Relevant bibliographies by topics / Obesity ; Type 2 diabetes ; Adipose Tissue

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Obesity ; Type 2 diabetes ; Adipose Tissue'

Author: Grafiati
Published: 4 June 2021
Last updated: 13 February 2022

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Journal articles on the topic "Obesity ; Type 2 diabetes ; Adipose Tissue"

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Lee, Min-Woo, Mihye Lee, and Kyoung-Jin Oh. "Adipose Tissue-Derived Signatures for Obesity and Type 2 Diabetes: Adipokines, Batokines and MicroRNAs." Journal of Clinical Medicine 8, no. 6 (June 14, 2019): 854. http://dx.doi.org/10.3390/jcm8060854.

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Obesity is one of the main risk factors for type 2 diabetes mellitus (T2DM). It is closely related to metabolic disturbances in the adipose tissue that primarily functions as a fat reservoir. For this reason, adipose tissue is considered as the primary site for initiation and aggravation of obesity and T2DM. As a key endocrine organ, the adipose tissue communicates with other organs, such as the brain, liver, muscle, and pancreas, for the maintenance of energy homeostasis. Two different types of adipose tissues—the white adipose tissue (WAT) and brown adipose tissue (BAT)—secrete bioactive peptides and proteins, known as “adipokines” and “batokines,” respectively. Some of them have beneficial anti-inflammatory effects, while others have harmful inflammatory effects. Recently, “exosomal microRNAs (miRNAs)” were identified as novel adipokines, as adipose tissue-derived exosomal miRNAs can affect other organs. In the present review, we discuss the role of adipose-derived secretory factors—adipokines, batokines, and exosomal miRNA—in obesity and T2DM. It will provide new insights into the pathophysiological mechanisms involved in disturbances of adipose-derived factors and will support the development of adipose-derived factors as potential therapeutic targets for obesity and T2DM.
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Sell, Henrike, and Jürgen Eckel. "Chemotactic cytokines, obesity and type 2 diabetes:in vivoandin vitroevidence for a possible causal correlation?" Proceedings of the Nutrition Society 68, no. 4 (August 24, 2009): 378–84. http://dx.doi.org/10.1017/s0029665109990218.

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A strong causal link between increased adipose tissue mass and insulin resistance in tissues such as liver and skeletal muscle exists in obesity-related disorders such as type 2 diabetes. Increased adipose tissue mass in obese patients and patients with diabetes is associated with altered secretion of adipokines, which also includes chemotactic proteins. Adipose tissue releases a wide range of chemotactic proteins including many chemokines and chemerin, which are interesting targets for adipose tissue biology and for biomedical research in obesity and obesity-related diseases. This class of adipokines may be directly linked to a chronic state of low-grade inflammation and macrophage infiltration in adipose tissue, a concept intensively studied in adipose tissue biology in recent years. The inflammatory state of adipose tissue in obese patients may be the most important factor linking increased adipose tissue mass to insulin resistance. Furthermore, chemoattractant adipokines may play an important role in this situation, as many of these proteins possess biological activity beyond the recruitment of immune cells including effects on adipogenesis and glucose homeostasis in insulin-sensitive tissues. The present review provides a summary of experimental evidence of the role of adipose tissue-derived chemotactic cytokines and their function in insulin resistancein vivoandin vitro.
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Søndergaard, Esben, and Michael D. Jensen. "Quantification of adipose tissue insulin sensitivity." Journal of Investigative Medicine 64, no. 5 (April 12, 2016): 989–91. http://dx.doi.org/10.1136/jim-2016-000098.

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In metabolically healthy humans, adipose tissue is exquisitely sensitive to insulin. Similar to muscle and liver, adipose tissue lipolysis is insulin resistant in adults with central obesity and type 2 diabetes. Perhaps uniquely, however, insulin resistance in adipose tissue may directly contribute to development of insulin resistance in muscle and liver because of the increased delivery of free fatty acids to those tissues. It has been hypothesized that insulin adipose tissue resistance may precede other metabolic defects in obesity and type 2 diabetes. Therefore, precise and reproducible quantification of adipose tissue insulin sensitivity, in vivo, in humans, is an important measure. Unfortunately, no consensus exists on how to determine adipose tissue insulin sensitivity. We review the methods available to quantitate adipose tissue insulin sensitivity and will discuss their strengths and weaknesses.
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Corvera, Silvia, and Olga Gealekman. "Adipose tissue angiogenesis: Impact on obesity and type-2 diabetes." Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 1842, no. 3 (March 2014): 463–72. http://dx.doi.org/10.1016/j.bbadis.2013.06.003.

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de Araújo, Iana M., Carlos E. G. Salmon, Andressa K. Nahas, Marcello H. Nogueira-Barbosa, Jorge Elias, and Francisco J. A. de Paula. "Marrow adipose tissue spectrum in obesity and type 2 diabetes mellitus." European Journal of Endocrinology 176, no. 1 (January 2017): 21–30. http://dx.doi.org/10.1530/eje-16-0448.

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ObjectiveTo assess the association of bone mass and marrow adipose tissue (MAT) with other fat depots, insulin resistance, bone remodeling markers, adipokines and glucose control in type 2 diabetes and obesity.Design and methodsThe study groups comprised 24 controls (C), 26 obese (O) and 28 type 2 diabetes. Dual-energy X-ray absorptiometry was used to determine bone mineral density (BMD). Blood samples were collected for biochemical measurements.1H Magnetic resonance spectroscopy was used to assess MAT in the L3 vertebra, and abdominal magnetic resonance imaging was used to assess intrahepatic lipids in visceral (VAT) and subcutaneous adipose tissue. Regression analysis models were used to test the association between parameters.ResultsAt all sites tested, BMD was higher in type 2 diabetes than in O and C subjects. The C group showed lower VAT values than the type 2 diabetes group and lower IHL than the O and type 2 diabetes groups. However, MAT was similar in the 3 groups. Osteocalcin and C-terminal telopeptide of type 1 collagen were lower in type 2 diabetes than those in C and O subjects. Moreover, at all sites, BMD was negatively associated with osteocalcin. No association was observed between MAT and VAT. No relationship was observed among MAT and HOMA-IR, leptin, adiponectin or Pref-1, but MAT was positively associated with glycated hemoglobin.ConclusionsMAT is not a niche for fat accumulation under conditions of energy surplus and type 2 diabetes, also is not associated with VAT or insulin resistance. MAT is associated with glycated hemoglobin.
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Zhang, Jun, Zhiwei Zhang, Yulei Ding, Peng Xu, Tingting Wang, Wenjing Xu, Huan Lu, et al. "Adipose Tissues Characteristics of Normal, Obesity, and Type 2 Diabetes in Uygurs Population." Journal of Diabetes Research 2015 (2015): 1–6. http://dx.doi.org/10.1155/2015/905042.

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Our results showed that, at the same BMI level, Uygurs have greater WHR values, abdominal visceral fat content, and diabetes risks than Kazaks. In addition, values of HDL-C in Uygur subjects were lower than those in Kazak subjects, and values of creatinine, uric acid, diastolic blood pressure, blood glucose, and fructosamine in Uygur male subjects were lower than those in Kazak male subjects. In contrast, systolic blood pressure values in Uygur subjects were greater than those in Kazak subjects, and blood glucose values were greater in Uygur female subjects than in Kazak female subjects. Additionally, in Uygurs, visceral adipose tissue expression levels ofTBX1andTCF21were greater in obesity group than in normal and T2DM groups and lower in T2DM group than in normal group (P<0.01). The visceral adipose tissue expression levels ofAPNin normal group was greater than those in obesity and T2DM groups, and visceral adipose tissue expression levels ofTNF-αandMCP-1in normal group were lower than those in obesity and T2DM groups (P<0.01). In conclusion, T2DM in Uygurs was mainly associated with not only distribution of adipose tissue in body, but also change in metabolic activity and adipocytokines secretion of adipose tissue.
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Blaak, E. E. "Fatty acid metabolism in obesity and type 2 diabetes mellitus." Proceedings of the Nutrition Society 62, no. 3 (August 2003): 753–60. http://dx.doi.org/10.1079/pns2003290.

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Disturbances in pathways of lipolysis and fatty acid handling are of importance in the aetiology of obesity and type 2 diabetes mellitus. There is evidence that a lowered catecholamine-mediated lipolytic response may play a role in the development and maintenance of increased adipose tissue stores. Increased adipose tissue stores, a disturbed insulin-mediated regulation of lipolysis and subnormal skeletal muscle non-esterified fatty acid (NEFA) uptake under conditions of high lipolytic rate may increase circulating NEFA concentrations, which may promote insulin resistance and cardiovascular complications. In addition, a disturbance of NEFA uptake by adipose tissue postprandially is also a critical determinant of plasma NEFA concentration. Furthermore, evidence is increasing that insulin-resistant muscle is characterised by a lowered ability to oxidise fatty acids. A dysbalance between fatty acid uptake and fatty acid oxidation may in turn be a factor promoting accumulation of lipid intermediates and triacylglycerols within skeletal muscle, which is strongly associated with skeletal muscle insulin resistance. The present review describes the reported disturbances in pathways of lipolysis and skeletal muscle fatty acid handling, and discusses underlying mechanisms and metabolic consequences of these disturbances.
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Dahik, Veronica D., Eric Frisdal, and Wilfried Le Goff. "Rewiring of Lipid Metabolism in Adipose Tissue Macrophages in Obesity: Impact on Insulin Resistance and Type 2 Diabetes." International Journal of Molecular Sciences 21, no. 15 (July 31, 2020): 5505. http://dx.doi.org/10.3390/ijms21155505.

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Obesity and its two major comorbidities, insulin resistance and type 2 diabetes, represent worldwide health issues whose incidence is predicted to steadily rise in the coming years. Obesity is characterized by an accumulation of fat in metabolic tissues resulting in chronic inflammation. It is now largely accepted that adipose tissue inflammation underlies the etiology of these disorders. Adipose tissue macrophages (ATMs) represent the most enriched immune fraction in hypertrophic, chronically inflamed adipose tissue, and these cells play a key role in diet-induced type 2 diabetes and insulin resistance. ATMs are triggered by the continuous influx of dietary lipids, among other stimuli; however, how these lipids metabolically activate ATM depends on their nature, composition and localization. This review will discuss the fate and molecular programs elicited within obese ATMs by both exogenous and endogenous lipids, as they mediate the inflammatory response and promote or hamper the development of obesity-associated insulin resistance and type 2 diabetes.
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Wang, Jing, Theodore P. Ciaraldi, and Fahumiya Samad. "Tissue Factor Expression in Obese Type 2 Diabetic Subjects and Its Regulation by Antidiabetic Agents." Journal of Obesity 2015 (2015): 1–8. http://dx.doi.org/10.1155/2015/291209.

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Objective.Increased coagulation activation may contribute to the high incidence of cardiovascular complications observed in obese and type 2 diabetes (T2D) subjects. Although tissue factor (TF), the primary initiator of coagulation is increased in obesity, its expression in adipose tissues and its association with metabolic parameters are unclear. We sought to compare TF expression in plasma and adipose tissues of obese subjects with and without T2D, its correlation with metabolic parameters, and regulation in response to antidiabetic drugs.MethodsSubjects were recruited from diabetes clinics and adipose tissue was obtained by needle biopsy of lower subcutaneous abdominal depot. For the intervention study, subjects were randomized into treatment groups with rosiglitazone or metformin for 4 months.Results.Plasma TF antigen, activity, and adipose TF mRNA were greater in obese T2D subjects compared with obese nondiabetics. Plasma TF activity correlated with fasting insulin, glucose, and free fatty acids, (FFAs), and adipose TF mRNA correlated with plasma FFA. Plasma TF activity was reduced by metformin and increased with rosiglitazone treatment.Conclusions.Specific diabetes-related metabolic parameters, but not obesity per se, are correlated with TF expression. Regulation of TF activity by different classes of antidiabetic drugs may relate to protective or adverse cardiovascular outcomes.
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Wu, Huaizhu, and Christie M. Ballantyne. "Metabolic Inflammation and Insulin Resistance in Obesity." Circulation Research 126, no. 11 (May 22, 2020): 1549–64. http://dx.doi.org/10.1161/circresaha.119.315896.

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Obesity is becoming an epidemic in the United States and worldwide and increases risk for many diseases, particularly insulin resistance, type 2 diabetes mellitus, and cardiovascular disease. The mechanisms linking obesity with these diseases remain incompletely understood. Over the past 2 to 3 decades, it has been recognized that in obesity, inflammation, with increased accumulation and inflammatory polarization of immune cells, takes place in various tissues, including adipose tissue, skeletal muscle, liver, gut, pancreatic islet, and brain and may contribute to obesity-linked metabolic dysfunctions, leading to insulin resistance and type 2 diabetes mellitus. Therapies targeting inflammation have shed light on certain obesity-linked diseases, including type 2 diabetes mellitus and atherosclerotic cardiovascular disease, but remain to be tested further and confirmed in clinical trials. This review focuses on inflammation in adipose tissue and its potential role in insulin resistance associated with obesity.
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Dissertations / Theses on the topic "Obesity ; Type 2 diabetes ; Adipose Tissue"

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Jones, Danielle Alice. "Adipose tissue as a mediator of inflammation and oxidative cellular damage in obesity and type 2 diabetes." Thesis, Swansea University, 2013. https://cronfa.swan.ac.uk/Record/cronfa42244.

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In the past 30 years the prevalence of obesity has almost trebled resulting in an increased incidence of type 2 diabetes mellitus (T2DM) and other co-morbidities. Visceral adipose tissue is believed to play a vital role in these conditions, but underlying mechanisms remain unclear. A close association exists between obesity, diabetes and oxidative stress, resulting in increased reactive oxygen species formation. The experiments in this thesis address this by searching for possible biochemical changes which may be specific for the onset of obesity related T2DM, as well as looking for genetic alterations at molecular and gene expression levels. This thesis also explored various techniques such as polymerase chain reaction (PCR), colorimetric assays and real-time RT-PCR. The aim was to investigate the role of adipose tissue in obesity and T2DM, focusing on markers of oxidative stress and gene expression in human visceral adipose tissue from subjects categorised as lean, obese and obese with T2DM. This cross-sectional study measured two markers of oxidative stress, two markers of DNA damage, gene expression analysis and identification of genes associated with T2DM and obesity. Specific gene sequencing was carried out on the glutathione reductase gene to determine possible gene variants. Results showed a paradoxical decrease in adipose markers of oxidative stress in subjects with obesity and T2DM. There appeared to be a protective mechanism in these subjects, displaying reduced levels of oxidative stress compared to other groups. This could be due to a significant proportion of these subjects being on ACE inhibitor and statin therapy, which may be confounding results and minimising the effects of the oxidative burden. Additionally, the same subjects showed an increased expression of the glutathione reductase gene. It is difficult to conclude if the decreased levels of oxidative stress in these subjects were a result of the increased glutathione reductase expression in the visceral adipose tissue or if there remains an unseen factor influencing the dramatic expression change seen in this group of subjects. No glutathione reductase gene variants were identified in these samples. This analysis highlighted that within this sample set, the impact of oxidative stress is in fact reversible as the antioxidant capacity in these subjects is evident, and in combination with correct drug therapy it may be possible to combat oxidative burden and reduce the subsequent damage inflicted upon the cells.
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Kumsaiyai, Warunee. "The impact of human adipose tissue on metabolic dysfunction in obesity and type 2 diabetes mellitus." Thesis, University of Warwick, 2014. http://wrap.warwick.ac.uk/67170/.

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This thesis sought to investigate how systemic lipids may contribute to the adipocyte derived inflammatory response and highlight how the adipocyte’s function can alter in different metabolic states which could contribute to the pathogenesis of type 2 diabetes mellitus (T2DM) and cardiovascular risk. Specifically, this thesis firstly examined the inflammatory nature of lipoprotein-associated phospholipase A2 (LpPLA2), a member of the phospholipase A2 super family of enzymes which previously has been shown to enhance Ox-LDL production in foam cells during arterial inflammation contributing to coronary artery disease. Therefore initial studies sought to (1) characterise PLA2 isoforms in lean, obese, T2DM abdominal subcutaneous (AbdSc) and omental (Om) in human adipose tissue (AT); (2) evaluate the role of lipids and inflammatory markers on circulating LpPLA2, and (3) determine the in vitro regulation of LpPLA2 in human adipocytes by its influence on LDL and Ox-LDL. AT and sera from lean, overweight, obese and T2DM subjects were taken. PLA2 gene expression was determined by microarray, RT-PCR and Western Blot. Associations between circulating LpPLA2 and metabolic parameters were investigated. The human adipocyte cell line, Chub-S7, was used to assess the effects of oxidized LDL (Ox-LDL) and LDL on PLA2 expression. LpPLA2 mRNA levels were higher in AbdSc AT than Om AT in obesity by 2-fold (P<0.05). The cPLA2 protein expression increased with obesity in AbdSc AT (P<0.01). T2DM showed increased LpPLA2 mRNA levels in AbdSc (P<0.001) and Om AT (P<0.01). Serum LpPLA2 showed positive correlations with cholesterol, TG, LDL, endotoxin and Ox-LDL (P<0.001) in non-diabetic subjects and with Ox-LDL (P<0.001), LDL (P<0.01) and cholesterol (P<0.05) in T2DM. In differentiated pre-adipocytes, activation of LpPLA2 protein expression was noted in response to LDL and Ox-LDL (P<0.001). The adipocyte appeared to be an active source of LpPLA2, altered by fat depot and metabolic state, with LpPLA2 protein expression induced by LDL and Ox-LDL, in vitro. Increased LpPLA2 protein from the adipocyte in obesity and/or T2DM could contribute to raise circulating Ox-LDL, as noted in other studies as well with increasing adiposity, which promotes further inflammation and atherosclerotic risk. Through the development of these current studies it appeared that how the adipocyte managed lipids was important to how the adipocyte may induce an inflammatory response and pathogenic factors. Therefore subsequent studies investigated how the change in metabolic state such as those derived in T2DM patients that undergo bariatric surgery may not necessarily reverse their inflammatory response. Previous studies from the team have shown that lipids may induce an innate immune response via toll like receptor (TLR) activation therefore subsequent investigations sought to consider the potential role of triglycerides (TG) as another mediator of inflammation. As such studies examined the specific impact of TG changes, pre- and post-bariatric surgery, on TLR expression in ex vivo AT and the in vitro effects of triglyceride rich lipoprotein (VLDL), on TLR expression in isolated human differentiated pre-adipocytes. Serum and AT was taken from a cohort of Obese, T2DM, female subjects prior to bariatric surgery and 6 months post-surgery. Human differentiated pre-adipocyte Chub S7 cells were again used to examine transcriptional effects of VLDL on TLR expression. Following surgical intervention, BMI (P<0.001), blood glucose (P<0.001), insulin (P<0.001), HOMA-IR (P<0.001), TG (P<0.05), Cholesterol (P<0.001) and LDL-cholesterol (P<0.05) were significantly improved. There was a significant reduction in TLR-4 mRNA post-surgery (P<0.01) irrespective of surgery type. It was also noted that subjects with the greatest drop (55.5% reduction) in TGs post-surgery (P<0.001) showed a significant correlated reduction in TLR4 mRNA expression (P<0.001). Whilst the in vitro treatment of differentiated Chub S7 cells highlighted VLDL induced TLR 4 mRNA expression (P<0.05) suggesting the inflammatory impact of lipids on adipocytes. These studies further highlighted that the reduction in AT inflammation appears dependent on how successfully subjects reduce their serum triglyceride, which appears supported by the in vitro findings. These studies suggest that bariatric surgery lead to metabolic improvement with weight loss, whilst dietary intervention is still required to ensure TGs reduce to reduce inflammation. Taken together, these studies and thesis highlight the diverse nature of lipids and their interaction with the adipocyte to impact on their inflammatory response. These data also highlight the importance to maintain a good systemic lipid profile low in TG to reduce adipocyte induced inflammation and that AT may represent an important therapeutic target to reduce inflammation, atherosclerotic risk and development of metabolic complications.
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Kaaman, Maria. "Role of inflammatory and mitochondria genes in adipose tissue and obesity /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-331-3/.

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Charles, Khanichi Nona. "Adipose tissue FABP deficiency promotes metabolic reprogramming and positively impacts healthspan." Thesis, Harvard University, 2014. http://dissertations.umi.com/gsas.harvard:11254.

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The adipose tissue lipid chaperones aP2 and mal1, also known as fatty acid binding proteins (FABPs), are significant molecules contributing to metabolic homeostasis, whereby their absence promotes physiological changes that improve systemic metabolism. Identification of palmitoleate as a lipokine generated in aP2-mal1 deficiency--originating from adipose and directing the lipogenic program in liver, established a role for these chaperones in linking adipocyte and hepatic function. We have recently demonstrated a functional role for secreted aP2 in the activation of gluconeogenesis and hepatic glucose output, further designating this molecule as an adipocyte-derived regulatory factor that influences liver metabolism. Key molecules linking the metabolism of nutrients in energy generating pathways are the nucleotide cofactors NAD and NADH. Together, these molecules function to coordinate the maintenance of redox reactions during normal cellular metabolism and act as required substrates for enzymes such as sirtuins and poly ADP-ribose polymerases. Using global metabolite profiling, we show that combined deficiency of the adipose tissue lipid chaperones aP2 and mal1 leads to a hepatic nucleotide imbalance resulting from metabolic reprogramming in liver. We demonstrate that this reprogramming of metabolite flux is accompanied by significant alterations in liver NAD metabolism and establish a role for aP2 in directing substrate utilization through inhibition of the rate-limiting enzyme for NAD synthesis, nicotinamide phosphoribosyltransferase. Several models for the proposed regulatory pathways that link nutrient metabolism to aging include mechanisms that are NAD dependent. Accordingly, we found that long-term FABP deficiency confers a strong resistance to aging related metabolic deterioration. Together, the findings presented in this thesis support a considerable role for FABPs in the regulation of NAD metabolism and healthspan.
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Brooks, Nicole E. "Fibroblast Growth Factor 21 Expression in Mice with Altered Growth Hormone Action: Links to Obesity, Type 2 Diabetes Mellitus, and Increased Longevity." Ohio University Honors Tutorial College / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=ouhonors1461161246.

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Lau, Tik-yan Ivy. "Macrophage-adipocyte cross-talk in the initiation of obesity-related insulin resistance and type 2 diabetes : role of adiponectin /." Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B4129046X.

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Lau, Tik-yan Ivy, and 劉荻茵. "Macrophage-adipocyte cross-talk in the initiation of obesity-related insulin resistance and type 2 diabetes: roleof adiponectin." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B4129046X.

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Choy, Steve. "Semi-mechanistic models of glucose homeostasis and disease progression in type 2 diabetes." Doctoral thesis, Uppsala universitet, Institutionen för farmaceutisk biovetenskap, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-273709.

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Type 2 diabetes mellitus (T2DM) is a metabolic disorder characterized by consistently high blood glucose, resulting from a combination of insulin resistance and reduced capacity of β-cells to secret insulin. While the exact causes of T2DM is yet unknown, obesity is known to be a major risk factor as well as co-morbidity for T2DM. As the global prevalence of obesity continues to increase, the association between obesity and T2DM warrants further study. Traditionally, mathematical models to study T2DM were mostly empirical and thus fail to capture the dynamic relationship between glucose and insulin. More recently, mechanism-based population models to describe glucose-insulin homeostasis with a physiological basis were proposed and offered a substantial improvement over existing empirical models in terms of predictive ability. The primary objectives of this thesis are (i) examining the predictive usefulness of semi-mechanistic models in T2DM by applying an existing population model to clinical data, and (ii) exploring the relationship between obesity and T2DM and describe it mathematically in a novel semi-mechanistic model to explain changes to the glucose-insulin homeostasis and disease progression of T2DM. Through the use of non-linear mixed effects modelling, the primary mechanism of action of an antidiabetic drug has been correctly identified using the integrated glucose-insulin model, reinforcing the predictive potential of semi-mechanistic models in T2DM. A novel semi-mechanistic model has been developed that incorporated a relationship between weight change and insulin sensitivity to describe glucose, insulin and glycated hemoglobin simultaneously in a clinical setting. This model was also successfully adapted in a pre-clinical setting and was able to describe the pathogenesis of T2DM in rats, transitioning from healthy to severely diabetic. This work has shown that a previously unutilized biomarker was found to be significant in affecting glucose homeostasis and disease progression in T2DM, and that pharmacometric models accounting for the effects of obesity in T2DM would offer a more complete physiological understanding of the disease.
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Thondam, S. K. "The role of Glucose dependent Insulinotropic Polypeptide (GIP) and other gut hormones in glucose regulation and adipose tissue metabolism in obesity and type 2 diabetes." Thesis, University of Liverpool, 2017. http://livrepository.liverpool.ac.uk/3007814/.

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Aims and hypothesis: Beyond the insulinotropic effects, glucose-dependent insulinotropic polypeptide (GIP) may regulate post-prandial lipid metabolism by promoting fat deposition and inflammation in adipose tissue after high fat diets. We hypothesised that GIP would have an anabolic action in subcutaneous adipose tissue (SAT) promoting non-esterified fatty acid (NEFA) re-esterification. We speculated these effects may be mediated by changes to the expression of key lipid metabolism enzymes and that GIP may promote inflammation by affecting the expression of key adipokines in SAT. We postulated that these effects may be different according to obesity status or glucose tolerance. Incretins and other gut hormones are affected by medications used in the treatment of T2DM. We hypothesised that metformin, a commonly used drug in T2DM, may influence the secretion of incretin and other gut hormones which may contribute to its pleotropic effects in glucose metabolism. Subjects/Methods: We recruited 31 participants, for 2 different studies. In the first study, 23 men in four categories, normoglycaemic lean (n=6), normoglycaemic obese, (n=6), obese with impaired glucose regulation (IGR) (n=6) and obese, T2DM (n=5) participated in a double-blind, randomised, crossover study involving a hyperglycaemic clamp with a 4-hour infusion of GIP or placebo (normal saline). Serum insulin, plasma NEFA concentrations, SAT triacylglycerol (TAG) content and gene expression of key lipid metabolism enzymes, lipoprotein lipase (LPL), adipose tissue triglyceride lipase (ATGL) and hormone sensitive lipase (HSL) and adipokine gene expression (TNF-α, MCP-1, osteopontin and adiponectin) in SAT were determined before and after the GIP/placebo infusions. In the second study, eight subjects (6 male and 2 female) were studied on two occasions for 6 hours following a standard mixed meal, before and after metformin monotherapy for at least 3 months. Blood samples were taken in the fasted state and at multiple time points after the mixed meal for measuring incretin hormone, glucagon like peptide (GLP-1), ghrelin (appetite regulatory gut hormone) and dipeptidyl peptidase –IV (DPP-IV) activity. Results: Study-1 The insulinotropic effect of GIP vs. placebo was greater in lean, obese and obese IGR groups with no significant effect in obese T2DM. In contrast, GIP lowered NEFA concentrations in obese T2DM concomitantly increasing the SAT-TAG content. Such effects were not observed in other groups. There was no change in gene expression of LPL, ATGL and HSL with GIP or placebo infusions. The gene expression of TNF-α was significantly higher in obese T2DM group and the expression of MCP-1 was higher in lean and obese subjects. Study-2 Metformin monotherapy in obese patients with T2DM was associated with significantly increased postprandial active GLP-1 concentrations. Conclusion: In T2DM, although the insulinotropic effect of GIP is impaired, the ability of GIP to promote fat storage seems intact lowering NEFA concentrations and increasing SAT lipid deposition which may further exacerbate obesity and insulin resistance. Oral hypoglycaemic agent metformin influences the incretin system by increasing GLP-1 concentrations and this may represent another important mechanism of its glucose-lowering effect.
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Lundholm, Lovisa. "Molecular mechanisms of estrogen action in relation to metabolic disease /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-392-4/.

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Books on the topic "Obesity ; Type 2 diabetes ; Adipose Tissue"

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Cinti, Saverio. Obesity, Type 2 Diabetes and the Adipose Organ. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-40522-3.

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Keum, NaNa, Mingyang Song, Edward L. Giovannucci, and A. Heather Eliassen. Obesity and Body Composition. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0020.

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In 2014, an estimated 1.9 billion adults worldwide were either overweight (BMI 25–29.9) or obese (BMI ≥30). The so-called obesity epidemic began in high-income, English-speaking countries in the early 1970s, but soon spread globally; more than one-third (38%) of all adults and 600,000 children under age five are overweight or obese, as are two-thirds (69%) of adults in the United States. Excessive body fat is a major cause of type 2 diabetes, hypertension, cardiovascular and liver disease, among other disorders, and has been designated a definite cause of at least fourteen cancer sites: breast (postmenopausal), colorectum, endometrium, esophagus (adenocarcinoma), gallbladder, kidney (renal cell), pancreas, gastric cardia, liver, ovary, prostate (advanced tumors), multiple myeloma, thyroid, and meningioma. Mechanisms by which adipose tissue are thought to promote tumor growth include the endocrine and metabolic effects of fat on sex hormones, growth factors, and inflammation, as well as local chemical or mechanical injury of gastrointestinal organs.
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Cinti, Saverio. Obesity, Type 2 Diabetes and the Adipose Organ: A Pictorial Atlas from Research to Clinical Applications. Springer, 2018.

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Cinti, Saverio. Obesity, Type 2 Diabetes and the Adipose Organ: A Pictorial Atlas from Research to Clinical Applications. Springer, 2019.

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Book chapters on the topic "Obesity ; Type 2 diabetes ; Adipose Tissue"

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Cinti, Saverio. "Murine Brown Adipose Tissue." In Obesity, Type 2 Diabetes and the Adipose Organ, 13–79. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-40522-3_2.

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Cinti, Saverio. "Human Brown Adipose Tissue." In Obesity, Type 2 Diabetes and the Adipose Organ, 81–105. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-40522-3_3.

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Wajchenberg, Bernardo Léo, and Ricardo V. Cohen. "Adipose Tissue and Type 2 Diabetes Mellitus." In Adipose Tissue and Adipokines in Health and Disease, 235–48. Totowa, NJ: Humana Press, 2014. http://dx.doi.org/10.1007/978-1-62703-770-9_16.

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Cinti, Saverio. "The Fasted Adipose Organ." In Obesity, Type 2 Diabetes and the Adipose Organ, 307–35. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-40522-3_10.

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Cinti, Saverio. "The Lactating Adipose Organ." In Obesity, Type 2 Diabetes and the Adipose Organ, 337–83. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-40522-3_11.

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Cinti, Saverio. "Murine Adipose Organ Development." In Obesity, Type 2 Diabetes and the Adipose Organ, 385–423. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-40522-3_12.

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Cinti, Saverio. "Warm-Acclimated Adipose Organ." In Obesity, Type 2 Diabetes and the Adipose Organ, 253–63. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-40522-3_8.

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Cinti, Saverio. "The Obese Adipose Organ." In Obesity, Type 2 Diabetes and the Adipose Organ, 265–305. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-40522-3_9.

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Cinti, Saverio. "Mixed Areas of Adipose Organ." In Obesity, Type 2 Diabetes and the Adipose Organ, 181–203. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-40522-3_6.

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Cinti, Saverio. "The Adipose Organ: Cold Acclimation." In Obesity, Type 2 Diabetes and the Adipose Organ, 205–51. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-40522-3_7.

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Conference papers on the topic "Obesity ; Type 2 diabetes ; Adipose Tissue"

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Patt, M., L. Massier, S. Tabei, T. Karlas, M. Blüher, A. Dietrich, M. Gericke, P. Kovacs, and R. Chakaroun. "FGF21 in Adipose Tissue Fibrosis, Obesity and Type 2 Diabetes." In Late Breaking Abstracts Diabetes Kongress 2021 – 55. Jahrestagung der DDG Präzisionsmedizin – Eine Reise in die Zukunft der Diabetologie www.diabeteskongress.de. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1730860.

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Al-Jaber, Hend Sultan, Layla Jadea Al-Mansoori, and Mohamed Aghar Elrayess. "The Role of GATA3 in Adipogenesis & Insulin Resistance." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0143.

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Background: Impaired adipogenesis plays an important role in the development of obesityassociated insulin resistance and type 2 diabetes. Adipose tissue inflammation is a crucial mediator of this process. In hyperglycemia, immune system is activated partially through upregulation of GATA3, causing exacerbation of the inflammatory state associated with obesity. GATA3 also plays a role as a gatekeeper of terminal adipocyte differentiation. Here we are examining the impact of GATA3 inhibition in adipose tissue on restoring adipogenesis, reversing insulin resistance and potentially lowering the risk of type 2 diabetes. Results: GATA-3 expression was higher in insulin resistant obese individuals compared to their insulin sensitive counterparts. Targeting GATA-3 with GATA-3 specific inhibitors reversed impaired adipogenesis and induced changes in the expression of a number insulin signaling-related genes, including up-regulation of insulin sensitivity-related gene and down-regulation of insulin resistance-related genes. Conclusion: GATA3 expression is higher in differentiating adipocytes from obese insulin resistant. Inhibiting GATA3 improves adipocytes differentiation and rescues insulin sensitivity in insulin resistant cells
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Faradzheva, S. S. "Estimation of adipose tissue using visual methods studies in patients with type 2 diabetes." In General question of world science. "Science of Russia", 2019. http://dx.doi.org/10.18411/gq-31-07-2019-36.

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Klimontov, V. V., D. M. Bulumbaeva, A. P. Lykov, O. N. Fazullina, N. P. Bgatova, N. B. Orlov, A. F. H. P. Pfeiffer, O. Pivovarova, and N. Rudovich. "Serum levels of WISP1/CCN4 in subjects with type 2 diabetes: the relationships with body fat distribution and adipose tissue dysfunction." In 2018 11th International Multiconference Bioinformatics of Genome Regulation and Structure\Systems Biology (BGRS\SB). IEEE, 2018. http://dx.doi.org/10.1109/csgb.2018.8544817.

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Islami, Dian Dini, Didik Gunawan Tamtomo, and Hanung Prasetya. "The Effect of Insulin Provision on the Risk Reduction of Type 2 Diabetes Mellitus: Meta-Analysis." In The 7th International Conference on Public Health 2020. Masters Program in Public Health, Universitas Sebelas Maret, 2020. http://dx.doi.org/10.26911/the7thicph.05.49.

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ABSTRACT Background: Insulin is the pivotal hormone regulating cellular energy supply and macronutrient balance, directing anabolic processes of the fed state. Insulin is essential for the intra-cellular transport of glucose into insulin-dependent tissues such as muscle and adipose tissue. The purpose of this study was to examine the effect of insulin provision on the risk reduction of type 2 diabetes mellitus. Subjects and Method: This was meta-analysis and systematic review. The study was conducted by collecting articles from PubMed, Google Scholar, and Springer Link databases, from 2010-2020. Keywords used “effect insulin” OR “giving insulin” AND “diabetes mellitus” OR “diabetes” AND “cross sectional” AND “adjusted odd ratio”. The inclusion criteria were full text, using English or Indonesia language, and using crosssectional study design. The articles were selected by PRISMA flow chart. The quantitative data were analyzed by RevMan 5.3. Results: A meta-analysis from 5 studies in Ethiopia, Northeast Ethiopia, Taiwan, African American, and South Korea, reported that insulin provision reduced the risk of diabetes mellitus (aOR= 1.89; 95% CI= 1.82 to 3.57; p= 0.05) with I2= 84%. Conclusion: Insulin provision reduced the risk of diabetes mellitus. Keywords: insulin, type 2 diabetes mellitus Correspondence: Dian Dini Islami. Masters Program in Public Health, Universitas Sebelas Maret. Jl. Ir. Sutami 36A, Surakarta 57126, Central Java. Email: dian.dinii94@gmail.com. Mobile: 085729483960. DOI: https://doi.org/10.26911/the7thicph.05.49
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Sherrod, Brandon, Shawn Gilbert, Krista Casazza, and Alan Eberhardt. "Design of a Torsion Tester for Measuring Murine Bone Properties for Studies on the Effects of Diabetes and Obesity." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14412.

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Conditions such as diabetes and obesity have been found to affect the mechanical integrity of bone. Studies have shown that diabetic rodent models exhibit lower levels of new bone formation during fracture healing 1, lower bone mineral density (BMD) 2, and increased risk of fracture 3. There are differences, however, in the bone integrity of bone samples from type I and type II diabetics, which is most likely due to obesity 2. Findings from research on obesity’s effects on bone integrity have been controversial; although there is an increase in bone mineral density (BMD) with increasing body mass index (BMI) and a decrease in fracture incidence in the central body regions in obese women compared to healthy weight women due to soft tissue padding, there is an increase in fracture incidence at extremeties 4. Other studies have shown that while cortical bone strength may not be adversely affected by high-fat diets, cancellous bone BMD and mechanical strength was significantly lower in high-fat diet mice than low-fat diet mice 5. In addition, extreme obesity has been associated with lower BMD despite the general trend of increased BMD with higher BMI 6.
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Chan, C., and S. Baek. "Model Based Surface Design to Incorporate the Effect of Soluble Cues." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53439.

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Many disease states such as obesity and Type 2 diabetes are polygenic and involve multiple organs with inter-related metabolic and vascular abnormalities, and furthermore are risk factors for other diseases such as nonalcoholic steatohepatitis (NASH), cardiovascular or Alzheimer’s diseases. Tissue engineering is attempting to address these diseases from the perspective of developing “spare” or “replacement” parts. Cell and tissue engineering integrates cellular and molecular biology with the principles and methods of chemical and mechanical engineering to develop biological substitutes that can restore, maintain, or control tissue function.
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