Bibliografías temáticas / Blood lipoproteins Metabolism

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Literatura académica sobre el tema "Blood lipoproteins Metabolism"

Autor: Grafiati
Publicado: 4 de junio de 2021
Última modificación: 29 de enero de 2023

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Artículos de revistas sobre el tema "Blood lipoproteins Metabolism"

1

Neary, Richard H., Mark D. Kilby, Padma Kumpatula, Francis L. Game, Deepak Bhatnagar, Paul N. Durrington, and P. M. Shaughn O'Brien. "Fetal and Maternal Lipoprotein Metabolism in Human Pregnancy." Clinical Science 88, no. 3 (March 1, 1995): 311–18. http://dx.doi.org/10.1042/cs0880311.

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1. Lipid, apolipoprotein concentration and composition were determined in maternal venous and umbilical arterial and venous blood at delivery by elective Caesarean section in 13 full-term pregnancies and in 25 healthy non-pregnant females. The indications of Caesarean section were a previous Caesarean section or breech presentation. None of the women was in labour and there were no other complications of pregnancy or fetal distress. 2. The objectives of the study were to establish whether the placenta has a role in feto-maternal cholesterol metabolism through either synthesis or transplacental cholesterol flux. The potential for free cholesterol diffusion between mother and fetus and rates of cholesterol esterification and transfer between lipoproteins were determined and related to the differences in composition between fetal and maternal lipoproteins. 3. Pregnant women had raised levels of all lipid and lipoprotein fractions compared with control subjects. The greatest increases were in free cholesterol and triacylglycerol (P < 0.0001). Lipoprotein (a) levels were significantly greater in the pregnant women [112(12.2) mg/l] than in the control women [50 (10.0) mg/l]. 4. The only significant correlation between maternal and fetal lipoprotein concentrations was in lipoprotein (a) levels (r = 0.791, P = 0.002). In both umbilical venous and arterial blood, concentrations of very-low- and low-density lipoproteins, particularly apolipoprotein B, cholesteryl ester and triacylglycerol, were lower than in maternal blood (P < 0.0001), but high-density lipoprotein levels were similar. 5. There was no umbilical arteriovenous differences in lipoprotein concentration or composition. This suggests that cholesterol synthesis or free cholesterol diffusion does not occur in the placenta. The relative concentrations of free cholesterol to phospholipid in maternal and fetal lipoproteins do not indicate the existence of a concentration gradient favouring free cholesterol diffusion across the placenta. 6. The esterification of free cholesterol was significantly reduced in maternal [17.7 (2.4) μmol h−1 l−1, P < 0.001] and fetal [6.7 (3.5) μmol h−1 l−1, P < 0.0001] compared with control [40.9 (13.2) μmol h−1 l−1] blood. 7. In fetal compared with maternal high-density lipoproteins the ratios cholesteryl ester/apoliproprotein A-I [0.84 (0.35) versus 0.40 (0.05), P < 0.01] and phospholipid/apolipoprotein A-I [1.66 (0.14) versus 0.58 (0.10), P < 0.0001] indicated lipid enrichment of these particles in the fetus. 8. Lipid enrichment of high-density lipoprotein is due in part to a marked reduction in transfer of cholesteryl ester in the fetus [1.0 (0.6) μmol h−1 l−1] compared with maternal [6.15 (1.3) μmol h−1 l−1, P = 0.004] and control [17.3 (7.2) μmol h−1 l−1, P < 0.0001] blood. 9. In conclusion, there was no evidence for involvement of the placenta in cholesterol metabolism during pregnancy. In fetal life high-density lipoproteins are lipid rich, partly because of a reduction in transfer of esterified cholesterol to other particles. Maternal and fetal lipoprotein levels are not correlated, although the results suggested that lipoprotein (a) levels may be related.
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2

Ohkawa, Ryunosuke, Hann Low, Nigora Mukhamedova, Ying Fu, Shao-Jui Lai, Mai Sasaoka, Ayuko Hara, et al. "Cholesterol transport between red blood cells and lipoproteins contributes to cholesterol metabolism in blood." Journal of Lipid Research 61, no. 12 (September 9, 2020): 1577–88. http://dx.doi.org/10.1194/jlr.ra120000635.

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Lipoproteins play a key role in transport of cholesterol to and from tissues. Recent studies have also demonstrated that red blood cells (RBCs), which carry large quantities of free cholesterol in their membrane, play an important role in reverse cholesterol transport. However, the exact role of RBCs in systemic cholesterol metabolism is poorly understood. RBCs were incubated with autologous plasma or isolated lipoproteins resulting in a significant net amount of cholesterol moved from RBCs to HDL, while cholesterol from LDL moved in the opposite direction. Furthermore, the bi-directional cholesterol transport between RBCs and plasma lipoproteins was saturable and temperature-, energy-, and time-dependent, consistent with an active process. We did not find LDLR, ABCG1, or scavenger receptor class B type 1 in RBCs but found a substantial amount of ABCA1 mRNA and protein. However, specific cholesterol efflux from RBCs to isolated apoA-I was negligible, and ABCA1 silencing with siRNA or inhibition with vanadate and Probucol did not inhibit the efflux to apoA-I, HDL, or plasma. Cholesterol efflux from and cholesterol uptake by RBCs from Abca1+/+ and Abca1−/− mice were similar, arguing against the role of ABCA1 in cholesterol flux between RBCs and lipoproteins. Bioinformatics analysis identified ABCA7, ABCG5, lipoprotein lipase, and mitochondrial translocator protein as possible candidates that may mediate the cholesterol flux. Together, these results suggest that RBCs actively participate in cholesterol transport in the blood, but the role of cholesterol transporters in RBCs remains uncertain.
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Imamura, Hiroyuki, Keiko Mizuuchi, and Reika Oshikata. "Physical Activity and Blood Lipids and Lipoproteins in Dialysis Patients." International Journal of Nephrology 2012 (2012): 1–6. http://dx.doi.org/10.1155/2012/106914.

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The relationship between physical activity and blood lipids and lipoproteins in dialysis patients is reviewed in the context of the potentially confounding factors such as nutritional intake, cigarette smoking, obesity, alcohol intake, and physical activity levels in the general population and additional confounding factors such as mode of dialysis and diabetes in dialysis patients. The known associations in the general population of physical activity with high-density-lipoprotein cholesterol subfractions and apolipoprotein A-I are more pronounced in hemodialysis patients than in peritoneal dialysis patients even after adjusting for these confounding factors. Examining studies on the effects of physical activity on blood lipids and lipoproteins, the most consistent observation is the noted decrease in triglycerides and increase in high-density-lipoprotein cholesterol and insulin sensitivity in hemodialysis patients. The changes in lipids and lipoproteins in hemodialysis patients could be caused by changes in activity levels of lipoprotein lipase, insulin sensitivity, and/or glucose metabolism. Future research investigating the relationship between physical activity and blood lipids and lipoproteins in dialysis patients should direct research towards the underlying mechanisms for changes in blood lipids and lipoproteins.
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4

Havel, R. J. "Lipid transport function of lipoproteins in blood plasma." American Journal of Physiology-Endocrinology and Metabolism 253, no. 1 (July 1, 1987): E1—E5. http://dx.doi.org/10.1152/ajpendo.1987.253.1.e1.

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Fatty acid and cholesterol transport in plasma lipoproteins evolved in the context of an open circulatory system in which lipoprotein particles are secreted directly into the blood and have ready access to cells in various tissues. In higher vertebrates with closed capillary beds, hydrolysis of triglycerides at capillary surfaces is required for efficient uptake of their component fatty acids into cells. Likewise, hydrolysis of cellular triglycerides in cells of adipose tissue precedes mobilization of the fatty acids and permits large amounts to be transported in the blood. However, in all Metazoa lipoproteins are secreted primarily from cells adjacent to an open microvascular bed. Uptake of lipoprotein particles as such into cells occurs in invertebrates and vertebrates alike, facilitated by binding to high-affinity receptors on cell surfaces. In vertebrates, a concentration gradient created between cholesterol in cells and lipoproteins by a cholesterol-esterifying enzyme that acts on lipoproteins promotes movement of cholesterol into the plasma compartment. Thus the strategies to transport poorly soluble lipids include enzymatic reactions at cell surfaces and in blood plasma as well as the processes of exocytosis and endocytosis.
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Ilves, Liis, Aigar Ottas, Liisi Raam, Mihkel Zilmer, Tanel Traks, Viljar Jaks, and Külli Kingo. "Changes in Lipoprotein Particles in the Blood Serum of Patients with Lichen Planus." Metabolites 13, no. 1 (January 6, 2023): 91. http://dx.doi.org/10.3390/metabo13010091.

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Lichen planus is a chronic inflammatory mucocutaneous disease that belongs to the group of papulosquamous skin diseases among diseases like psoriasis, a widely studied disease in dermatology. The aim of the study was to identify the changes between the blood sera of lichen planus patients and healthy controls to widen the knowledge about the metabolomic aspect of lichen planus and gain a better understanding about the pathophysiology of the disease. We used high-throughput nuclear magnetic resonance (NMR) spectroscopy to measure the levels of blood serum metabolites, lipoproteins and lipoprotein particles. Dyslipidemia has relatively recently been shown to be one of the comorbidities of lichen planus, but the changes in the components of lipoproteins have not been described yet. We found statistically significant changes in the concentrations of 16 markers regarding lipoproteins, which included the components of intermediate-density lipoproteins, low-density lipoproteins and large low-density lipoproteins. We propose that the detected changes may increase the risk for specific comorbidities (e.g., dyslipidemia) and resulting cardiovascular diseases, as the turnover and hepatic uptake of the altered/modified lipoprotein particles are disturbed.
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Stellaard, Frans. "From Dietary Cholesterol to Blood Cholesterol, Physiological Lipid Fluxes, and Cholesterol Homeostasis." Nutrients 14, no. 8 (April 14, 2022): 1643. http://dx.doi.org/10.3390/nu14081643.

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Dietary cholesterol (C) is a major contributor to the endogenous C pool, and it affects the serum concentration of total C, particularly the low-density lipoprotein cholesterol (LDL-C). A high serum concentration of LDL-C is associated with an increased risk for atherosclerosis and cardiovascular diseases. This concentration is dependent on hepatic C metabolism creating a balance between C input (absorption and synthesis) and C elimination (conversion to bile acids and fecal excretion). The daily C absorption rate is determined by dietary C intake, biliary C secretion, direct trans-intestinal C excretion (TICE), and the fractional C absorption rate. Hepatic C metabolism coordinates C fluxes entering the liver via chylomicron remnants (CMR), LDL, high-density lipoproteins (HDL), hepatic C synthesis, and those leaving the liver via very low-density lipoproteins (VLDL), biliary secretion, and bile acid synthesis. The knowns and the unknowns of this C homeostasis are discussed.
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7

Kersten, Sander. "Peroxisome Proliferator Activated Receptors and Lipoprotein Metabolism." PPAR Research 2008 (2008): 1–11. http://dx.doi.org/10.1155/2008/132960.

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Plasma lipoproteins are responsible for carrying triglycerides and cholesterol in the blood and ensuring their delivery to target organs. Regulation of lipoprotein metabolism takes place at numerous levels including via changes in gene transcription. An important group of transcription factors that mediates the effect of dietary fatty acids and certain drugs on plasma lipoproteins are the peroxisome proliferator activated receptors (PPARs). Three PPAR isotypes can be distinguished, all of which have a major role in regulating lipoprotein metabolism. PPARαis the molecular target for the fibrate class of drugs. Activation of PPARαin mice and humans markedly reduces hepatic triglyceride production and promotes plasma triglyceride clearance, leading to a clinically significant reduction in plasma triglyceride levels. In addition, plasma high-density lipoprotein (HDL)-cholesterol levels are increased upon PPARαactivation in humans. PPARγis the molecular target for the thiazolidinedione class of drugs. Activation of PPARγin mice and human is generally associated with a modest increase in plasma HDL-cholesterol and a decrease in plasma triglycerides. The latter effect is caused by an increase in lipoprotein lipase-dependent plasma triglyceride clearance. Analogous to PPARα, activation of PPARβ/δleads to increased plasma HDL-cholesterol and decreased plasma triglyceride levels. In this paper, a fresh perspective on the relation between PPARs and lipoprotein metabolism is presented. The emphasis is on the physiological role of PPARs and the mechanisms underlying the effect of synthetic PPAR agonists on plasma lipoprotein levels.
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Muscella, Antonella, Erika Stefàno, and Santo Marsigliante. "The effects of exercise training on lipid metabolism and coronary heart disease." American Journal of Physiology-Heart and Circulatory Physiology 319, no. 1 (July 1, 2020): H76—H88. http://dx.doi.org/10.1152/ajpheart.00708.2019.

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Blood lipoproteins are formed by various amounts of cholesterol (C), triglycerides (TGs), phospholipids, and apolipoproteins (Apos). ApoA1 is the major structural protein of high-density lipoprotein (HDL), accounting for ~70% of HDL protein, and mediates many of the antiatherogenic functions of HDL. Conversely, ApoB is the predominant low-density lipoprotein (LDL) Apo and is an indicator of circulating LDL, associated with higher coronary heart disease (CHD) risk. Thus, the ratio of ApoB to ApoA1 (ApoB/ApoA1) is used as a surrogate marker of the risk of CHD related to lipoproteins. Elevated or abnormal levels of lipids and/or lipoproteins in the blood are a significant CHD risk factor, and several studies support the idea that aerobic exercise decreases CHD risk by partially lowering serum TG and LDL-cholesterol (LDL-C) levels and increasing HDL-C levels. Exercise also exerts an effect on HDL-C maturation and composition and on reverse C transport from peripheral cells to the liver to favor its catabolism and excretion. This process prevents atherosclerosis, and several studies showed that exercise training increases heart lipid metabolism and protects against cardiovascular disease. In these and other ways, it more and more appears that regular exercise, nutrition, and strategies to modulate lipid profile should be viewed as an integrated whole. The purpose of this review is to assess the effects of endurance training on the nontraditional lipid biomarkers, including ApoB, ApoA1, and ApoB/ApoA1, in CHD risk.
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Belozerov, Evgeniy Stepanovich, Nelli Alekseevna Shchukina, Aleksandr Leonidovich Smetanin, Anton Igorevich Andriyanov, Oksana Gennadievna Korosteleva, and Elena Sergeevna Martynova. "LIPID METABOLISM IN YOUNG MILITARY MEN." Ulyanovsk Medico-biological Journal, no. 4 (December 26, 2022): 120–27. http://dx.doi.org/10.34014/2227-1848-2022-4-120-127.

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The purpose of the paper is to assess the influence of the nutritional factor on lipid metabolism in young military men.
 Materials and methods. The objects of the study were young conscripted men aged 19.3±1.2, who feed on combined arms ration (n=71). Lipid metabolism indicators (cholesterol, triglycerides, high-density lipoprotein, low density lipoprotein, very low density lipoproteins and atherogenic index) were assessed in military men. For this purpose, chromatography-mass spectrometry (Beckman Coulter AU480 automatic biochemical analyzer) was used. The study was conducted in the consultative and diagnostic polyclinic of the medical and diagnostic center, Military Medical Academy. The assessment of the studied indicators was made 60 days apart in the autumn-winter period. Nonparametric methods were used for statistical processing of experimental data. Risk analysis of the potential influence of the nutritional factor on lipid metabolism was carried out.
 Results. Differences in the lipoprotein content in the servicemen blood serum at the beginning and end of trial were random. Levels of cholesterol levels and low density lipoproteins, as well as atherogenic index decreased significantly.
 Conclusion. During the study, no statistically significant negative changes in lipid metabolism were found.
 Risk assessment of potential violation of the nutritional status in young military men indicates a favorable effect of nutrition on their lipid metabolism.
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Garmish, O. "The nature of metabolic disorders of blood lipoproteins as the basis for the pathogenesis of atherosclerosis in patients with inflammatory joint diseases." Bukovinian Medical Herald 24, no. 4 (96) (November 26, 2020): 12–18. http://dx.doi.org/10.24061/2413-0737.xxiv.4.96.2020.97.

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Objective of this study was to determine the characteristics of the metabolic disorders of lipids and lipoproteins (LP) in the blood in 112 patients with systemic rheumatic diseases.Material and methods. In all patients, the level of C-reactive protein (CRP), the content of malonic aldehyde (MA) in circulating monocytes, in blood plasma, and catalase activity were determined. The presence and severity of pro-atherogenic status were evaluated by the content of modified low-density lipoproteins (LDL) and very-low-density lipoproteins (VLDL) in the blood, which was determined by the bioassay method using peritoneal mouse macrophages. The immunogenicity of modified LР was determined by the content in the circulating immune complexes (CIC) of cholesterol (Сhol) and triglycerides (TG). The spectrum of lipids and LP in the blood was evaluated in detail with an additional determination of the plasma level of proteins apoB and apoA-1 were determined.Results. The obtained results show the existence in the examined patients of significant systemic inflammation in conjunction with the distinct proatherogenic metabolic state that was revealed by lipoprotein modification with the appearance in them of auto-antigenic properties. These changes appeared despite the absence of significant traditional atherogenic risk factors. The results of the paired correlative analysis showed the existence of strong dependence between indexes of systemic inflammation, proatherogenic and immunogenic lipoprotein modification. Conclusions. When determining proatherogenic disorders of lipid and blood lipoproteins metabolism in patients with systemic rheumatic diseases, it is necessary to focus not on traditional risk factors, which may remain within normal values, but on the content of apoA-1, apoB proteins, their ratio, and the determination of modified lipoproteins blood and the severity of the autoimmune reaction to them.
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Tesis sobre el tema "Blood lipoproteins Metabolism"

1

Owen, Alice. "The effects of estrogens and phytoestrogens on the metabolism and oxidation of plasma lipoproteins /." Title page, contents and abstract only, 1999. http://web4.library.adelaide.edu.au/theses/09PH/09pho968.pdf.

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Mamo, John Charles Louis. "Plasma lipoprotein triacylglycerol metabolism in sheep : a thesis submitted to the University of Adelaide in fulfilment of the requirements for the degree of Doctor of Philosophy." Title page, contents and introduction only, 1986. http://web4.library.adelaide.edu.au/theses/09PH/09phm265.pdf.

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Willcox, Karen Kay. "EFFECTS OF AGING AND NUTRITION ON PLASMA LIPOPROTEINS IN NONHUMAN PRIMATES." Thesis, The University of Arizona, 1985. http://hdl.handle.net/10150/275320.

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Hacquebard, Mirjam Rebecca. "Alpha-tocopherol acquisition by plasma lipoproteins and changes in lipoprotein profile after cardiac surgery." Doctoral thesis, Universite Libre de Bruxelles, 2008. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/216586.

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Alpha-tocopherol, the most abundant form of vitamin E in man, is transported in the circulation by plasma lipoproteins. It plays important roles, not only in preventing lipid peroxidation, but also in modulating several cell functions such as cell signaling and gene expression. While chylomicrons transport dietary alpha-tocopherol after intestinal absorption, LDL and HDL are the major carriers of alpha-tocopherol in fasting plasma and largely contribute to its delivery to cells and tissues. Exchanges of alpha-tocopherol occur between plasma lipoproteins. In addition, alpha-tocopherol transfers have also been observed, in both directions, between plasma lipoproteins and artificial chylomicrons such as intravenous lipid emulsion particles used in parenteral nutrition. In acute conditions, intravenous supply of vitamin E via lipid emulsions, which bypasses the intestinal tract, may offer some advantages over oral administration to rapidly increase alpha-tocopherol plasma concentration. However, many questions remain unanswered regarding kinetics and factors facilitating vitamin E exchanges between lipid emulsions and plasma lipoproteins. The first part of this work aimed at characterizing alpha-tocopherol transfers between alpha-tocopherol rich emulsion particles and plasma lipoproteins as well as the potential for plasma proteins to modulate such transfers. An in vitro model of incubation was used in which emulsion triglyceride concentration was relatively low and lipoprotein levels comparable to those commonly found in the circulation. Results indicate a high capacity for LDL and HDL to acquire extra-amounts of alpha-tocopherol by rapid mass transfers from alpha-tocopherol-rich emulsion particles. Data further shows that, at a fixed alpha-tocopherol concentration provided by emulsion particles, the limiting factor for alpha-tocopherol enrichment is not the capacity of plasma lipoproteins to accommodate extra-amounts of alpha-tocopherol but the facilitating effect of plasma proteins on alpha-tocopherol transfer, the duration of the incubation and possibly the competition between different acceptor particles. Two lipid transfer proteins, PLTP and CETP, appear to largely mediate facilitation of alpha-tocopherol transfer; however, other plasma proteins may be involved. Data further shows that alpha-tocopherol enriched LDL and HDL can readily transfer newly acquired alpha-tocopherol to cells, without any regulation by plasma proteins.<p>Short-term prophylactic vitamin E supplementation has been suggested to be beneficial in some patients in acute conditions who present reduced plasma vitamin E concentrations in association with important changes in plasma lipids and severe oxidative stress. However, it was not clear whether low plasma vitamin E concentration in critically ill patients is related to changes in the composition of plasma lipoproteins or to a decrease in the number of alpha-tocopherol carriers. In the second part of this work, two clinical studies were conducted to analyze changes of lipoprotein concentration and composition in relation to inflammatory reaction and oxidative stress in selected subgroups of critically ill patients, namely patients undergoing cardiac surgery with different procedures. Important changes in LDL and HDL lipid content were observed, some of which contrast with previous observations made in critically ill septic patients. The reduced plasma level of alpha-tocopherol measured after cardiac surgery is entirely due to a reduced number of circulating LDL and HDL particles. Data suggests that such reduced number in alpha-tocopherol carriers post-surgery may impede the delivery of alpha-tocopherol to cells in conditions of increased requirements due to oxidative stress. Avoidance of extracorporeal circulation during cardiac surgery does not reduce inflammation-related changes in plasma lipids but largely prevents oxidative stress. This data on changes occurring in plasma lipoproteins may help to better define strategies against pro-inflammatory changes or oxidative stress. If further studies would confirm a clinical benefit with evidence-based rationale, alpha-tocopherol enriched lipid emulsions may be used to guarantee a sufficient alpha-tocopherol supply in acute conditions associated with fewer alpha-tocopherol transporters and increased requirements due to high risk of oxidative tissue injury.<p><br>Doctorat en Sciences biomédicales et pharmaceutiques<br>info:eu-repo/semantics/nonPublished
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Oviedo, Landaverde Irene. "Disruption of LDL receptor-like gene function in Caenorhabditis elegans." Thesis, McGill University, 2004. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=81419.

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dsc-4(qm182), a mutation that suppresses the lengthened defecation cycle of clk-1 also suppresses the delay in germline development. dsc-4 encodes a putative orthologue of microsomal triglyceride transfer protein (MTP), a protein essential for the assembly and secretion of apo-B-containing low density lipoproteins (LDL). The effect of dsc-4 on clk-1(qm30), coupled to studies of apoB homologues in worms led to a model suggesting the possibility of using C. elegans in the study of LDL-like lipoprotein particles. The impact of the level of lipoproteins is particularly evident in the germline developmental rate of the worms.<br>We report here a further elucidation of clk-1 mutants in the study of the biology of LDL-like particles. In particular, we investigated the effect of targeting LDL receptor-like genes by RNA interference (RNAi) on the egg laying rate of clk-1(qm30). We find positive modulating effects by disruption of these putative LDL receptors. In confirmation of our model of lipoprotein metabolism in clk-1 mutants, we find that disruption of these putative LDL receptors produces strikingly different effects in wild-type, clk-1(qm30) or clk-1(qm30); dsc-4(qm182) animals.<br>In addition, we report unexpected effects of various clk-1 alleles on the phenotypes of animals in which lrp-1 and rme-2 are disrupted. Specifically, we observe an allele specific amelioration of the phenotypes associated with disruption of these genes (abnormal molting and sterility, respectively). We discuss the possible significance of these findings. (Abstract shortened by UMI.)
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6

Bouna, Moussa Tandia. "Interaction des complexes lipides cationiques / ADN avec les composants du plasma." Doctoral thesis, Universite Libre de Bruxelles, 2005. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/211013.

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Gellar, Lauren A. "The Effect of Glycemic Index and Glycemic Load on Glucose Control, Lipid Profiles and Anthropometrics Among Low-Income Latinos With Type 2 Diabetes: A Dissertation." eScholarship@UMMS, 2011. https://escholarship.umassmed.edu/gsbs_diss/522.

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Background The incidence of type 2 diabetes has increased dramatically, particularly among Latinos. While several studies suggest the beneficial effect of lowering glycemic index and glycemic load in patients with type 2 diabetes, no data exists regarding this issue in the Latino population. The purpose of this study was to determine the effect of lowering glycemic index and glycemic load on diabetes control, lipid profiles and anthropometrics among Latinos with type 2 diabetes. Methods Subjects participated in a 12 month randomized clinical trial. The intervention targeted diabetes knowledge, attitudes and behavioral capabilities related to diabetes self management with content including nutrition and physical activity. The nutrition protocol emphasized reduction in glycemic index, fat, salt and portion size and increase in fiber. The control group was given usual care. Measurements included Hba1c, fasting glucose, total cholesterol (TC), low density lipoproteins (LDL) and high density lipoproteins (HDL), HDL:LDL ratio, TC:HDL ratio, waist circumference and BMI and were collected at baseline, 4 and 12-months. Results Two hundred fifty two Latino adults with type 2 diabetes participated in the study. Baseline mean HbA1C was 8.98% (SD=1.87), BMI was 34.76 kg/cm (SD=6.94), age was 56 (SD=11.18) years and 76% were female. Reduction in glycemic index was positively associated with a reduction in logHbA1c (p=0.006), HDL:LDL ratio (p=0.037) and waist circumference (p=0.003) overtime, but not with fasting glucose, TC, LDL and HDL, TC:HDL ratio, body weight or BMI. No significant associations were found between glycemic load and any measures. Conclusion Results suggest that lowering glycemic index may have a positive effect on some markers of diabetes control, lipid profiles and anthropometrics among Latinos with type 2 diabetes, but not others. While statistically significant reductions in GI and GL were noted, the actual reduction was small. Thus, greater reduction in GI and GL may be needed for clinical significance and greater effect on metabolic outcomes. Future research should target populations with higher baseline GI and GL.
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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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Owen, Alice 1972. "The effects of estrogens and phytoestrogens on the metabolism and oxidation of plasma lipoproteins." 1999. http://web4.library.adelaide.edu.au/theses/09PH/09pho968.pdf.

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Includes bibliographical references (leaves 172-217). Examines the effects of estrogens and phytoestrogens on plasma lipoprotein levels and other risk factors for cardiovascular disease, including the oxidisability of low density lipoprotein
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Owen, Alice 1972. "The effects of estrogens and phytoestrogens on the metabolism and oxidation of plasma lipoproteins / Alice Jane Owen." Thesis, 1999. http://hdl.handle.net/2440/19821.

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Includes bibliographical references (leaves 172-217).<br>viii, 217 leaves : ill. ; 30 cm.<br>Examines the effects of estrogens and phytoestrogens on plasma lipoprotein levels and other risk factors for cardiovascular disease, including the oxidisability of low density lipoprotein<br>Thesis (Ph.D.)--University of Adelaide, Dept. of Physiology, 1999
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Libros sobre el tema "Blood lipoproteins Metabolism"

1

J, Halpern M., ed. Lipid metabolism and its pathology. New York: Plenum Press, 1985.

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2

Workshop on Lipoprotein Heterogeneity (1986 Rockville, Md.). Proceedings of the Workshop on Lipoprotein Heterogeneity, Rockville, Maryland, September 29, 30, and October 1, 1986. Edited by Lippel Kenneth. [Bethesda, Md.]: U.S. Dept. of Health and Human Services, National Institutes of Health, 1987.

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John, Betteridge, Illingworth D. Roger 1945-, and Shepherd J. 1944-, eds. Lipoproteins in health and disease. London: Arnold, 1999.

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4

1945-, Fruchart J. C., and Shepherd J. 1944-, eds. Human plasma lipoproteins. Berlin: De Gruyter, 1989.

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5

International Dresden Lipid Symposium (9th 1997 Dresden, Germany). Advances in lipoprotein and atherosclerosis researh, diagnostic and treatment: Proceedings of the 9th International Dresden Lipid Symposium, held at Dresden, June 27-29, 1997. Edited by Hanefeld Markolf. Jena: G. Fischer, 1998.

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International Dresden Lipid Symposium (7th 1991 Dresden, Germany). Advances in lipoprotein and atherosclerosis research, diagnostics and treatment: Proceedings of the 7th International Dresden Lipid Symposium 1991 Held at Dresden, June 9-11, 1991. Edited by Dude H, Hanefeld Markolf, and Jaross W. Stuttgart: Gustav Fischer Verlag Jena, 1991.

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International Symposium on Drugs Affecting Lipid Metabolism (8th 1983 Philadelphia, Pa.). Drugs affecting lipid metabolism VIII. New York: Plenum Press, 1985.

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International Meeting on Atherosclerosis and Cardiovascular Diseases. (7th 1989 Bologna, Italy). Atherosclerosis and cardiovascular disease: 7° international meeting, Bologna, September 1989. Edited by Descovich G. C. Bologna: Editrice Compositori, 1989.

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International Meeting on Atherosclerosis and Cardiovascular Diseases. (6th 1986 Bologna, Italy). Atherosclerosis and cardiovascular diseases: 6° international meeting, Bologna, October 1986. Edited by Descovich G. C and Lenzi S. Bologna: Editrice Compositori, 1987.

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Parker, James N., and Philip M. Parker. Abetalipoproteinemia: A bibliography and dictionary for physicians, patients, and genome researchers [to internet references]. San Diego, CA: ICON Health Publications, 2007.

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Capítulos de libros sobre el tema "Blood lipoproteins Metabolism"

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Aviram, Michael. "Effect of Lipoproteins and Platelets on Macrophage Cholesterol Metabolism." In Blood Cell Biochemistry, 179–208. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4757-9531-8_7.

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Bergmann, Sybille, Cornelia Mix, Gabriele Siegert, Catleen Uhlig, Peter Richter, and Werner Jaross. "Which Effects Does Early HRT Have on Perimenopausal Changes in the Lipoprotein Profile, Glucose Metabolism, and the Blood Coagulation-Fibrinolysis System?" In Medical Science Symposia Series, 135–39. Dordrecht: Springer Netherlands, 1997. http://dx.doi.org/10.1007/978-94-011-5560-1_21.

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Cegla, Jaimini, and James Scott. "Lipid disorders." In Oxford Textbook of Medicine, edited by Timothy M. Cox, 2055–97. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0232.

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High blood cholesterol and high blood triglycerides are causal risk factors for atherosclerotic cardiovascular disease, which remains the leading cause of death in the developed world. Lipid and lipoprotein metabolism—cholesterol, triglycerides, and fat-soluble vitamins are transported with specific proteins in the blood as multimeric complexes called lipoproteins. Lipid and lipoprotein metabolism are effected by three principal physiological processes: (1) intestinal absorption of dietary lipid and transport in the blood of dietary lipid and lipids, principally derived from the liver (as triglyceride-rich lipoproteins) to peripheral tissues for catabolism by skeletal and cardiac muscle or storage in adipose tissue; (2) return of triglyceride-rich lipoprotein remnants to the liver, hepatic synthesis of low-density lipoprotein, and the transport of cholesterol between peripheral tissues and the liver; and (3) reverse cholesterol transport by high-density lipoprotein (HDL) between peripheral tissues and the liver. Dyslipidaemias are disorders of lipoprotein metabolism in which there is elevation of total cholesterol and/or triglycerides, often accompanied by reduced levels of HDL cholesterol. Causes of dyslipidaemia—particular lipid disorders including polygenic hypercholesterolaemia, familial hypercholesterolaemia, combined hypercholesterolaemia and hypertriglyceridaemia, familial combined hyperlipidaemia, familial dysbetalipoproteinaemia (also called type 3 hyperlipoproteinaemia), and severe hypertriglyceridaemia, as well as secondary or aggravating factors. Management of dyslipidaemia—the key questions are: (1) what classes of lipoproteins and lipids are increased or decreased in the patient’s plasma? (2) Does the patient has a primary (genetic) or secondary (acquired) dyslipidaemia (often contributions from both influences)? (3) Is the patient at risk of atherosclerotic cardiovascular disease or acute pancreatitis? (4) What other risk factors (e.g. hypertension or diabetes) are present? (5) What treatments might be used to address these abnormalities?
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Larry Durstine, J., and Andrea Summer. "Physical Activity, Exercise, Blood Lipids, and Lipoproteins." In Lipid Metabolism and Health, 265–82. CRC Press, 2005. http://dx.doi.org/10.1201/9781420038422.ch12.

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Mc Auley, Mark T., and Amy E. Morgan. "Cholesterol transport in blood, lipoproteins, and cholesterol metabolism." In Cholesterol, 227–58. Elsevier, 2022. http://dx.doi.org/10.1016/b978-0-323-85857-1.00025-0.

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Si Nguyen, Van, Xuan Truong Tran, Thanh Duy Vo, and Quang Truong Le. "Residual Cardiovascular Risk Factors in Dyslipidemia." In Risk Factors for Cardiovascular Disease. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.100046.

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Cardiovascular disease poses a major challenge for the 21st century. Although good control of blood pressure and type 2 diabetes and reducing low-density lipoprotein-cholesterol levels can improve cardiovascular outcomes, a substantial residual risk remains existed after treatment in most patient populations. Recently, many efforts have been directed at finding the important role of low high-density-lipoprotein cholesterol, high triglycerides, especially triglyceride-rich lipoproteins and lipoprotein (a) in the metabolism of atherosclerotic plaque formation Therefore, based on the recent evidence, identification and treatment of these risk factors may play a role in optimizing therapeutic strategy, particularly in high risk subjects along with conventional treatment. In clinical practice, adequate attention should be paid when screening and managing residual cardiovascular risk factors in dyslipidemia in term of individualized approach. The ongoing trials will give more answers to elucidate this important area.
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Gelson, William, and Alexander Gimson. "Structure and function of the liver, biliary tract, and pancreas." In Oxford Textbook of Medicine, edited by Jack Satsangi, 3032–42. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0315.

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The liver, sited in the right upper quadrant of the abdomen, comprises eight segments, each of which is a complete functional unit with a single portal pedicle and a hepatic vein. Within the functional segments, the structural unit is the hepatic lobule, a polyhedron surrounded by four to six portal tracts containing hepatic arterial and portal venous branches from which blood perfuses through sinusoids, surrounded by walls of hepatocytes that are a single cell thick and lined by specialized endothelial cells with ‘windows’ (fenestrae), to the centrilobular region and the central hepatic veins. Bile secreted through the canalicular membrane of the hepatocyte collects in biliary canaliculi, from which it passes through the biliary tract into the gut. The liver secretes bile, which aids digestion by emulsifying lipids, and has a central role in metabolism of (1) bilirubin, from haem; (2) bile salts, the principal mechanism for clearance of cholesterol; (3) carbohydrates; (4) amino acids and ammonia; (5) proteins, most circulating plasma proteins being produced by hepatocytes; and (6) lipid and lipoproteins. The pancreas lies in the retroperitoneum and is composed of (1) an exocrine portion centred on acini, producing an alkaline secretion containing digestive enzymes including serine proteases, exopeptidases, and lipolytic enzymes, draining through a ductal system into the duodenum; and (2) the islets of Langerhans, which secrete insulin (also glucagon, somatostatin, and pancreatic polypeptide).
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Elliott, Perry, Pier D. Lambiase, and Dhavendra Kumar. "Familial hypercholesterolaemia." In Inherited Cardiac Disease, 343–48. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198829126.003.0012.

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Familial hypercholesterolaemia (FH) is an inborn error of metabolism that leads to accumulation of low-density lipoprotein cholesterol (LDL-C) particles in the blood and premature coronary artery atherosclerosis. This chapter covers the clinical criteria for the diagnosis of FH, the genetics that underpins the condition, cascade testing, premature coronary heart disease, and treatment methods.
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Alhassan, Sofiya, and Peter Grandjean. "Essential Laboratory Methods for Blood Lipid and Lipoprotein Analysis." In Lipid Metabolism and Health, 117–45. CRC Press, 2005. http://dx.doi.org/10.1201/9781420038422.ch7.

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Ejaz, Mahnoor, Areena Suhail Khan, Faiza Naseer, and Alvina Gul. "Metabolic Syndromes." In Omics Technologies for Clinical Diagnosis and Gene Therapy: Medical Applications in Human Genetics, 242–68. BENTHAM SCIENCE PUBLISHERS, 2022. http://dx.doi.org/10.2174/9789815079517122010018.

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Metabolic Syndromes (MetS) are recognized as a cluster of risk factors which are known to increase the likelihood of obesity, type 2 diabetes (T2D) and cardiovascular disorders (CVDs). It is significant to understand disease pathology in order to discover a pathological mechanism leading to the development of MetS. Elevated triglycerides, increased blood pressure, hyperglycemia (increased blood glucose levels), low levels of High-density lipoprotein (HDL) cholesterol and elevated waist circumference are key parameters in diagnosing MetS. Various therapeutic interventions have been developed for treating metabolic diseases like polypills which are commonly known as combination pills, along with the fixed dose combinations. In addition to pharmacological handling, surgical treatment is also showing success in treating MetS such as Bariatric treatment. With the emerging experimental techniques, gene therapy allows the replacement of a defective gene with a healthy one, which may eventually reverse the disease. Leptin Gene Therapy, ZFN Gene Editing, CRISPR/ Cas9 genome editing are different platforms of gene therapy which are showing promising results in treating the metabolic disease. Novel experimental approaches and pharmacological treatments can provide a better insight into metabolic syndrome and its related complications, thereby reducing its global burden.
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Actas de conferencias sobre el tema "Blood lipoproteins Metabolism"

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Prado, Vanildo, Daniel Buttros, Luciana Buttros de Paula, Benedito de Sousa Almeida Filho, Heloisa Maria de Luca Vespoli, Carla Kamya Pessoa, Eduardo Pessoa, and Eliana Aguiar Petri Nahás. "EVALUATION OF METABOLIC SYNDROME AND OBESITY IN BREAST CANCER SURVIVORS SUBJECTED TO INTERDISCIPLINARY APPROACH: A PROSPECTIVE COHORT STUDY." In Abstracts from the Brazilian Breast Cancer Symposium - BBCS 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s2081.

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Objective: The aim of this study was to assess the occurrence of metabolic syndrome (MetS), obesity, and abdominal obesity during the first year after a diagnosis of breast cancer. Methods: This prospective observational study included women with a recent diagnosis of breast cancer. Women aged ≥40 years, with a recent diagnosis of breast cancer, were included. The clinical, anthropometric, and biochemical analyses were performed. Women with three or more diagnostic criteria were considered with MetS as follows: waist circumference (WC) &gt; 88 cm; triglycerides (TG) ≥150 mg/dL; high-density lipoprotein 30 kg/m2 and abdominal obesity with WC &gt;88cm. The measurements were carried out in three moments: first medical assessment (T0m), six months (T6m), and 12 months later (T12m). All patients underwent the interdisciplinary assessment (i.e., nutritional and psychological) at T0m. For statistical analysis, the ANOVA with repeated measures and the chi-square test of trend were used. Results: A total of 72 women with breast cancer were included, with a mean age of 58.4±10.7 years. In the assessment of MetS, BMI, and WC, no difference was observed in the occurrence between the three moments. When comparing the individual metabolic syndrome criteria between the three moments, there was only a statistical difference in the TG and glycemia criteria. The analysis of blood glucose showed a decrease in mean values, with a value of 106.6 mg/dL-T0m, 100.46 mg/dL-T6m, and 98.96 mg/dL-T12m (p=0.004). Regarding TG, an increase in mean values was observed, with a value of 121 mg/dL-T0m, 139.4 mg/dL-T6m, and 148.46 mg/dL-T12m (p=0.003). No cancer treatment showed an impact on the measured criteria. Conclusion: The interdisciplinary approach on the breast cancer survivors demonstrated a positive impact on the control of metabolic syndrome, obesity, and abdominal obesity on the first year of follow-up. Additionally, glycemic indices showed a significant decrease, but an increase in TG values was observed.
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Al Kudsi, Dana Samir, Sara Zeyad Hamad, Hanan Mohamed Al Keldi, Abdelhamid Kerkadi, Abdelali Agouni, and Reem Omar Salih. "The Association between Zinc and Copper and Cardiometabolic Risk Factors in Adults." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2021. http://dx.doi.org/10.29117/quarfe.2021.0143.

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Cardiometabolic risk (CMR) factors increase the likelihood of developing cardiovascular diseases (CVD). In Qatar, 24% of the total deaths are attributed to CVDs. Several nutritional disturbances have been linked to high risk of CVD. Many studies have discussed the effects of zinc (Zn) and copper (Cu) on CMR factors; however, evidence has been controversial. This investigated the association between CMR factors and the status of Zn, Cu, and Zn/Cu ratio. A total of 575 Qatari adults (≥18 years) were obtained from Qatar Biobank. Plasma levels of Zn and Cu were determined using inductively coupled plasma mass spectrometry (ICP-MS). Anthropometric data and CMR factors were determined using standard methods. Adjusted associations between minerals and CMR were estimated by logistic regression. The associations’ strength was tested using partial correlation. Zn was not strongly correlated (p-value˃0.01) or significantly associated with CMR factors and metabolic syndrome (MetS). Cu levels correlated positively with body mass index (BMI) (0.23; p˂0.001), pulse rate (PR) (0.18; p˂0.001), total cholesterol (0.13; p=0.01), and high-density lipoproteins (HDL) (0.27; p˂0.001); and negatively with diastolic blood pressure (DBP) (−0.13; p=0.01). High Cu significantly decreased the risk of MetS (0.121; p˂0.001). Furthermore, Zn/Cu ratio positively correlated with waist circumference (0.13; p=0.01), systolic blood pressure (0.13; p˂0.01), and DBP (0.14; p˂0.01); and negatively with BMI (−0.19; p˂0.001), PR (−0.17; p˂0.001), and HDL (−0.27; p˂0.001). High Zn/Cu ratio increased the prevalence of low HDL (4.508; p˂0.001) and MetS (5.570; p˂0.01). These findings suggest that high Cu levels are associated with a protective effect on DBP, HDL, and MetS and that high plasma Zn/Cu ratio is associated with the risk of low HDL and MetS. We recommend future studies to focus on minerals status among abdominally obese and prediabetic subjects because of the probable link between low serum Zn and Cu and insulin resistance and CVD.
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