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1

Nye, Colleen Klocek. "Assessing the Role of Glyceroneogenesis in Triglyceride Metabolism." Case Western Reserve University School of Graduate Studies / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=case1216141039.

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2

Relas, Heikki. "Metabolism of squalene in triglyceride-rich lipoproteins in humans." Helsinki : University of Helsinki, 2001. http://ethesis.helsinki.fi/julkaisut/laa/kliin/vk/relas/.

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3

Björkegren, Johan. "Triglyceride-rich lipoproteins : postprandial metabolism and composition in relation to atherosclerosis /." Stockholm, 1998. http://diss.kib.ki.se/search/diss.se.cfm?19980515bjor.

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4

Peterson, Jonathan M., Marcus M. Seldin, Zhikui Wei, Susan Aja, and G. William Wong. "CTRP3 Attenuates Diet-induced Hepatic Steatosis by Regulating Triglyceride Metabolism." Digital Commons @ East Tennessee State University, 2013. https://dc.etsu.edu/etsu-works/72.

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CTRP3 is a secreted plasma protein of the C1q family that helps regulate hepatic gluconeogenesis and is downregulated in a diet-induced obese state. However, the role of CTRP3 in regulating lipid metabolism has not been established. Here, we used a transgenic mouse model to address the potential function of CTRP3 in ameliorating high-fat diet-induced metabolic stress. Both transgenic and wild-type mice fed a high-fat diet showed similar body weight gain, food intake, and energy expenditure. Despite similar adiposity to wild-type mice upon diet-induced obesity (DIO), CTRP3 transgenic mice were strikingly resistant to the development of hepatic steatosis, had reduced serum TNF-α levels, and demonstrated a modest improvement in systemic insulin sensitivity. Additionally, reduced hepatic triglyceride levels were due to decreased expression of enzymes (GPAT, AGPAT, and DGAT) involved in triglyceride synthesis. Importantly, short-term daily administration of recombinant CTRP3 to DIO mice for 5 days was sufficient to improve the fatty liver phenotype, evident as reduced hepatic triglyceride content and expression of triglyceride synthesis genes. Consistent with a direct effect on liver cells, recombinant CTRP3 treatment reduced fatty acid synthesis and neutral lipid accumulation in cultured rat H4IIE hepatocytes. Together, these results establish a novel role for CTRP3 hormone in regulating hepatic lipid metabolism and highlight its protective function and therapeutic potential in attenuating hepatic steatosis.
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5

Starling, Raymond D. "Effects of exercise and diet on muscle triglyceride." Virtual Press, 1996. http://liblink.bsu.edu/uhtbin/catkey/1019481.

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The purpose of this investigation was to examine the effects of exercise and diet on muscle triglyceride. Seven endurance-trained men completed a 120min cycling bout at 65% of V O2max in an attempt to lower muscle glycogen and triglyceride. Each subject then ingested an isocaloric, high-carbohydrate (HI-CHO; 83% of kcal) or high-fat (HI-FAT; 68% of kcal) diet for the ensuing 24 h. A 1600 kJ cycling time trial was completed following this 24-h dietary period. Muscle glycogen concentration before (571±38 vs. 599±41 mmol•kg dw-1) and after (241±36 vs. 285±41 mmol•kg dw-1) the 120-min cycling bout was not different (P>0.05) between the HI-CHO and HI-FAT trials, respectively. Muscle triglyceride concentration before (33.0±2.3 vs. 37.0±2.1 mmol•kg dw-1) and after (30.9±2.4 vs. 32.8±1.6 mmol•kg dw-1) the 120-min cycling bout was also not different between the HI-CHO and HI-FAT trials, respectively. In addition, muscle triglyceride did not decrease significantly during the cycling bout for the HI-CHO (2.1±2.1 mmol•kg dw-1) or HI-FAT (4.2±1.8 mmol•kg dw-1) trial. Over the 24-h dietary period, a significantly greater amount of glycogen was resynthesized during the HI-CHO (308±41 mmol•kg dw-1) versus the HI-FAT trial (42±23 mmol•kg dw-1). Muscle triglyceride concentration increased 11.9±1.6 mmol•kg dw-1 (P<0.05) and decreased 3.4±1.8 mmol•kg dw-1 (P>0.05) during the 24-h dietary period for the HI-FAT and HI-CHO trials, respectively. Cycling performance time was significantly greater during the HI-FAT (139.3±7.1 min) compared to the HICHO (117.1±3.2) trial. The average V02 (3.40±0.12 vs. 2.96±0.17 L•min-1) and RER (0.89±0.01 vs. 0.82±0.01) during the time trial were higher for the HI-CHO than the HI-FAT trial, respectively. These data demonstrate that a small, insignificant amount of muscle triglyceride is utilized during prolonged, moderate-intensity cycling. Furthermore, 24 h of a high-fat diet increased muscle triglyceride concentration and reduced endurance performance.<br>Human Performance Laboratory
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6

Crawford, Lynne Mary. "The regulation of triglyceride metabolism in the liver and adipose tissue." Thesis, University of Glasgow, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.263457.

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7

Martinez, Alvaro. "Triglyceride metabolism and antiretroviral therapy in HIV infection : role of ApoAV." Paris 6, 2008. http://www.theses.fr/2008PA066070.

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Les thérapies antirétrovirales (ARV) efficaces ont transformé l’évolution et le pronostic de l'infection par le virus de l’immunodéficience humaine (VIH), du fait d’un meilleur contrôle de la réplication virale et de la restauration de certaines fonctions immunitaires. Les thérapies ARV couramment utilisées depuis 10 ans comprennent isolement ou de manière combinée des inhibiteurs de la protéase (IP) et/ou des inhibiteurs de la transcriptase inverse du VIH. Néanmoins, les thérapies ARV ont l’inconvénient d’induire des anomalies lipidiques (notamment une augmentation des triglycérides (TG) et du cholestérol (C) circulants), potentiellement associées à un surrisque de maladie cardiovasculaire. De manière plus spécifique, les traitements ARV contenant des IP semblent être pourvoyeurs d’anomalies plus fréquentes ou plus prononcées, notamment des lipoprotéines riches en TG (LRT). TG et C sont transportés dans la circulation sanguine par des complexes macromoléculaires appelés lipoprotéines (e. G. VLDL, LDL et HDL). Les taux sanguins de lipoprotéines résultent de l'équilibre entre leur synthèse, par les organes producteurs, leur remodelage et leur clearance. Les lipides sont transportés par la voie dite endogène depuis le foie jusque vers les tissus périphériques par les VLDL et LDL, alors que les HDL transportent principalement du cholestérol depuis les tissus périphériques jusque vers le foie par la voie dite inverse. Le métabolisme des lipoprotéines est effectuée sous des mécanismes fortement modulé par, entre autres facteurs, d’apolipoproteins (apo), d’enzymes (e. G. LPL) et de protéines de transfert des lipides (e. G. CETP). L'apoAV a été récemment identifiée comme un régulateur important du métabolisme des TG. Synthétisée principalement par le foi elle circule dans le sang associée aux HDL et VLDL. Le but principal de nos travaux était d’explorer les modifications du métabolisme lipidique induit par les IP chez l'homme et de déterminer les mécanismes qui les sous-tendent, avec un accent particulier porté à l’apoAV. Une première approche était d’explorer de manière prospective pendant 24 semaines les modifications du métabolisme des lipoprotéines chez 58 patients VIH+ sous une combinaison fixe d’ARV contenant l’IP Lopinavir (Lpv). Une augmentation (+94%) précoce et significative (p<0,001) des taux plasmatiques des LRT était constatée des la 2e semaine. De manière surprenante une forte augmentation (+28%, p<0,001) tardive du taux de cholestérol HDL (HDL-C) était constatée à 24 semaines. Le HDL-C était le seul paramètre lipidique corrélé à l'exposition au Lopinavir. De plus, en parallèle à l'augmentation des LRT, nous avons observé une forte augmentation de l’apoE (+27%) et de l'apoB (+11%) dans la population globale. A l’inverse, l’apoAV n’augmentait de manière significative que chez les patients naïfs de traitement ARV (+40%), alors qu’elle était constamment élevée chez les sujets prétraité. La fraction de l'apoAV associée aux HDL dans la circulation sanguine, était inchangée après 24 semaines de traitement avec Lpv, suggérant que l'augmentation de l'apoAV circulante était provoquée par l'augmentation des VLDL. De manière concomitante l’activité LPL (-31%) et de l’activité CETP (-3,4%) diminuaient significativement (p<0,02), suggérant une diminution de la clearance des LRT et une altération du transport inverse du cholestérol chez les patients traités par IP. Les marqueurs inflammatoires (CRP, TNFα et sTNF-RI) restaient dans les fourchettes normales de concentration avant et après 24 semaines de traitement. L’ensemble de ces observations suggèrent que: 1º) Malgré une augmentation significative de tous les paramètres lipidiques classiquement considérées comme athérogénes, les dyslipidémies étaient rares; 2º) Des effets biologiques spécifique du Lpv sur la seule fraction de HDL, résultant possiblement d’une baisse de l’activité CETP ; 3º) l’augmentation des LRT et de l’apoAV en parallèle pourrait résulter d’une baisse de l’activité LPL induite par le traitement ARV. En conséquence, nous nous sommes proposé d’explorer les éventuels mécanismes par lesquels la LPL et l’apoAV pourraient interagir pour moduler le métabolisme des TG.
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8

Izumi, Ryouta. "CRISPR/Cas9-mediated Angptl8 knockout suppresses plasma triglyceride concentrations and adiposity in rats." Kyoto University, 2019. http://hdl.handle.net/2433/242910.

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9

Mahat, Bimit. "The Effects of Hypoxia on Human Adipose Tissue Lipid Storage and Mobilization Functions: From Primary Cell Culture to Healthy Men." Thesis, Université d'Ottawa / University of Ottawa, 2017. http://hdl.handle.net/10393/36865.

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Adipose tissue plays a central role in the regulation of lipid storage and mobilization. A tight control between adipose tissue lipid storage and mobilization functions must be exerted to prevent an overload of lipids at other organs such as the heart, liver and skeletal muscles, and favor the risk of developing metabolic disorders, such as Type 2 diabetes and cardiovascular diseases (CVD). There is strong evidence from animal studies that low oxygen levels (hypoxia) are noted in adipose tissue as the mass of the organ excessively expands and, in turn, exacerbates some adipose tissue functions. Whether hypoxia exposure, which could be derived from reduced environmental oxygen availability, disease or a combination of both, affects adipose tissue lipid storage and mobilization functions in humans is not well known. Using in vitro and in vivo approaches, this thesis aimed at characterizing the effects of hypoxia on human adipose tissue lipid storage and lipid mobilization functions. Study I investigated how hypoxia can modulate human adipose functions such as lipid storage and lipid mobilization in vitro. Study II examined whether acute intermittent hypoxia, which simulates obstructive sleep apnea, affects adipose tissue lipid storage/mobilization functions and triglyceride levels in healthy young men in postprandial state. Study III tested the effect of an acute 6-hour continuous exposure to hypoxia (fraction of inspired oxygen (FIO2) = 0.12)) on plasma triglyceride levels in healthy young men in the fasting state. Study I indicates that both acute (24h) and chronic (14d) hypoxia (3%, and 10% O2) modulate human adipose tissue lipid storage and mobilization functions in a different manner. Study II demonstrates that acute exposure to intermittent hypoxia (6h) is sufficient to increase plasma non-esterified fatty acids (NEFA) levels, as well as insulin levels, but does not alter circulating triglyceride or subcutaneous adipose tissue lipid storage and/or mobilization capacity ex vivo in healthy men. Study III shows that acute exposure to normobaric hypoxia increases circulating NEFA and glycerol concentrations but did not translate in altering circulating triglycerides in fasting healthy men. In conclusion, our observations suggest that an exposure to reduced oxygen levels impairs human adipose tissue storage and/or mobilization functions, a phenomenon known in the development of metabolic disorders, such as Type 2 diabetes and CVD.
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10

Nilsson, Lennart. "Regulation of plasminogen activator inhibitor-1 : role of triglyceride-rich lipoproteins, fatty acids and fibrate compounds /." Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3443-6/.

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11

Wen, Xiao-Yan. "Characterization of a mouse insertional mutation lpd associated with a defect in triglyceride metabolism." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1995. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/NQ28158.pdf.

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12

Burgess, P. "The influence of different energy sources on hepatic microsomal enzyme activity and triglyceride metabolism." Thesis, University of Newcastle Upon Tyne, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.234400.

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13

區和盛 and Wo-shing Au. "Regulation of microsomal triglyceride transfer protein gene byinsulin: the involvement of MAPKerk cascadeand HNF-1." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2001. http://hub.hku.hk/bib/B31225615.

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14

Stears, Anna J. "The effect of adiposity on triglyceride metabolism in men and women with and without Type 2 Diabetes Mellitus." Thesis, University of Southampton, 2011. https://eprints.soton.ac.uk/375271/.

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15

Cooper, David L., Derek E. Murrell, David Roane, and Sam Harirforoosh. "Effects of Formulation Design on Niacin Therapeutics: Mechanism of Action, Metabolism, and Drug Delivery." Digital Commons @ East Tennessee State University, 2015. https://dc.etsu.edu/etsu-works/7166.

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Niacin is a highly effective, lipid regulating drug associated with a number of metabolically induced side effects such as prostaglandin (PG) mediated flushing and hepatic toxicity. In an attempt to reduce the development of these adverse effects, scientists have investigated differing methods of niacin delivery designed to control drug release and alter metabolism. However, despite successful formulation of various orally based capsule and tablet delivery systems, patient adherence to niacin therapy is still compromised by adverse events such as PG-induced flushing. While the primary advantage of orally dosed formulations is ease of use, alternative delivery options such as transdermal delivery or polymeric micro/nanoparticle encapsulation for oral administration have shown promise in niacin reformulation. However, the effectiveness of these alternative delivery options in reducing inimical effects of niacin and maintaining drug efficacy is still largely unknown and requires more in-depth investigation. In this paper, we present an overview of niacin applications, its metabolic pathways, and current drug delivery formulations. Focus is placed on oral immediate, sustained, and extended release niacin delivery as well as combined statin and/or prostaglandin antagonist niacin formulation. We also examine and discuss current findings involving transdermal niacin formulations and polymeric micro/nanoparticle encapsulated niacin delivery.
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16

Liu, Ke-di. "The interaction of obesity and age and their effect on adipose tissue metabolism in the mouse." Thesis, University of Cambridge, 2019. https://www.repository.cam.ac.uk/handle/1810/290384.

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Numerous studies have investigated how bulk lipid metabolism is influenced in obesity and in particular how the composition of triglycerides found in the cytosol change with increased adipocyte expansion. However, in part reflecting the analytical challenge the composition of cell membranes, and in particular glycerophospholipids, an important membrane component, have been seldom investigated. Cell membrane components contribute to a variety of cellular processes including maintaining organelle functionality, providing an optimized environment for numerous proteins and providing important pools for metabolites, such as choline for one-carbon metabolism and S-adenosylmethionine for DNA methylation. Here, I have conducted a comprehensive lipidomic and transcriptomic study of white adipose tissue in mice that become obese either through genetic modification (ob/ob genotype), diet (high-fat diet) or a combination of the two across the life course. Specifically, I demonstrated that the changes in triglyceride metabolism that dominate the overall lipid composition of white adipose tissue were distinct from the compositional changes of glycerophospholipids. These latter lipids became more unsaturated to maintain the fluidity and normal function of the membrane in the initiation of obesity but then turned saturated after long-term administration of HFD and aging. This suggests that while triglycerides within the adipose tissue may be a relatively inert store of lipids, the compositional changes occur in cell membranes with more far-reaching functional consequences in both obesity and aging. The two-phase change of phospholipids can be correlated well with transcriptional and one-carbon metabolic changes within the adipocytes. The transcriptomic study demonstrated that the lipid metabolic pathways regulated by the peroxisome, AMPK, insulin and PPARγ signaling were activated in the initiation of obesity but inhibited in the adipose tissue of old ob/ob mice along with up-regulated inflammation pathways. The brown and white adipose tissue of PPARα-knock-out mice were also studied by lipidomic tools to get a deeper understanding of the effect of the peroxisome and PPAR system on adipose tissue and lipid metabolism during obesity. Most of the lipids were increased and became more saturated and shorter in adipose tissues of PPARα null mice, which is in good accordance with the results of the former animal study. In conclusion, my work using different rodent models and multi-omics techniques demonstrated a protective metabolic mechanism activated in the initiation but impaired at the end of the processes of obesity and aging, which could be an explanation of the similarity of obesity and aging in terms of high incidence of the metabolic syndrome and related diseases.
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17

Tsai, Yu-Hwai. "Regulatory effects of medium chain triglyceride (8:0+10:0) and lauric acid (12:0) and APO(A) polymorpohism on plasma lipoprotein cholestrol metabolism and LP(A) concentrations /." The Ohio State University, 1998. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487951214937113.

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18

Mazur, Andrzej. "Contribution a l'etude de l'infiltration lipidique du foie chez la vache laitiere en debut de lactation." Clermont-Ferrand 2, 1986. http://www.theses.fr/1986CLF21040.

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19

Chatterjee, Cynthia. "Purinergic Signaling and Autophagy Regulate the Secretion of High-Density Lipoprotein and Hepatic Lipase." Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/24027.

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Dyslipidemia can be a comorbidity of both insulin-resistance and atherosclerosis. Hypertriglyceridemia is common in hyperglycemia and is associated with hypoalphalipoproteinemia (low HDL) and with altered nucleotide or purinergic signaling. We therefore hypothesized that extracellular nucleotides may affect hepatic lipoprotein metabolism. Our studies confirm this view and show that nucleotides regulate cellular proteolytic pathways in liver cells and thereby control lipoprotein secretion and their metabolism by hepatic lipase (HL). Treatment of liver cells with the nucleotide, adenosine diphosphate (ADP), stimulates VLDL-apoB100 and apoE secretion, but blocks HDL-apoA-I and HL secretion. ADP functions like a proteasomal inhibitor to block proteasomal degradation and stimulate apoB100 secretion. Blocking the proteosome is known to activate autophagic pathways. The nucleotide consequently stimulates autophagic degradation in liver cells and increases cellular levels of the autophagic proteins, LC3 and p62. Confocal studies show that ADP increases cellular LC3 levels and promotes co-localization of LC3 and apoA-I in an autophagosomal degradation compartment. ADP acts through the G-protein coupled receptor, P2Y13, to stimulate autophagy and block both HDL and HL secretion. Overexpression of P2Y13 increases cellular LC3 levels and blocks the induction of both HDL and HL secretion, while P2Y13 siRNA reduce LC3 protein levels and cause up to a ten-fold stimulation in HDL and HL secretion. P2Y13 gene expression regulates autophagy through the insulin receptor (IR-β). A reduction in P2Y13 expression increases the phosphorylation of IR-β and protein kinase B (Akt) >3-fold, while increasing P2Y13 expression inhibits the activation of IR-β and Akt. Experiments with epitope-labeled apoA-I and HL show that activation of purinergic pathways has no effect on the internalization and degradation of extracellular apoA-I and HL, which confirms the view that nucleotides primarily impact intracellular protein transport and degradation. In conclusion, elevated blood glucose levels may promote dyslipidemia by stimulating purinergic signaling through P2Y13 and IR-β and perturbing the intracellular degradation and secretion of both HDL and VLDL.
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20

Chambaz, Jean. "Metabolisme des acides gras essentiels par les hepatocytes de rat en culture." Paris 6, 1988. http://www.theses.fr/1988PA066669.

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La composition en apolipoproteines des lipoproteines synthetisees et secretees par des hepatocytes a ete caracterisee par immuntransfert et immunolocalisation. Les mecanismes de constitution et secretion de pools de lipides porteurs des acides gras essentiels sont caracterises
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21

Borel, Patrick. "Effets du son et du germe de ble sur l'activite in vitro de la lipase pancreatique, et sur la digestion et le metabolisme des lipides chez le rat." Aix-Marseille 2, 1987. http://www.theses.fr/1987AIX22078.

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22

Petkevicius, Kasparas. "The role of macrophage intracellular lipid partitioning in glucose and lipid homeostasis during obesity." Thesis, University of Cambridge, 2019. https://www.repository.cam.ac.uk/handle/1810/285429.

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Obesity-associated metabolic disorders are amongst the most prevalent causes of death worldwide. Understanding how obesity leads to the development of the Metabolic Syndrome (MetS) and cardiovascular disease (CVD) will enable the development of novel therapies that dissociate obesity from its cardiometabolic complications. Our laboratory views the functional capacity of white adipose tissue (WAT), the organ designed for safe lipid storage, as a key factor in the development of MetS and CVD. At a genetically-defined stage of the aberrant WAT expansion that occurs during obesity, adipocytes undergo a functional failure, resulting in an impaired control of serum free fatty acid (FFA) concentration. In such setting, FFAs and their metabolic derivatives accumulate in other organs, where they cause lipotoxicity, leading to the development of insulin resistance and CVD. We therefore aim to understand the pathophysiological mechanisms that induce adipocyte dysfunction. The past two decades of research have established the immune system as an important regulator of WAT function. The number of adipose tissue macrophages (ATMs), the most abundant immune cell type in WAT, increases during obesity, resulting in WAT inflammation. Multiple genetic and pharmacological intervention studies of murine models of obesity have assigned a causal link between ATM pro-inflammatory activation and WAT dysfunction. However, while the propagation of inflammation in ATMs during obesity has been extensively studied, factors triggering ATM inflammatory activation are less clear. Recently, our lab has observed lipid accumulation in the ATMs isolated from obese mice. Lipid-laden ATMs were pro-inflammatory, leading us to hypothesise that aberrant lipid build-up in macrophages triggers WAT inflammation during obesity. This thesis expands on the initial findings from our lab and describes two novel mechanisms that potentially contribute to lipid-induced inflammatory activation of ATMs. In chapter 3, the role of de novo phosphatidylcholine (PC) synthesis pathway during lipotoxicity in macrophages is addressed. The first part of the chapter demonstrates that lipotoxic environment increased de novo PC synthesis rate in bone marrow-derived macrophages (BMDMs) and ATMs, and that loss of rate-limiting enzyme in de novo PC synthesis pathway, CTP:phosphocholine cytidylyltransferase a (CCTa) diminished saturated FFA-induced inflammation in BMDMs. In the second part, I show that macrophage-specific CCTa deletion did not impact on the development of WAT inflammation or systemic insulin resistance, but had a minor benefitial effect on hepatic gene transcription during obesity. Chapter 4 develops on recent observations of interactions between sympathetic nerves and macrophages in WAT. In the first part of the chapter, I demonstrate that stimulating B2-adrenergic receptor (B2AR), the main receptor for sympathetic neurotransmitter norepinephrine in macrophages, enhanced intracellular triglyceride storage by up-regulating diacylglycerol O-acyltransferase 1 (Dgat1) gene expression in BMDMs. The second part of the chapter shows that macrophage-specific B2AR deletion did not modulate systemic glucose and lipid metabolism during obesity, but mice lacking B2ARs in macrophages demonstrated augmented hepatic glucose production on a chow diet. Furthermore, systemic B2AR blockade or macrophage-specific B2AR deletion in mice did not affect the thermogenic response to cold exposure. Chapter 5 includes the characterisation of B2AR stimulation-induced changes to the global cellular proteome of BMDMs, and a subsequent validation of the role of candidate transcription factors in regulating B2AR agonism-induced gene expression in BMDMs.
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Padilla, Nadège. "Effets des différentes techniques de chirurgie bariatrique sur le métabolisme des lipoprotéines riches en triglycérides(LRT) intestinales et hépatiques chez le patient obèse." Thesis, Aix-Marseille, 2014. http://www.theses.fr/2014AIXM5020/document.

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Introduction/objectif : La dyslipidémie des sujets obèses insulinorésistants est principalement caractérisée par une augmentation plasmatique des LRT hépatiques (LRT-apo-B100) et intestinales (LRT-apo-B48). La chirurgie bariatrique, largement pratiquée dans le traitement de l'obésité, est associée à l'amélioration de nombreuses anomalies métaboliques. Nous avons étudié l'effet de la chirurgie bariatrique sur le métabolisme des LRT intestinales et hépatiques.Méthodes/résultats : Le métabolisme des LRT de 22 patients obèses non diabétiques bénéficiant d'une chirurgie bariatrique : sleeve gastrectomie (SG ; n=12) ou bypass gastrique (BP ; n=10) a été étudié par une méthode d'enrichissement isotopique stable (D3-L-Leucine) en alimentation continue. Chaque sujet a réalisé deux études cinétiques : une 1 mois avant et une 6 mois après la chirurgie. Le résultat principal est une diminution de la taille du pool de LRT-apo-B100 après une SG et un BP (p&lt;0,01) expliquée par une augmentation du taux de clairance des LRT-apo-B100 (SG : p&lt;0,05) sans diminution du taux de production. Le pool de LRT-apo-B48 est significativement réduit après une SG (p&lt;0,05), sans explication claire à part une tendance à la diminution du taux de production. La diminution du pool de LRT-apo-B100 est significativement corrélée à la diminution de la concentration en apo-CIII dans le groupe entier.Conclusion : Cette étude est la première étude cinétique réalisée chez l'Homme explorant les mécanismes d'amélioration du métabolisme des LRT après une chirurgie bariatrique. Cette amélioration du métabolisme peut contribuer à la diminution de la mortalité cardiovasculaire observée après une chirurgie bariatrique<br>Introduction and objective: The dyslipidemia of insulin-resistant obese patients is widely characterised by the elevation of plasma triglyceride-rich lipoproteins (TRL) of both hepatic (TRL-apoB-100) and intestinal (TRL-apoB-48) origin. Bariatric surgery is a well-established and effective modality for the treatment of obesity, and is associated with improvements in a number of metabolic abnormalities that are associated with obesity. Here, we have investigated the effect of bariatric surgery on intestinal and hepatic TRL metabolism. Approach and Results: Twenty two non-diabetic, obese subjects undergoing bariatric surgery: sleeve gastrectomy (SG; n=12) and gastric bypass (BP; n=10) were studied using a stable isotope (D3-L-Leucine) enrichment methodology, in the constant fed state. Each subject underwent two lipoprotein turnover studies: 1 month before and 6 months after surgery. The main finding was a reduction in TRL-apo-B100 concentration following both SG and BP procedures (P&lt;0.01 for both), explained by an increase in TRL-apo-B100 fractional catabolic rate (P&lt;0.05 for SG) without a reduction in production rate. TRL-apo-B48 concentration was significantly reduced following SG, with no clear explanation other than a trend towards reduction in production rate. The reduction of TRL-apo-B100 concentration was significantly associated with a reduction of plasma apo-CIII in the pooled group of patients undergoing bariatric surgery. Conclusions: This is the first human kinetic study to explore the mechanism of improvement of TRL metabolism following bariatric surgery. These effects may contribute to the decrease of cardiovascular mortality after surgery
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24

Cushing, Emily Malcolm. "Regulation of plasma triglycerides by ANGPTL4 and GPIHBP1." Diss., University of Iowa, 2018. https://ir.uiowa.edu/etd/6399.

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The absorption, packaging, and delivery of fat to appropriate peripheral tissues is essential for maintaining metabolic homeostasis, and defects or dysregulation of these processes can contribute to metabolic disorders such as diabetes, obesity, and hyperlipidemia. In the intestine, dietary fat is packaged into triglyceride-rich lipoprotein particles and delivered to peripheral tissues through the circulatory system. Lipolysis of lipoprotein triglycerides requires the enzyme lipoprotein lipase (LPL) and takes place on the luminal surface of capillary endothelial cells. Lipolysis by LPL is regulated in part by two proteins, GPIHBP1 and ANGPTL4. GPIHBP1, a GPI-anchored protein of capillary endothelial cells, is responsible for transporting LPL across endothelial cells to the capillary lumen. Without this transport, LPL becomes mislocalized to the interstitial space and cannot access triglyceride-rich lipoproteins, resulting in severe hypertriglyceridemia. Conversely, ANGPTL4 inhibits LPL and ANGPTL4 deficiency results in increased LPL activity and lower plasma triglyceride levels. Our goal is to understand how the interactions between LPL, GPIHBP1, and ANGPTL4 influence the delivery of triglyceride-derived fatty acids to tissues. In this thesis, I (1) use mouse models to elucidate the function of ANGPTL4 in regulating the clearance of diet-derived fat from plasma, (2) describe a mechanism for GPIHBP1-independent plasma triglyceride clearance observed in mice lacking both GPIHBP1 and ANGPTL4, and (3) propose that this GPIHBP1-independent mechanism is also operative in Gpihbp1–/– mice following a high fat diet challenge. The contributions of this thesis are significant because they close a gap in our knowledge of how and where ANGPTL4 functions, as well as indicating that, when ANGPTL4 is suppressed or absent altogether, a GPIHBP1-independent mechanism can function to clear plasma triglycerides.
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BURGNELLE-MAYEUR, CAMILLE. "Influence du gene de nanimse (dw) sur le metabolisme lipidique de la poule pondeuse." Paris 7, 1988. http://www.theses.fr/1988PA077024.

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26

Morin, Renée. "The Effect of Acute Intermittent Hypoxia on Postprandial Lipid Metabolism." Thesis, Université d'Ottawa / University of Ottawa, 2020. http://hdl.handle.net/10393/40537.

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Background: Obstructive sleep apnea (OSA) consists of repeated, involuntary breathing suspension during sleep. These events induce rapid depletion/repletion of blood/tissue oxygen content, a phenomenon known as intermittent hypoxia. Aside from causing daytime sleepiness, the most important health consequence of OSA is a 2-fold increase in cardiovascular (CVD) risk. Animal studies provide evidence that intermittent hypoxia, a simulating model of OSA, causes important rise in plasma TG, especially in the postprandial state. However, the underpinning mechanisms linking intermittent hypoxia to altered postprandial TG levels remain unknown. As such, the objective of this study was to characterize the effects of acute intermittent hypoxia on postprandial TG levels in 2 distinct lipoprotein subtypes in humans: chylomicrons which are secreted by the intestine and carry dietary lipids, and denser TG carriers (mainly VLDL) which are secreted by the liver and carry endogenous lipids. Methods: The research consisted of a randomized crossover design. In collaboration with the Sleep laboratory at Montfort Hospital, 7 individuals diagnosed with moderate sleep apnea were recruited through phone calls as well as 8 healthy individuals without OSA from the University of Ottawa. While lying on a bed, participants were given a meal after which they were exposed for 6 hours to normoxia or intermittent hypoxia corresponding to moderate OSA, e.g. 15 hypoxic events per hour. Blood lipid levels were measured hourly.  Results: Plasma TG levels increased over time in both experimental conditions and tended to be greater under 6-h exposure to intermittent hypoxia (p=0.093, effect size ηp2= 0.383.). This trend toward higher total plasma TG under intermittent hypoxia was attributable to increased levels in denser TG carrying lipoproteins such as VLDL and CM remnants (p= 0.009, ηp2 = 0.173).  Conclusion: Acute intermittent hypoxia, a simulating model of obstructive sleep apnea, tends to negatively affect postprandial TG levels, which is attributable to an increase in denser TG carrying lipoprotein levels such as VLDL and CM remnants. These results lend support to the increase in blood lipid levels in animal studies observing the effect of acute hypoxia in mice.  Contribution to advancement of knowledge: This proposed research will allow a better understanding of the mechanisms by which obstructive sleep apnea may alter blood lipid profile. This information will be beneficial to the treatment of obstructive sleep apnea related dyslipidemia and contribute to reduce CVD risk in the large proportion of obstructive sleep apnea patients who are reluctant to current treatment avenues.
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27

Emerson, Sam R. "Postprandial metabolism and inflammation: novel insights focusing on true-to-life application." Diss., Kansas State University, 2017. http://hdl.handle.net/2097/35605.

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Doctor of Philosophy<br>Department of Human Nutrition<br>Sara Rosenkranz<br>The aims of this dissertation were to provide innovative, applicable insights regarding the impact of single-meal consumption on metabolic and inflammatory responses in the acute post-meal (“postprandial”) period. In Chapter 2, the connection between large postprandial glucose and triglyceride (TG) fluxes and cardiovascular disease (CVD) risk were reviewed. A new marker of metabolic status, Metabolic Load Index (MLI), calculated by adding glucose and TG, was proposed based on several considerations: 1) independent associations between postprandial glucose and TG with CVD risk, although the substrates are considered to increase risk through similar mechanisms; 2) postprandial glucose and TG responses are interrelated; and 3) meals consumed in daily life typically contain both carbohydrate and fat. MLI may be useful in characterizing metabolic status/risk in both clinical and research settings. Chapter 3 was a systematic review with the purpose of objectively describing postprandial responses (i.e. magnitude and timing) to a high-fat meal (HFM) in five commonly assessed inflammatory markers: interleukin (IL)-6, C-reactive protein (CRP), tumor necrosis factor (TNF)-α, IL-1β, and IL-8. IL-6 increased in >70% of studies, starting at ~1.4 pg/mL pre-meal and peaking at ~2.9 pg/mL ~6 hours post-HFM. Other markers (CRP, TNF-α, IL-1β, and IL-8) did not change after the HFM in the majority of studies. These findings suggest that IL-6 is an inflammatory marker that routinely increases following HFM consumption. Future postprandial studies should further investigate IL-6, as well as explore novel markers of inflammation. In Chapter 4, we compared the metabolic and inflammatory responses to a HFM (17 kcal/kg, 60% fat), representative of meals used in previous postprandial studies, to two meal trials that were more reflective of typical eating patterns: a moderate-fat meal (MFM; 8.5 kcal/kg, 30% fat), and a biphasic meal (BPM), in which the MFM was consumed twice, three hours apart. The HFM elicited a greater total area-under-the-curve (tAUC) TG response (1348.8 ± 783.7 mg/dL x 6 hrs) compared to the MFM (765.8 ± 486.8 mg/dL x 6 hrs; p = 0.0005) and the BPM (951.8 ± 787.7 mg/dL x 6 hrs; p = 0.03), but the MFM and BPM were not different (p = 0.72). It appears that the large postprandial TG response observed in previous studies may not be representative of the daily metabolic challenge for many individuals. Chapter 5 assessed the impact of both aging and chronic physical activity level on postprandial metabolic responses by comparing three groups: younger active (YA), older active (OA), and older inactive (OI) adults. The TG tAUC response was lower in YA (407.9 ± 115.1 mg/dL x 6 hr) compared to OA (625.6 ± 169.0 mg/dL x 6 hr; p = 0.02) and OI (961.2 ± 363.6 mg/dL x 6 hr; p = 0.0002), while the OA group TG tAUC was lower than OI (p = 0.02). Thus, it is likely that both aging and chronic physical activity level impact the postprandial metabolic response. This series of projects provides needed clarification regarding the postprandial metabolic and inflammatory responses to single-meal intake, particularly in the context of real-life application.
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Najjar, Amal. "Etude quantitative de la sécrétion de lipase, de la lipolyse et du stockage de lipides chez Yarrowia lipolytica lors de sa croissance en présence d'huile d'olive." Thesis, Aix-Marseille 2, 2010. http://www.theses.fr/2010AIX22100/document.

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La sécrétion de lipase, la lipolyse extracellulaire et l’absorption des acides gras (AGL) ont été étudiés chez Yarrowia lipolytica (YL) en présence d’huile d’olive et/ou de sucrose. Des mesures d’activité lipase et d’immuno-révélation ont montré que l’activité lipase présente dans le milieu de culture provenait principalement de la lipase YLLIP2. L’huile d’olive induit la production de lipase qui est principalement associée aux cellules pendant les premières heures de cultures. YLLIP2 est ensuite libérée dans le milieu de culture avant d’être totalement dégradée par les protéases. Les triglycérides (TG) sont dégradés alors que la lipase est encore attachée aux cellules. Les produits de lipolyse présents dans le milieu de culture et à l’intérieur des cellules ont été quantifiés par chromatographie TLC-FID et GC. Les niveaux intracellulaires d’AGL et de TG augmentent transitoirement et dépendent de la source de carbone utilisée. Une accumulation maximum de 37,8 % w/w de lipides est observée avec l’huile d’olive seule. Cette étude montre que la levure YL est un modèle intéressant pour étudier la lipolyse extracellulaire et l’absorption des acides gras par les cellules<br>Lipase secretion, extracellular lipolysis and fatty acid (FFA) uptake were quantified in Yarrowia lipolytica (YL) grown in the presence of olive oil and/or sucrose. Lipase assays and western blot analysis indicated that the lipase activity measured in YL cultures mainly resulted from YLLIP2 lipase. Lipase production was triggered by olive oil and YLLIP2 remained associated with the yeast cells during the first hours of culture. It was then released in the culture medium before it was totally degraded by the alkaline protease. Olive oil triglycerides (TG) were degraded when the lipase was still attached to the cell wall. The fate of lipolysis products in the culture medium and inside the yeast cell were investigated by quantitative TLC-FID and GC analysis. Intracellular levels of FFA and TG increased transiently and were dependent on the carbon sources. A maximum fat storage of 37.8% w/w was observed with olive oil alone. The present study shows that yeasts are interesting models for studying extracellular lipolysis and fat uptake by the cell
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Mourot, Jacques. "Contribution à l'étude du rôle des phytostérols sur le métabolisme du cholestérol et des lipides chez le rat." Nancy 1, 1989. http://www.theses.fr/1989NAN10351.

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30

LE, FUR CATHERINE. "Interaction entre le stress et les variations nycthemerales sur le metabolisme des lipides (doctorat : nutrition)." Lille 2, 1999. http://www.theses.fr/1999LIL2T014.

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31

Giribela, Aricia Helena Galvão. "Avaliação da influência da menopausa no tamanho das partículas da HDL e na sua capacidade de receber lipídios de uma nanoemulsão semelhante à LDL." Universidade de São Paulo, 2007. http://www.teses.usp.br/teses/disponiveis/5/5139/tde-23102007-111819/.

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Concentração de apolipoproteína A-1 (1.5±0.3; 1.5±0.2g/l). O tamanho da HDL também foi igual entre os dois grupos (8.8±0.8; 9.0±0.5 nm, respectivamente). A menopausa também não afetou a transferência de lípides da LDE para a HDL (em % total de radioatividade/10mg HDL/h), CE (0.5±0.3; 0.5±0.2, respectivamente), CL (0.9±0.2; 0.9±0.2), TG (0.6±0.2;0.6±0.2) e PL (3.0±0.7; 3.3±1.0). Conclusão: A menopausa não Introdução: A concentração plasmática da HDL é um fator de risco importante e independente para a prevenção da doença aterosclerótica, principalmente na mulher. Seu metabolismo e suas características estruturais e funcionais também têm sido estudados como fatores de risco. Neste estudo, foram comparadas mulheres de mesma faixa etária na pré e na pós-menopausa, para determinar a influência da menopausa sobre o tamanho da HDL e sobre a habilidade desta lipoproteína em receber lipídios de lipoproteínas doadoras, um processo que depende de proteínas de transferência e da composição e estrutura da HDL. Métodos: Vinte e duas mulheres saudáveis, normolipidêmicas na pré e dezoito na pós-menopausa, de idades entre 40-50 anos foram estudadas. Os grupos não diferiam em IMC, glicemia, colesterol total, LDL, triglicérides, apo A1 e apo B. Uma nanoemulsão artificial foi usada como modelo de LDL (LDE) para doar lípides para a HDL. LDE marcada radioativamente com 3 H-triglicérides (TG) e 14 C-colesterol livre (CL) ou 3 H- ésteres colesterol (CE) e 14 C-fosfolipídios (PL) foram incubados com as amostras de plasma por 1 hora. Após a precipitação química do sobrenadante contendo HDL, foi contada a radioatividade. O tamanho da HDL foi medido por espalhamento da luz laser. Resultados: A concentração da HDL nos dois grupos não diferiu, demonstrada pela concentração de HDL colesterol (61±12; 61±14 mg/dl respectivamente) e influenciou o tamanho das partículas HDL e um importante parâmetro funcional que é a habilidade da HDL de receber lipídios.<br>Objective: HDL levels are important for atherosclerosis prevention especially in the female gender, but functional aspects of the lipoprotein are also important. In this study, post-menopausal were compared to pre-menopausal women in the same age range to determine the influence of menopause upon the HDL size and ability of the lipoprotein to receive lipids from donor lipoproteins, a process that depends on transfer proteins and on HDL composition and structure. Methods: Twenty-two pre and eighteen postmenopausal, healthy and normolipidemic women, aged 40-50 yr. Both groups did not differ in BMI and plasma glucose, total and HDL cholesterol, triglycerides and apo B concentration. An artificial nanoemulsion (LDE) was used as a model of LDL to donate lipids to HDL. LDE labeled with 3 H-triglicerides (TG) and 14 C-free cholesterol (FC) or 3 H-cholesteryl esters (CE) and 14 C-phospholipids (PL) incubated with plasma samples for 1h. After chemical precipitation, the supernatant containing HDL was counted for radioactivity. HDL size was measured by laser-light-scattering. Results: HDL concentration of pre and post menopausal women did not differ as estimated by HDL cholesterol (61±12; 61±14 mg/dl respectively) and apo A1 concentration (1.5±0.3; 1.5±0.2g/l). HDL size also did not differ (8.8±0.8; 9.0±0.5 nm, respectively). Menopause also did not affect the transfer of lipids from LDE to HDL (in % of total radioactivity/10mg HDL/h), namely CE (0.5±0.3; 0.5±0.2, respectively), FC (0.9±0.2; 0.9±0.2), TG (0.6±0.2;0.6±0.2) and PL (3.0±0.7; 3.3±1.0). Conclusion: The menopause does not affect the size and an important functional parameter that is the ability of HDL to receive lipids.
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Näsström, Birgit. "Lipoprotein lipase in hemodialysis patients and healthy controls : effects of heparin." Doctoral thesis, Umeå universitet, Medicin, 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-340.

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Mortality from cardiovascular disease in patients on chronic hemodialysis (HD) is 10 to 20 times greater than in the general population. One major risk factor is renal dyslipidemia, characterised by an impaired catabolism of triglyceride (TG)-rich lipoproteins with accumulation of atherogenic remnant particles. A contributing factor may be derangement of the lipoprotein lipase (LPL) system, the major lipase in the catabolism of TG-rich lipoproteins. The functional pool of LPL is located at vascular surfaces, and is released by heparin into the circulating blood and extracted and degraded by the liver. Unfractionated heparin (UFH) is commonly used during dialysis to avoid clotting in the extracorporeal devices, but is increasingly replaced by various low molecular weight heparin (LMWH) preparations. Plasma LPL activity is usually lower after injection of LMWH which is therefore said to release less LPL and cause less disturbance of lipoprotein metabolism than UFH. However, animal studies have revealed that LMWH is as efficient as UFH in releasing LPL but is less efficient in retarding hepatic uptake. The aim of this study was to explore the effects of UFH and a LMWH (dalteparin) on LPL activity and TG concentrations in HD-patients compared with healthy controls, matched for age and gender. A disturbed LPL system might contribute to an impaired lipoprotein metabolism, and hence, an aggravated cardiovascular condition. An 8-hour primed infusion of UFH to controls gave rise to an initial peak of LPL activity within 30 minutes. The activity then dropped by almost 80% over the next two hours and levelled off to a plateau that corresponded to 15% of the peak level. When UFH was infused to HD-patients the curve for LPL activity resembled that for controls, but was reduced by 50% during the peak, while the plateau activities were comparable. The interpretation was that the functional pool, represented by the initial peak, was impaired in HD-patients, while the production of lipase molecules, reflected by the plateau, was only marginally reduced. During the peak of LPL activity TG decreased in both groups, but less in HD-patients, as was expected from the lower circulating lipase activity. During the plateau phase with low lipase activity, TG increased towards and beyond baseline values. When dalteparin was infused, the same pattern of plasma LPL activity was observed, although remarkably reduced. In controls the peak was only 30% and the subsequent plateau 40% compared with the activities during the UFH infusion. A bolus of UFH given when the LPL activity had levelled off to a plateau brought out about the same amount of activity, regardless of whether dalteparin or UFH had been infused. The conclusion was that both heparin preparations had reduced endothelial LPL to a similar extent, but that dalteparin less efficiently retarded the hepatic uptake of the enzyme. As a consequence to this, TG tended to reach higher levels after the dalteparin infusion. The LPL activities were further reduced in HD-patients during infusion with dalteparin, the peak was only 27% and the plateau 35% compared with the activities when UFH was infused. There was no decrease in TG, but rather a continuous increase, suggesting a profound depletion of functional LPL. In another study in HD-patients, two anticoagulation regimes based on present clinical practice were compared, and the doses were adjusted to the respective manufacturers recommendation. UFH was administered as a primed infusion, whereas dalteparin was given only as a single bolus pre-dialysis, not followed by an infusion. The results were in line with those in the experimental studies and indicate that also in the clinical setting LMWH interferes with the LPL system as least as much as an infusion of UFH does, and temporarily impairs lipolysis of TG. This interference might, in consequence, contribute to an aggravated cardiovascular condition in HD-patients.
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Matos, Eduardo Pompeo de. "Resposta do sistema imunológico e do metabolismo intermediário de ratos wistar machos tratados com nonilfenol etoxilado." reponame:Repositório Institucional da UCS, 2018. https://repositorio.ucs.br/11338/3859.

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O nonilfenol etoxilado (NPE) é um desregulador endócrino que está presente no meio ambiente devido ao seu uso como detergente nos processos de limpeza de efluentes industriais. O objetivo deste trabalho foi avaliar a influência do NPE sobre o sistema imune adaptativo em ratos Wistar machos. Nestes animais foram avaliados o efeito do NPE sobre as células linfocitárias periféricas através da realização de hemograma e do perfil linfocitário adaptativo, analisando os marcadores de superfície CD4, CD8, CD28 e CD45 RA. Foi também avaliado o efeito do tratamento sobre o fígado e baço, bem como sobre o metabolismo intermediário, através das análises de glicemia, triglicerídeos e colesterol. Os dados não demonstraram diferenças significativas em relação ao índice hepático e esplênico. O nível de triglicerídeos apresentou um aumento de 50% nos grupos tratados, na avaliação dos níveis de colesterol e glicose não foi demonstrado diferenças significativas entre os grupos. Os resultados indicaram que o número de linfócitos e monócitos dos grupos tratados tiveram uma queda significativa de aproximadamente 25% e 50% em relação ao grupo controle. Foi demonstrado que o número de células fortemente marcadas quanto à presença da proteína CD45RA High na superfície celular dos linfócitos é maior nas células dos ratos do grupo tratado e que o tratamento aumenta a relação entre as células CD45RA High/Dim. Esses resultados levantam a hipótese que as células aumentadas nos grupos tratados apresentam fenótipo de membrana compatível com células T terminalmente diferenciadas (TEMRA). Este estudo forneceu dados novos sobre a ação do NPE, até onde se tem conhecimento, é a primeira pesquisa a constatar a presença elevada de células TEMRA em animais tratados com NPE, contribuindo com um novo foco para futuras pesquisas dessa substância.<br>Conselho Nacional de Desenvolvimento Científico e Tecnológico, CNPq<br>Ethoxylated nonylphenol (NPE) is an endocrine disruptor that is present in the environment because of its use as a detergent in the industrial effluent cleaning processes. The objective of this work was to evaluate the influence of ethoxylated nonylphenol (NPE) on the adaptive immune system in male Wistar rats. In these animals, the effect of NPE on peripheral lymphocyte cells was evaluate by performing hemogram and adaptive lymphocytic profile, analyzing CD4, CD8, CD28 and CD45 RA surface markers. The effect of treatment on the liver and spleen, as well as on the intermediate metabolism, was also evaluate through glycemic, triglyceride and cholesterol analyzes. The data did not show significant differences in relation to the hepatic and splenic index. The level of triglycerides presented a 50% increase in the treated groups; in the evaluation of cholesterol and glucose levels, no significant differences between the groups were demonstrate. The results indicated that both, the number of lymphocytes and monocytes of the treated groups had a significant decrease of approximately 25% and 50% relative to the control group. The number of strongly labeled cells for the presence of the CD45RA High protein on the cell surface of the lymphocytes showed to be higher in the cells of the mice in the treated group and that the treatment increases the ratio between the CD45RA High/Dim cells. These results raise the hypothesis that enlarged cells in the treated groups exhibit terminally differentiated T cell (TEMRA). This study provided new data on the action of NPE, to the best of our knowledge, is the first research to verify the elevated presence of TEMRA cells in animals treated with NPE. In addition, these findings contribute a new focus for future research on this substance.
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del, Bas Prior Josep Maria. "Modulation of hepatic lipoprotein metabolism by dietary procyanidins." Doctoral thesis, Universitat Rovira i Virgili, 2007. http://hdl.handle.net/10803/8662.

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INTRODUCTION<br/>During the past decade, Nutrition research has been subjected to a shift of focus, from epidemiology and physiology to the comprensión of the molecular basis of nutrients actions.<br/>Thus, the new "-omics" disciplines transcriptomics, proteomics or metabolomics, provide the tools to understand the molecular mechanisms involved in the modulation of gene expression by nutrients. The study of the beneficial properties of wine procyanidins has not avoided this shift of focus. Thus, from the initial studies which defined the "French paradox", to nowadays, a wide array of studies have been focused in defining the properties of the non-alcoholic components of red wine, mainly flavonoids, a family of polyphenolic compounds. The objectives of this thesis have been to define the molecular mechanisms by which grape procyanidins modulate the hepatic metabolism of lipoproteins, reducing the risk of cardiovascular disease and other pathologies which basis is found in the dysregulation of the lipoprotein metabolism.<br/>SUMMARY<br/>In the present thesis, the effect of procyanidins in the hepatic lipoprotein metabolism has been studied. With this objective, HepG2, HeLa and CV-1 cells have been used as invitro models. In vivo studies have been performed in Wistar rats and C57BL6 mice, wild-type and transgenic mice lacking SHP (NR0B2) and FXR (NR5H1).<br/>RESULTS<br/>1. Procyanidins improve plasma lipid profile in the postprandial phase in rats. A single oral dose of procyanidins decreases plasma triglycerides and ApoB levels to 50% of control values. In addition LDL-Cholesterol is significantly reduced, thus improving the atherosclerotic risk index.<br/>2. Procyanidins display a triglyceride-lowering effect both in vivo and in vitro. In rat and mouse, procyanidin treatment triggers a hypotriglyceridemic response. In HepG2 cultures, procyanidins down-regulate the secretion of triglycerides and ApoB, thus showing that these flavonoids act directly on hepatic cells. This fact strongly suggests that, in vivo, a direct action of procyanidins on the liver contributes to their hypotriglyceridemic response.<br/>3. Nuclear receptor Small Heterodimer Partner (SHP) is a target of procyanidins in hepatic cells. Procyanidins modulate the expression of SHP, rapidly increasing its expression in rat liver as well as in HepG2 cultured cells.<br/>4. SHP mediates the triglyceride-lowering activity of procyanidins in vitro and in vivo. When SHP expression is silenced in HepG2 or abolished in SHP-null mice, procyanidins lose their hypotriglyceridemic activity. In contrast, in SHP-silenced HepG2 cells, procyanidins are still able to reduce apoB secretion. Hence, procyanidins reduce triglyceride via a SHP-dependent mechanism, whereas they reduce apoB in a SHPindependent manner.<br/>5. Nuclear receptor Farnesoid X Receptor (FXR) is an essential mediator of the hypotriglyceridemic action of procyanidins upstream SHP. Oral gavage of procyanidins to FXR-null mice have not a hypotriglyceridemic effect. Moreover, luciferase based in vitro assays showed that procyanidins increase the transcriptional activity of FXR. Thus, FXR is an essential component of the signalling pathway used by procyanidins to elicit the triglyceride lowering effect.<br/>6. Key genes of the inflammation process are targets of procyanidins in liver, in the postprandial phase. Oral administration of procyanidins to rats rapidly downregulates the expression, in liver, of transcription factor Egr1, a mediator of the hepatic inflammatory response, and several acute-phase proteins, namely haptoglobin, fibrinogen B and alpha-1 antitrypsin. In addition, expression of DUSP6, a component of the ERK1/2 subfamily of MAPK, is repressed by this treatment. Nfkbia, a repressor of NF-kB activity, is overexpressed upon procyanidin treatment. This expression pattern strongly suggests that procyanidins attenuate the pro-inflammatory state associated to the postprandial phase.<br>INTRODUCCIÓN<br/>Durante la pasada década, la investigación en nutrición se ha visto sujeta a un cambio en sus objetivos, pasando de los estudios basados en la fisiología y la epidemiología a la comprensión de las bases moleculares implicadas en las acciones biológicas de los nutrientes. Así, las nuevas disciplinas, como la biología molecular o las "-omics", transcriptómica, proteómica o metabolómica, proporcionan las herramientas para el estudio de los mecanismos moleculares implicados en la modulación génica por nutrientes.<br/>El estudio de las propiedades beneficiosas del vino no ha evitado este cambio de foco. Así, desde los primeros estudios que definieron la "paradoja francesa", hasta la actualidad, una ámplia gama de estudios se han dedicado a definir las propiedades de los componentes no alcohólicos del vino, mayoritariamente, los Flavonoides, una familia de compuetos polifenólicos. El objetivo de esta tesis ha sido definir los mecanismos moleculares mediante los cuales las procianidinas de uva modulan el metabolismo de lipoproteínas en el hígado, disminuyendo así el riesgo cardiovascular y diferentes patologías cuya base se encuentra en la desregulación del metabolismo lipoproteico.<br/>MEMORIA<br/>Durante esta tesis se ha estudiado el efecto de las procianidinas sobre el metabolismo lipoproteico en el hígado. Con este objetivo se han usado líneas celulares como modelo in vitro, tanto hepatocitos (HepG2) como líneas accesorias (HeLa y CV-1). Como modelos para el estudio de las procianidinas in vivo se han usado ratas de la cepa Wistar y ratones de la cepa C57BL6, tanto wild-type como dos líneas de transgénicos, Knockout para SHP (NR0B2) y FXR (NR5H1).<br/>RESULTADOS<br/>Se han obtenido los siguientes resultados:<br/>Las procianidinas de uva disminuyen los niveles de lipoproteínas ricas en triglicéridos, así como mejoran los índices de riesgo cardiovascular en ratas.<br/>Estos efectos se deben a la modulación de la expresión génica en el hígado, tejido adiposo y músculo entre otras acciones.<br/>El mecanismo por el cual las procianidinas disminuyen las lipoproteínas ricas en triglicéridos ha sido estudiado in Vitro (HepG2) e in vivo (C57BL6 wild-type y knockout para SHP). Se han definido dos mecanismos principales. El primero implica la señalización de las procianidinas por una vía dependiente de SHP (Small heterodimer partner, NR0B2), un receptor nuclear. El segundo mecanismo es independiente de SHP e inhibe la expresión de MTP (enzima controlador de la síntesis de lipoproteínas) y consecuente secreción de un menor número de lipoproteínas de muy baja densidad (VLDL).<br/>Por encima de SHP, se ha definido FXR (Farnesoid X receptor) como sensor de las procianidinas mediante el uso de ratones C57BL6 KO para FXR y sistemas reporter basados en luciferasa. Estableciendo que el mecanismo de señalización de las procianidinas pasa por FXR, que a su vez induce la expresión de SHP y este inhibe la expresión de SREBP1, factor de transcripción clave para la síntesis de lípidos, disminuyendo así la cantidad de lípidos hepáticos y, consecuentemente, la secreción de lipoproteínas.<br/>DISCUSIÓN<br/>La modulación del metabolismo de lipoproteínas es el principal objetivo para el tratamiento de las diferentes patologías relacionadas con dislipemias. Así, la definición de las procianidinas de uva como agentes hipolipidémicos, las convierte en un componente de la dieta de alta importancia para prevenir y mejorar una ámplia gama de patologías, desde la aterogénesis hasta otros estados metabólicos alterados, causantes de la resistencia a la insulina o el síndrome metabólico.<br/>Por otro lado, el establecimiento de los mecanismos moleculares implicados en los efectos de las procianidinas de uva, aumenta el conocimiento sobre estos compuestos, así como su aplicabilidad en diferentes estados metabólicos alterados. De esta manera, se ha propuesto que la activación de FXR podría usarse como una estrategia en el tratamiento de la hiperlipidemia o la resistencia a la insulina. Así, las procianidinas emergen como un importante agente terapéutico, cuya importancia radica en la amplia presencia de estos compuestos en la dieta.
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35

Chi, Xun. "Extracellular regulation of LPL activity by angiopoietin-like proteins." Diss., University of Iowa, 2017. https://ir.uiowa.edu/etd/5729.

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Dyslipidemia often accompanies metabolic diseases such as obesity and type II diabetes mellitus and represents a risk factor for cardiovascular disease. Clearance of triglycerides from the plasma is mediated by lipoprotein lipase (LPL), which hydrolyzes the triglycerides in chylomicrons and VLDL, liberating fatty acids for tissue uptake. LPL functions in the capillaries of the heart, adipose tissue, and skeletal muscle where LPL is anchored to the capillary wall by its endothelial cell transporter GPIHBP1. LPL activity is regulated by several factors including three members of the angiopoietin-like (ANGPTL) family–ANGPTL3, ANGPTL4, and ANGPTL8. How these proteins interact with LPL, especially in the physiological context of LPL anchored to endothelial cells by GPIHBP1, has not been well characterized. In my studies of ANGPTL4, I found when LPL is bound to GPIHBP1, it is partially, but not completely, protected from inactivation by ANGPTL4. Inactivation of LPL by ANGPTL4 leads to the dissociation of active LPL dimers into inactive monomers and I found that these monomers have a greatly reduced affinity for GPIHBP1. ANGPTL4 can be cleaved in vivo, separating the N-terminal coiled-coil domain from the C-terminal fibrinogen like-domain. I found the N-terminal domain alone is a much more potent LPL inhibitor than the full-length protein, even though both appear to have similar binding affinities for LPL-GPIHBP1 complexes. When I investigated ANGPTL3, I found ANGPTL3 itself is not a potent inhibitor of LPL at physiological concentrations, and unlike ANGPTL4, cleavage of ANGPTL3 does not improve its ability to inhibit LPL. Instead I found that ANGPTL3 forms a complex with ANGPTL8, a complex that only forms efficiently when the two proteins are co-expressed, and that this complex allows ANGPTL3 to bind and inhibit LPL. My data provide new insights into how ANGPTL proteins regulate LPL activity and the delivery of fat to tissues.
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36

Kimura, Rino. "Studies on the attenuation effects of intestinal PPARα activation on postprandial hyperlipidemia". Kyoto University, 2014. http://hdl.handle.net/2433/188757.

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Kyoto University (京都大学)<br>0048<br>新制・課程博士<br>博士(農学)<br>甲第18319号<br>農博第2044号<br>新制||農||1021(附属図書館)<br>学位論文||H26||N4826(農学部図書室)<br>31177<br>京都大学大学院農学研究科食品生物科学専攻<br>(主査)教授 河田 照雄, 教授 伏木 亨, 教授 金本 龍平<br>学位規則第4条第1項該当
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37

GUENDOUZI, KARIM. "Role de la triglyceride lipase hepatique dans le metabolisme des lipoproteines de haute densite : caracterisation biochimique et devenir cellulaire des particules." Toulouse 3, 1999. http://www.theses.fr/1999TOU30104.

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Les lipoproteines de haute densite (hdl) jouent un role essentiel dans le transport retour du cholesterol des tissus peripheriques vers le foie. Ce role des hdl est sous-tendu par des remaniements particulaires sous l'action de diverses enzymes du compartiment vasculaire telle que la triglyceride lipase hepatique (tgl-h). La tgl-h, de par son activite triacylglycerol lipase, va scinder des hdl 2 enrichies en triglycerides (hdl 2-tg) en deux particules : les pre 1 hdl, premiers accepteurs du cholesterol cellulaire, et les hdl 2 lipolysees, nommees remnants de hdl 2 (hdl 2-r), tres vite captees par le foie (barrans (1994), j. Biol. Chem 269:11572-11577). Leur analyse biochimique et physique montre que les hdl 2-r perdent une molecule d'apo a-i, 60% des triglycerides et 15% des phospholipides par comparaison aux hdl 2-tg. L'etude de la fluidite lipidique a mis en evidence une rigidification de la surface et du cur des hdl 2-r par rapport aux hdl 2-tg. De plus, la conformation de l'apo a-i des hdl 2-r est modifiee dans la partie nh 2-terminale comme le suggerent les changements d'immunoreactivite de l'apo a-i vis a vis d'anticorps monoclonaux. L'analyse de l'interaction cellulaire des particules avec des cellules d'hepatome montre que les hdl 2-tg se lient uniquement a une famille de sites de basse affinite. Par contre, les hdl 2-r, issus du traitement par la tgl-h, sont capables de se lier a la fois a des sites de basse mais aussi de haute affinite avec des parametres de liaison comparables a ceux decrits pour les hdl 3 (barbaras (1994), biochemistry 33:2335-2340). Enfin, l'analyse du devenir intracellulaire suggere que la liaison de haute affinite des hdl 2-r pourrait moduler l'internalisation des particules par les sites de basse affinite. Cette regulation (en cours d'etude) permettrait de mieux comprendre les mecanismes intervenant lors de la captation hepatique des hdl. L'ensemble de ces resultats souligne ainsi l'importance de la tgl-h dans le catabolisme des hdl.
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38

BRANDIZZI, LAURA I. V. "Metabolismo de quilomicrons em pacientes portadores de doenca arterial coronaria." reponame:Repositório Institucional do IPEN, 2002. http://repositorio.ipen.br:8080/xmlui/handle/123456789/11017.

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39

Cohen, Jonathan. "The regulation of postprandial lipemia in man." Doctoral thesis, University of Cape Town, 1989. http://hdl.handle.net/11427/27177.

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The regulation of the serum triglyceride responses to fat ingestion have been examined in normolipidemic men. To evaluate the existing methods for comparing chylomicron-triglyceride clearance, the oral and intravenous fat tolerance tests and a steady state duodenal perfusion method were compared. Good correlations (r > 0.8) were found between each of these methods. Since the intravenous fat tolerance test is independent of fat absorption, these data suggested that the serum triglyceride response to fat feeding was largely determined by the rate of chylomicron-triglyceride clearance. To determine the influence of the quantity and type of meal fat on postprandial serum triglyceride concentrations, the serum triglyceride responses to three different doses of dairy cream, and to standard doses of olive and sunflower oil were examined. For a given type of fat, the magnitude of postprandial lipemia (the integrated serum triglyceride excursion) varied directly with the quantity of fat in the meal. This finding suggested that the chylomicron- triglyceride clearance system(s) did not become saturated even after large fat meals. In addition, it appeared that the hormonal factors released in response to fat ingestion (some of which are known to increase lipoprotein lipase activity in vitro) did not increase the rate of chylomicron-triglyceride clearance. If the quantity of fat in a meal was fixed, then postprandial lipemia increased with increasing saturation of the triglyceride fatty acids. These differences did not appear to reflect differences in triglyceride absorption. Since acute fat feeding per se did not appear to stimulate chylomicron-triglyceride clearance, the effects of dietary proteins and carbohydrates were studied. The addition of up to 35g protein to a standard test meal did not affect postprandial lipemia. These results were supported by the observation that protein ingestion did not affect intravenous fat tolerance. Postprandial serum triglyceride concentrations were significantly influenced by carbohydrate ingestion. Fructose (50g) and sucrose (100g) markedly increased postprandial lipemia, although glucose ingestion did not. In agreement with earlier studies, glucose ingestion decreased serum triglyceride concentrations 2 hours after the meal. This effect was abolished by intraduodenal fat administration and by substituting starch for glucose in the test meal. The effects of glucose could be reproduced by iso-osmotic quantities of urea, however. These findings suggested that glucose ingestion did not increase chylomicron -triglyceride clearance. It is more likely that glucose delayed the absorption of triglycerides by slowing gastric emptying, and that this effect was partly related to the increased osmolarity of glucose- containing meals. The effects of chronic exercise on postprandial lipemia and chylomicron-triglyceride clearance were determined in endurance- adapted athletes. The serum triglyceride responses to large and small fat meals were lower in athletes than in sedentary men with comparable fasting triglyceride concentrations. These differences were not eliminated by a single bout of acute exercise in the sedentary men. The clearance of intravenously administered lntralipid, and chylomicron -triglyceride clearance assessed from steady state chylomicron-triglyceride concentrations during duodenal fat perfusion were faster in athletes than in the sedentary men. These data suggested that the low postprandial lipemia in athletes reflects increased chylomicron-triglyceride clearance caused by increased activity of the triglyceride clearing system(s). Given these considerations. it appears that the pathway(s) for chylomicron triglyceride clearance are extremely efficient in normal men and that these pathways are not subject to acute physiological regulation.
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40

Hewitt, Kylie N. "The liver phenotype of the aromatase knockout (ArKO) mouse." Monash University, Dept. of Biochemistry and Molecular Biology, 2003. http://arrow.monash.edu.au/hdl/1959.1/9465.

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41

Souza, Francisca das Chagas do Amaral. "Efeito do consumo de peixes gordurosos amazônicos sobre o metabolismo lipídico de ratos wistar." Universidade Federal do Amazonas, 2006. http://tede.ufam.edu.br/handle/tede/3109.

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Made available in DSpace on 2015-04-20T12:31:39Z (GMT). No. of bitstreams: 1 - PDF.pdf: 156224 bytes, checksum: d8d6c26c25fefd22c60ea2b135c6dbc3 (MD5) Previous issue date: 2006-08-04<br>Fundação de Amparo à Pesquisa do Estado do Amazonas<br>Obesity is a disease that occurs due to the unbalance between the ingested energy and the spent energy to maintain the vital processes. Obesity has incresingly wrong and reached, nowadays, and epidemic level. It has also been considered the main public health issues in modern society. It is asociated with the rising risk of developing Diabetes Melliteus, cardiovascular diseases, dislipodemia, and several other chronic diseases. The diet based on fat maybe crucial reason to develop such diseases. The fishing also provides a large sort of food to thousands of local inhabitants nutrional development. Among the most well-known and consumed Amazon fish there is Tambaqui (Colossoma macropomum), Matrinxã (Brycon cephalus) and Mapará (Hypophthalmus edentatus), which are all considered very fat species. And so, the main purpose of this essay is to analyse the effects of a diet based on Amazon fat fish (Mapará, Matrinxã and Tambaqui) on male mice lipydic metabolism from wistar blood line. They were feeded with Adlibitum for 14 days. To make it happen doses of total cholesterol and triglycerids, glycoses, proteins and plasma lipydic fraction were made. The rate of lypogenesis again in vivo has been measured on RET, EPI, FIG and CARC, by incorporating 3 H2O in lipy. Our results show that the enrichment of a diet based on Amazon fat fish has altered the mice lipydic metabolism, dicreased effectively the lipid plasmatic concentration (Col. TG, e LDL) and increased the HDL besides the lipolitic activity on fatty tissues has grown after 4 weeks of feeding. Admiting that the ingestion of hiperlipydic diets may have caused an aterogenic effect, mainly because they have reduced certain lipydic fractions that have been claimed to cause serious vascular problems.<br>A obesidade é uma doença que ocorre como conseqüência do desequilibro no balanço entre energia ingerida e a gasta para a manutenção de processos vitais. A obesidade possui prevalência crescente, assumindo atualmente caráter epidêmico, sendo considerada um dos principais problemas de saúde pública na sociedade moderna. Ela está associada com o aumento do risco de desenvolve diabetes mellitus, doenças cardiovasculares, dislipidemias e inúmeras outras doenças crônicas. As dietas ricas em lipídios podem ser um fator determinante para o desenvolvimento de tais doenças. A pesca contribui na oferta de alimentos e para o desenvolvimento nutricional de milhares de habitantes da região. Dentre os mais conhecidos e consumidos peixes da Amazônia estão o tambaqui (Colossoma macropomum), a matrinxã (Brycon cephalus) e o mapará (Hypophthalmus edentatus), os quais são consideradas espécies bastante gordurosas. Desta forma objetivo deste trabalho foi avaliar os efeitos da dieta de peixes gordurosos (mapará, matrinxã e tambaqui) da Amazônia sobre o metabolismo lipídico de ratos machos da linhagem wistar. Assim foram alimentados ad libitum por 30 dias. Para tanto foram realizadas as dosagens de colesterol total e triglicérideos, glicose, proteínas e frações lipídicas do plasma. a taxa de lipogênese de novo in vivo foi medida nos tecidos RET, EPI, FIG e CARC, por meio da incorporação de 3H2O em lipídios. Nossos resultados mostram que o enriquecimento da dieta com peixes amazônicos gordurosos alterou o metabolismo lipídico dos ratos, diminuindo de forma efetiva a concentração plasmática de lipídios (Col. TG, e LDL) e aumentando o HDL. Além disso, a atividade lipolítica nos tecidos adiposos aumentou após 4 semanas de alimentação. Sugerindo que a ingestão de dietas hiperlipídicas pode ter efeito aterogênico, principalmente, por diminuírem determinadas frações lipídicas, que tem sido responsabilizada por causar graves problemas vasculares.
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42

Åkesson, Nilsson Gunilla. "Determination of chlorinated fatty acids using SPE, XSD and GC/MS with particular regard to cultured human cells /." Uppsala : Dept. of Environmental Assessment, Swedish Univ. of Agricultural Sciences, 2004. http://epsilon.slu.se/a493.pdf.

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43

JOANNIC, JEAN-LUC. "Effet des glucides et des lipides alimentaires sur le metabolisme post-prandial des lipoproteines riches en triglycerides chez l'homme sain." Paris 7, 1997. http://www.theses.fr/1997PA077121.

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L'objectif de ce travail est d'explorer chez l'homme sain l'influence de la qualite des aliments glucidiques et lipidiques et de leur mixite sur la triglyceridemie post-prandiale au travers d'hormones post-prandiales (insuline et leptine) et des proprietes physico-chimiques des lipoproteines riches en triglycerides (chylomicrons, vldl, idl). Les repas mixtes isocaloriques et iso-lipido-glucidiques avaient trois parametres stables : les teneurs en proteine, en acides gras satures et polyinsatures n-3. Les repas etaient composes de riz d'index glycemique (ig) faible ou de puree instantanee d'ig eleve, associes a des huiles riches en acies monoinsatures (agmi, 70% de c18 : 1n-9) ou en acides gras polyinsatures (agpi, 56% de c18 : 2n-6). Trois etudes ont ete menees. La premiere consistait a chercher les effets de ces repas sur les reponses glycemiques et insulinemiques, la deuxieme a evaluer l'intensite de faim et a doser la concentration de leptine plasmatique au cours des repas riz et agpi et puree et agmi ; la troisieme a etudier le metabolisme des lipoproteines riches en triglycerides. Les agpi induisent une glycemie et une insulinemie plus faibles par rapport aux agmi, 30 mn apres le repas, independamment du type de glucides. Les glucides affectent ces reponses metaboliques plus tardivement. L'intensite de faim est plus elevee a 4 h, 5 h, 6 h apres le repas a base de riz et d'agpi par rapport au repas a base de puree et d'agmi, sans modification des taux de leptine plasmatique. Le repas a base de riz augmente la triglyceridemie tardivement (4 h et 8 h) au travers des chylomicrons essentiellement, par rapport au repas a base de puree, independamment des lipides. Apres le rapas, a 30 mn, les agmi augmentent la triglyceridemie par rapport aux agpi. Cette augmentation est caracterisee par un enrichissement des chylomicrons en triglycerides au detriment des esters de cholesterol. En conclusion, la nature des glucides et des lipides des repas affecte linsulinemie, la glycemie et la triglyceridemie a l'etat post-prandial. Il serait interessant de reproduire ces resultats chez des sujets diabetiques, obeses ou hypertriglyceridemiques afin de tenter d'etablir des recommendations alimentaires dans le but de diminuer les facteurs de risques des maladies cardiovasculaires.
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44

Rech, Giovana. "Efeitos de dieta suplementada com serragem de Pinus sp. miceliada com Pycnoporus sanguineus sobre o metabolismo de ratos diabéticos." reponame:Repositório Institucional da UCS, 2016. https://repositorio.ucs.br/handle/11338/2259.

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Submitted by Ana Guimarães Pereira (agpereir@ucs.br) on 2017-04-13T17:31:31Z No. of bitstreams: 1 Dissertacao Giovana Rech.pdf: 196743 bytes, checksum: c2a7f372a48a43103520ef163e0726eb (MD5)<br>Made available in DSpace on 2017-04-13T17:31:31Z (GMT). No. of bitstreams: 1 Dissertacao Giovana Rech.pdf: 196743 bytes, checksum: c2a7f372a48a43103520ef163e0726eb (MD5) Previous issue date: 2017-04-13<br>Coordenação de Aperfeiçoamento de Pessoal de Nível Superior, CAPES.
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45

Ferreira, Darkiane Fernandes. "Papel do receptor toll-like 4 no metabolismo lipídico hepático." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/5/5167/tde-26112014-085554/.

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Estudos recentes têm demonstrado uma participação importante do receptor toll-like 4 (TLR4) na evolução de doenças envolvendo desordens metabólicas, como a doença do fígado gorduroso não-alcoólico (NAFLD). No entanto, as alterações do metabolismo lipídico que poderiam ser influenciadas pela ativação do TLR4 são desconhecidas. Neste estudo propomos caracterizar o papel do receptor TLR4 no metabolismo de lipídios no fígado de camundongos deficientes para o receptor de LDL, um modelo que desenvolve NAFLD quando submetido a uma dieta rica em gordura saturada e colesterol. Camundongos controle (C57 black6), deficientes para o receptor de LDL (LDLrKO), deficientes para o receptor TLR4 (TLR4KO) ou deficientes para ambos (duplo KO) receberam dieta controle ou hiperlipídica por quatro, oito ou doze semanas. Após o tratamento e sacrifício dos animais, avaliamos o perfil de lipídios plasmáticos, o conteúdo de lipídios do fígado e a expressão gênica de enzimas relacionadas à síntese e degradação de triglicerídeos (TG) e colesterol no fígado. O perfil inflamatório no fígado também foi avaliado. A dieta hiperlipídica induziu uma hipertrigliceridemia e hipercolesterolemia nos animais LDLr KO e duplo KO, sendo que o grupo duplo KO apresentou níveis séricos inferiores de triglicérides (TG) e ácidos graxos livres a partir de oito semanas de tratamento em comparação aos animais LDLrKO. A dieta hiperlipídica também induziu um aumento significativo no conteúdo de TG e de colesterol no fígado de todos os grupos. Na análise da expressão gênica não foram encontradas diferenças na expressão de proteínas relacionadas à síntese de triglicérides e colesterol (ApoB100, MTTP, GPAT1 e GPAT4) entre os grupos. Porém houve aumento significativo na expressão de proteínas relacionadas à oxidação de ácidos graxos (CPT1, MTP, ACOX, PBE, tiolase) e à síntese de ácidos biliares (CYP7a1) no grupo duplo KO em comparação ao grupo LDLr KO. No perfil inflamatório, a expressão de F4/80 demonstrou infiltração de macrófagos significativamente elevada no grupo LDLrKO tratado com a dieta hiperlipídica comparada a todos os outros grupos. No entanto, houve maior expressão de IL-6, IL-1beta e TNF-alfa no grupo duplo KO em comparação ao grupo LDLr KO. Nossos dados sugerem que a ativação do TLR4 no fígado de animais alimentados com uma dieta hiperlipídica pode contribuir para o acúmulo de lipídios e início da esteatose hepática. Estratégias para a inativação hepática do TLR4 podem diminuir a NAFLD não somente devido a diminuição da inflamação, mas por aumentar a oxidação de ácidos graxos no fígado<br>Recent studies have shown an important role of toll-like receptor 4 (TLR4) in the evolution of diseases involving metabolic disorders, such as non-alcoholic fatty liver disease (NAFLD). However, changes in lipid metabolism regulated by TLR4 activation are still unknown. In this study, we characterized the role of TLR4 receptor in hepatic lipid metabolism of mice deficient for the LDL receptor, a model that develops NAFLD when exposed to a diet rich in saturated fat and cholesterol. We investigated the role of TLR4 activation in the pathogenesis of diet-induced NAFLD by crossing LDLr KO mice with the TLR4 knockout mice (double KO). Animals were fed for 4, 8 or 12 weeks with high-fat diet (HFD) containing 18% saturated fat and 1.25% cholesterol. We evaluated plasma lipid profile, hepatic lipid content and gene expression of enzymes related to the synthesis and degradation of triglycerides and cholesterol in the liver. Liver inflammatory status was also investigated. We observed that HFD induced hypertriglyceri-demia and hypercholesterolemia in LDLr KO and double KO mice, but double KO animals presented lower serum levels of triglycerides and free fatty acids after eight weeks of treatment. HFD also induced a significant increase in liver contents of triglycerides (TG) and of cholesterol in all groups. We did not find differences in the expression of proteins related to triglycerides and cholesterol synthesis (ApoB100, MTTP, GPAT1, GPAT4) between the groups. However, we observed a significant increase in the expression of proteins related to fatty acid oxidation (CPT1, MTP, ACOX, PBE, tiolase ) and bile acid synthesis (CYP7a1) in double KO group in comparison to LDLr KO. Regarding the inflammatory process, F4/80 expression was elevated in LDLr KO mice fed HFD when compared to all groups. On the other hand, IL-6, IL-1beta e TNF-alfa expression was induced by HFD only in double KO mice. Taken together, our results show that TLR4 activation in liver from mice fed on a high-fat diet may contribute to lipid accumulation and steatosis onset. Strategies regarding localized TLR4 inactivation may increase the oxidation of fatty acids and improve NAFLD not only due to decreased inflammation
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46

Carneiro, Marcia Maria. "Metabolismo de quilomícrons e aterosclerose subclínica em portadores de hipercolesterolemia familiar heterozigótica." Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/5/5131/tde-23112011-192759/.

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A hipercolesterolemia familiar (HF) é uma doença caracterizada por elevadas concentrações do colesterol das lipoproteínas de baixa densidade (LDL) e doença coronariana (DAC) prematura. Os remanescentes de quilomícrons são removidos principalmente pelo seu receptor específico (RLP), mas também pelo receptor da LDL. Este último encontra-se defeituoso na maior parte dos casos de HF e poderia levar a menor remoção plasmática dos quilomícrons. Há controvérsias se existem distúrbios do metabolismo dos quilomícrons em portadores de HF. Mais ainda não se sabe se estes defeitos poderiam contribuir para o desenvolvimento de DAC na HF. O objetivo deste estudo foi avaliar se portadores de HF apresentam defeitos na remoção plasmática de quilomícrons artificiais e seus remanescentes em relação a indivíduos normolipidêmicos. Foi avaliado também em estudo transversal se existe associação da cinética dos quilomícrons com a presença de DAC subclínica medida pela calcificação da artéria coronária (CAC). Foram estudados 36 pacientes portadores de HF e 50 controles normolipidêmicos pareados para idade e sexo. A remoção plasmática dos quilomícrons foi medida pelo decaimento radioisotópico da emulsão de quilomícrons artificiais injetada após jejum. A CAC foi determinada por tomografia computadorizada cardíaca nos portadores de HF. As taxas fracionais de remoção (TFR) dos quilomícrons e de seus remanescentes representadas pelo decaimento do 14C-éster de colesterol (TFR 14C-CE em min-1) foram menores nos portadores de HF em comparação aos normolipidêmicos: mediana (intervalos) 0,0013 (1,5.10-9;0,082) vs. 0,012 (1,51.10-9;0,017) p= 0,001. Não houve diferença em relação à remoção dos triglicérides da emulsão representada pelo decaimento da 3H-triglicérides (TFR 3H-TG em min-1) entre os grupos: 0,027 (0,0004;0,23) e 0,03 (0,0004;0,4) respectivamente nos grupo HF e controle (p= 0,26). Não foram encontradas diferenças significativas nas TFR tanto do 14C-CE 0,0007 (1,47. 10-9; 0,082) e 0,0013 (1,6. 10-9; 0,038) p= 0,67 como do 3H-TG 0,025 (0,0004; 0,07) e 0,0029 (0,009; 0,23), p=0,80 respectivamente nos portadores de HF apresentando (n=20) ou não CAC (n= 16). Em conclusão os portadores de HF apresentaram diminuição significativa da remoção dos quilomícrons e seus remanescentes em comparação com normolipidêmicos. Contudo, não foi encontrada associação entre esses distúrbios e a presença da DAC subclínica<br>Familial hypercholesterolemia (FH) is characterized by high concentrations of low density lipoproteins (LDL) cholesterol and early onset of coronary artery disease (CAD). Chylomicron remnants are removed mainly by their specific receptors (RLP) but also by the LDL receptor. The latter is defective in most cases of FH and could lead to lower plasma removal of chylomicrons and their remnants. There is controversy whether there are disorders of chylomicron metabolism in patients with FH. Moreover, it is unclear if these defects could contribute to the development of CAD in FH. The aim of this study was to evaluate whether there are defects on the removal from plasma of chylomicrons and their remnants in FH patients in comparison with normolipidemic subjects. We also evaluated in a cross sectional study the association of chylomicron kinetics with the presence of subclinical CAD represented by coronary artery calcification (CAC). We studied 36 patients with FH and 50 normolipidemic controls matched for age and sex. The plasma removal of chylomicrons was measured by isotopic decay of artificial chylomicron emulsion injected after fasting. CAC was determined by cardiac computed tomography in FH patients. The fractional catabolic rates (FCR) of chylomicrons and remnants removal represented by 14C-cholesteryl ester decay (14C-CE FCR in min-1) were lower in FH in comparison with normolipidemics: median (ranges) 0.0013 (1.47.10-9; 0.082) vs. 0.012 (1.51.10-9, 0.169) p = 0.001. There was no difference regarding the removal of emulsion triglyceride represented by 3H-triglyceride decay of ( 3H- TG FCR in min-1) between the groups: 0.026 (0.0004; 0.23) and 0.031 (0.0004; 0.4) respectively in FH and in normolipidemics (p = 0.264). There were no significant differences in both the 14C-CE FCR 0.0007 (1.47.10-9; 0.08) and 0.0013 (1.61.10-9; 0.038) p = 0.67 and in the 3H-TG FCR 0.025 (0.0004; 0.075) and 0.029 (0.0095; 0.23), p = 0.80 respectively in FH patients presenting (n = 20) or not CAC (n = 16). In conclusion patients with FH had a significant decrease on the removal from plasma of chylomicrons and their remnants compared with normolipidemics. However, no association between these disorders and the presence of CAC was found
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47

Mangeney-Andréani, Marise. "Perturbations du metabolisme lipidique induites par la d-galactosamine : action de l'acide clofibrique." Paris 6, 1987. http://www.theses.fr/1987PA066018.

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48

Nlend, Albert Emmanuel. "Etude de l'influence de différents types d'acides gras sur le métabolisme glucidique chez le sujet diabétique non insulinodépendant." Bordeaux 2, 1996. http://www.theses.fr/1996BOR2P110.

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49

Latorre, Luque Jèssica. "Relevance of the epigenetic regulation exercised by hepatic microRNAs in the fatty liver arena: from the bedside to the bench." Doctoral thesis, Universitat de Girona, 2020. http://hdl.handle.net/10803/671499.

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Non-alcoholic fatty liver disease (NAFLD) has become the leading cause of chronic liver disease worldwide, involving a spectrum of disturbances mainly characterized by fatty acid infiltration and fat deposition in the liver parenchyma. Given that alterations in epigenetic mechanisms have been associated with hepatic metabolic disorders, we focused on the relevance of microRNAs (miRNAs) in the pathophysiology of NAFLD. In this thesis, an analysis of hepatic miRNAs comparing patients with and without NAFLD has shown that the disease is associated with an altered miRNA profile, and that the expression of specific miRNAs is related to changes in gene expression and impaired glucose and lipid metabolism. Additionally, altered regulation of miRNAs has been demonstrated through modulation of AMPK in cell and animal models. Finally, specific miRNAs were observed to partially rescued fatty acid overload and modified lipid profiles within hepatocytes, stressing their potential as epigenetic regulators to combat NAFLD<br>La malaltia de fetge gras no alcohòlic (NAFLD) s’ha convertit en la causa principal de les malalties hepàtiques cròniques a nivell mundial, caracteritzada per la infiltració massiva d’àcids grassos al parènquima hepàtic. Tenint en compte que alteracions en els mecanismes epigenètics s’han associat a trastorns metabòlics del fetge, ens centrem en la rellevància dels microRNAs (miRNAs) en la fisiopatologia de NAFLD. En aquesta tesi, un anàlisi de miRNAs hepàtics comparant pacients amb i sense NAFLD ha demostrat que la malaltia està associada amb un perfil de miRNAs alterat, i que l’expressió d’alguns miRNAs està relacionada amb canvis en l’expressió gènica i amb alteracions en el metabolisme glucídic i lipídic. Addicionalment, s’ha demostrat una alteració de la regulació dels miRNAs a través de la modulació de AMPK en models cel·lulars i animals. I finalment, s’han identificat el potencial terapèutic de miRNAs específics per combatre l’acumulació inadequada d’àcids grassos als hepatòcits
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50

Courchesne-Loyer, Alexandre. "Étude de la stimulation cétogénique chez l’adulte en bonne santé : impact sur le métabolisme énergétique cérébral." Thèse, Université de Sherbrooke, 2016. http://hdl.handle.net/11143/10569.

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Le cerveau humain est un organe très métaboliquement actif. Cet énorme besoin énergétique l’expose à un risque accru de détérioration causée par un dérèglement de ce métabolisme. Dans la phase précoce de la maladie d’Alzheimer, un hypométabolisme cérébral du glucose est observé. Cette carence énergétique serait à l’origine des détériorations observée lors du développement de cette maladie. Le cerveau a accès à une autre source endogène d’énergie : les cétones. Les cétones sont particulièrement importantes pour le cerveau puisqu’il ne possède pas la capacité d’utiliser les acides gras comme source énergétique à l’instar des autres organes. Les cétones sont issues de la β-oxydation hépatique des acides gras. Ils sont produits en situation de jeûne lorsque les niveaux circulants de glucose et d’insuline sont bas. Les cétones se sont déjà montré efficaces dans le traitement de divers troubles neurologiques comme l’épilepsie. Par contre, outre les diètes cétogènes et le jeûne prolongé, il n’existe pas de traitement efficace pour maintenir une cétonémie modérée chez l’adulte. Le métabolisme énergétique cérébral en situation de cétose modérée reste encore mal compris dans cette population. Les travaux de cette thèse se sont donc concentrés à étudier la possibilité d’une combinaison d’approche nutritionnelle et pharmacologique afin de stimuler la cétogenèse chez l’adulte. Ils ont aussi exploré les changements de métabolisme cérébral chez l’adulte durant une cétose modérée. L’objectif de la première étude était d’étudier le potentiel du bezafibrate à stimuler la cétogenèse induite par une supplémentation en triglycérides de moyennes chaînes (MCT). Cette première étude a démontré que le bezafibrate avait peu d’effet sur la stimulation de la cétogenèse induite par les MCT et que le facteur limitant dans cette stimulation était donc la disponibilité des substrats et non la capacité cétogène des cellules hépatiques. L’objectif de la seconde étude était d’étudier les changements de capture des cétones et du glucose au cerveau durant un état de cétose modérée chez l’adulte. Les résultats de cette deuxième étude ont montré que la capture des cétones au cerveau est directement proportionnelle à leur concentration plasmatique. Cette étude a aussi démontré que la capture cérébrale des cétones était directement reliée à leur concentration plasmatique alors que la capture cérébrale du glucose est modulée par les besoins énergétiques du cerveau. Une stimulation cétogénique chez des personnes atteintes de déclin cognitif pourrait donc aider à rétablir la balance énergétique et ralentir l’apparition des symptômes chez ces personnes mais cet effet devra être étudié dans une étude ultérieure.<br>Abstract : The human brain is the most metabolically active organ of the body. This high need for energy exposes it to an increase risk in case of hypometabolism. Such a glucose hypometabolism is seen during the early stages of Alzheimer’s disease. This factor is believed to be one of the cause of the disease. Ketones are the main alternate substrate for the human brain. Ketones are particularly important since, unlike other organs, the brain can not use fatty acids as alternative fuel. Ketones are mainly produce through β-oxidation of fatty acid by the liver. This happens mainly during fasting when circulating levels of glucose and insulin are low. Studies have shown that ketones can have a therapeutic effect in a variety of neurological diseases, mainly epilepsy and Alzheimer’s disease. Nevertheless, apart from ketogenic diet and prolonged fasting, there is currently no effective ways to induce and maintain moderate ketosis in adults. Brain energy metabolism under moderate ketosis remains also misunderstood in this population. This thesis aimed look at the effect of a combination of a pharmacological treatment and a nutritional supplementation to induce moderate sustain ketosis in adults. It also studied the effect of a moderate ketosis on brain energy metabolism in adults. The aim of the first study was to study the effect of a pharmacological treatment, bezafibrate, on the potentiation of the ketogenic effect induced by a medium-chain triglycerides (MCT) supplementation. The results of this study that bezafibrate had little effect on the ketosis induced by a MCT supplementation and, therefore, that the limiting factor in human ketosis was not the liver cells capacity to produce ketones but the availability of substrates for ketogenesis. The aim of the second study was to study the impact of a nutritional moderate ketosis on brain glucose and ketone uptake. The results of this study showed a direct correlation between brain ketone uptake and plasma ketone concentrations. This study also showed that brain ketone uptake is regulated by blood ketone concentration whereas brain glucose uptake is regulated by the brain energy needs. Further studies should then look if such a moderate ketosis induced in cognitively impaired patients could re-equilibrate the energy balance in the brain and then slow the apparition of clinical symptoms in this population.
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