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1
Cohen, Paul, and Bruce M. Spiegelman. "Cell biology of fat storage." Molecular Biology of the Cell 27, no. 16 (August 15, 2016): 2523–27. http://dx.doi.org/10.1091/mbc.e15-10-0749.
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The worldwide epidemic of obesity and type 2 diabetes has greatly increased interest in the biology and physiology of adipose tissues. Adipose (fat) cells are specialized for the storage of energy in the form of triglycerides, but research in the last few decades has shown that fat cells also play a critical role in sensing and responding to changes in systemic energy balance. White fat cells secrete important hormone-like molecules such as leptin, adiponectin, and adipsin to influence processes such as food intake, insulin sensitivity, and insulin secretion. Brown fat, on the other hand, dissipates chemical energy in the form of heat, thereby defending against hypothermia, obesity, and diabetes. It is now appreciated that there are two distinct types of thermogenic fat cells, termed brown and beige adipocytes. In addition to these distinct properties of fat cells, adipocytes exist within adipose tissue, where they are in dynamic communication with immune cells and closely influenced by innervation and blood supply. This review is intended to serve as an introduction to adipose cell biology and to familiarize the reader with how these cell types play a role in metabolic disease and, perhaps, as targets for therapeutic development.
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Frayn, Keith N. "Adipose tissue and the insulin resistance syndrome." Proceedings of the Nutrition Society 60, no. 3 (August 2001): 375–80. http://dx.doi.org/10.1079/pns200195.
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Obesity is associated with insulin resistance. Insulin resistance underlies a constellation of adverse metabolic and physiological changes (the insulin resistance syndrome) which is a strong risk factor for development of type 2 diabetes and CHD. The present article discusses how accumulation of triacylglycerol in adipocytes can lead to deterioration of the responsiveness of glucose metabolism in other tissues. Lipodystrophy, lack of adipose tissue, is also associated with insulin resistance. Any plausible explanation for the link between excess adipose tissue and insulin resistance needs to be able to account for this observation. Adipose tissue in obesity becomes refractory to suppression of fat mobilization by insulin, and also to the normal acute stimulatory effect of insulin on activation of lipoprotein lipase (involved in fat storage). The net effect is as though adipocytes are ‘full up’ and resisting further fat storage. Thus, in the postprandial period especially, there is an excess flux of circulating lipid metabolites that would normally have been ‘absorbed’ by adipose tissue. This situation leads to fat deposition in other tissues. Accumulation of triacylglycerol in skeletal muscles and in liver is associated with insulin resistance. In lipodystrophy there is insufficient adipose tissue to absorb the postprandial influx of fatty acids, so these fatty acids will again be directed to other tissues. This view of the link between adipose tissue and insulin resistance emphasises the important role of adipose tissue in ‘buffering’ the daily influx of dietary fat entering the circulation and preventing excessive exposure of other tissues to this influx.
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Sütt, Silva, Emmelie Cansby, Alexandra Paul, Manoj Amrutkar, Esther Nuñez-Durán, Nagaraj M. Kulkarni, Marcus Ståhlman, et al. "STK25 regulates oxidative capacity and metabolic efficiency in adipose tissue." Journal of Endocrinology 238, no. 3 (September 2018): 187–202. http://dx.doi.org/10.1530/joe-18-0182.
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Whole-body energy homeostasis at over-nutrition critically depends on how well adipose tissue remodels in response to excess calories. We recently identified serine/threonine protein kinase (STK)25 as a critical regulator of ectopic lipid storage in non-adipose tissue and systemic insulin resistance in the context of nutritional stress. Here, we investigated the role of STK25 in regulation of adipose tissue dysfunction in mice challenged with a high-fat diet. We found that overexpression of STK25 in high-fat-fed mice resulted in impaired mitochondrial function and aggravated hypertrophy, inflammatory infiltration and fibrosis in adipose depots. Reciprocally, Stk25-knockout mice displayed improved mitochondrial function and were protected against diet-induced excessive fat storage, meta-inflammation and fibrosis in brown and white adipose tissues. Furthermore, in rodent HIB-1B cell line, STK25 depletion resulted in enhanced mitochondrial activity and consequently, reduced lipid droplet size, demonstrating an autonomous action for STK25 within adipocytes. In summary, we provide the first evidence for a key function of STK25 in controlling the metabolic balance of lipid utilization vs lipid storage in brown and white adipose depots, suggesting that repression of STK25 activity offers a potential strategy for establishing healthier adipose tissue in the context of chronic exposure to dietary lipids.
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Corvera, Silvia. "Adipose tissue: from amorphous filler to metabolic mastermind." Biochemist 43, no. 2 (March 19, 2021): 16–20. http://dx.doi.org/10.1042/bio_2021_113.
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Adipose tissue plays a central role in the control of systemic glucose homeostasis through two major mechanisms: fat storage and secretion of specific cytokines known as adipokines. Fat storage in adipose tissue is critically important, as it prevents lipid deposition in liver and muscle, which in turn results in insulin resistance and increased risk of type 2 diabetes. Secretion of adipokines, such as leptin, protects from fuel depletion through appetite control, and other adipokines control fuel distribution and utilization. Fat storage capacity of adipose tissue increases through two mechanisms, adipocyte hypertrophy and adipocyte hyperplasia. Adipose tissue depots expand differently in diverse individuals and confer varying degrees of metabolic disease risk. There are multiple adipocyte subtypes that together mediate the functions of adipose tissue. They do so through specialized functions such as thermogenesis, which burns fuel to maintain core temperature, and through selective secretion of different adipokines. Much progress has been made in understanding the mechanisms by which adipose tissue controls systemic metabolism, increasing our hope of developing new, effective therapies for metabolic diseases.
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Sharma, Deepika, Swati Sharma, and Preeti Chauhan. "Acetylation of Histone and Modification of Gene Expression via HDAC Inhibitors Affects the Obesity." Biomedical and Pharmacology Journal 14, no. 1 (March 28, 2021): 153–61. http://dx.doi.org/10.13005/bpj/2110.
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Obesity is due to imbalance between energy intake and energy expenditure. Adipose tissues are the main site for the fat storage as well as for dissipation. There are two types of adipose tissues: white adipose tissue, which store fat as triglyceride, brown adipose tissue, which burns the fat into energy through the thermogenesis due to uncoupling protein1 present in inner mitochondrial membrane. Histone acylation causes changes in the chromatin structure without causing any change in the deoxyribonucleic acidsequence and thus regulate gene expression.Histonedeacetylase causes the deacylation of histone and interfere with function of histone. Thus histonedeacetylase inhibitors alter the expression of thermogenic gene encoding uncoupling protein 1, peroxisome proliferator activated receptor γ and also causes browning or beiging of white adipose tissue and increases the energy expenditure.
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Liu, Lulu, Mei Mei, Shumin Yang, and Qifu Li. "Roles of Chronic Low-Grade Inflammation in the Development of Ectopic Fat Deposition." Mediators of Inflammation 2014 (2014): 1–7. http://dx.doi.org/10.1155/2014/418185.
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Pattern of fat distribution is a major determinant for metabolic homeostasis. As a depot of energy, the storage of triglycerides in adipose tissue contributes to the normal fat distribution. Decreased capacity of fat storage in adipose tissue may result in ectopic fat deposition in nonadipose tissues such as liver, pancreas, and kidney. As a critical biomarker of metabolic complications, chronic low-grade inflammation may have the ability to affect the process of lipid accumulation and further lead to the disorder of fat distribution. In this review, we have collected the evidence linking inflammation with ectopic fat deposition to get a better understanding of the underlying mechanism, which may provide us with novel therapeutic strategies for metabolic disorders.
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Votruba, Susanne B., and Michael D. Jensen. "Short-term regional meal fat storage in nonobese humans is not a predictor of long-term regional fat gain." American Journal of Physiology-Endocrinology and Metabolism 302, no. 9 (May 1, 2012): E1078—E1083. http://dx.doi.org/10.1152/ajpendo.00414.2011.
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Although body fat distribution strongly predicts metabolic health outcomes related to excess weight, little is known about the factors an individual might exhibit that predict a particular fat distribution pattern. We utilized the meal fatty acid tracer-adipose biopsy technique to assess upper and lower body subcutaneous (UBSQ and LBSQ, respectively) meal fat storage in lean volunteers who then were overfed to gain weight. Meal fatty acid storage in UBSQ and LBSQ adipose tissue, as well as daytime substrate oxidation (indirect calorimetry), was measured in 28 nonobese volunteers [ n = 15 men, body mass index = 22.1 ± 2.5 (SD)] before and after an ∼8-wk period of supervised overfeeding (weight gain = 4.6 ± 2.2 kg, fat gain = 3.8 ± 1.7 kg). Meal fat storage (mg/g adipose tissue lipid) in UBSQ ( visit 1: 0.78 ± 0.34 and 1.04 ± 0.71 for women and men, respectively, P = 0.22; visit 2: 0.71 ± 0.24 and 0.90 ± 0.37 for women and men, respectively, P = 0.08) and LBSQ ( visit 1: 0.60 ± 0.23 and 0.48 ± 0.29 for women and men, respectively, P = 0.25; visit 2: 0.62 ± 0.24 and 0.65 ± 0.23 for women and men, respectively, P = 0.67) adipose tissue did not differ between men and women at either visit. Fractional meal fatty acid storage in UBSQ (0.31 ± 0.15) or LBSQ (0.19 ± 0.13) adipose tissue at visit 1 did not predict the percent change in regional body fat in response to overfeeding. These data indicate that meal fat uptake trafficking in the short term (24 h) is not predictive of body fat distribution patterns. In general, UBSQ adipose tissue appears to be a favored depot for meal fat deposition in both sexes, and redistribution of meal fatty acids likely takes place at later time periods.
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Miranda, Diego A., Ji-Hyun Kim, Long N. Nguyen, Wang Cheng, Bryan C. Tan, Vera J. Goh, Jolene S. Y. Tan, et al. "Fat Storage-inducing Transmembrane Protein 2 Is Required for Normal Fat Storage in Adipose Tissue." Journal of Biological Chemistry 289, no. 14 (February 11, 2014): 9560–72. http://dx.doi.org/10.1074/jbc.m114.547687.
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Trayhurn, Paul, and John H. Beattie. "Physiological role of adipose tissue: white adipose tissue as an endocrine and secretory organ." Proceedings of the Nutrition Society 60, no. 3 (August 2001): 329–39. http://dx.doi.org/10.1079/pns200194.
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The traditional role attributed to white adipose tissue is energy storage, fatty acids being released when fuel is required. The metabolic role of white fat is, however, complex. For example, the tissue is needed for normal glucose homeostasis and a role in inflammatory processes has been proposed. A radical change in perspective followed the discovery of leptin; this critical hormone in energy balance is produced principally by white fat, giving the tissue an endocrine function. Leptin is one of a number of proteins secreted from white adipocytes, which include angiotensinogen, adipsin, acylation-stimulating protein, adiponectin, retinol-binding protein, tumour neorosis factor a, interleukin 6, plasminogen activator inhibitor-1 and tissue factor. Some of these proteins are inflammatory cytokines, some play a role in lipid metabolism, while others are involved in vascular haemostasis or the complement system. The effects of specific proteins may be autocrine or paracrine, or the site of action may be distant from adipose tissue. The most recently described adipocyte secretory proteins are fasting-induced adipose factor, a fibrinogen–angiopoietin-related protein, metallothionein and resistin. Resistin is an adipose tissue-specific factor which is reported to induce insulin resistance, linking diabetes to obesity. Metallothionein is a metal-binding and stress-response protein which may have an antioxidant role. The key challenges in establishing the secretory functions of white fat are to identify the complement of secreted proteins, to establish the role of each secreted protein, and to assess the pathophysiological consequences of changes in adipocyte protein production with alterations in adiposity (obesity, fasting, cachexia). There is already considerable evidence of links between increased production of some adipocyte factors and the metabolic and cardiovascular complications of obesity. In essence, white adipose tissue is a major secretory and endocrine organ involved in a range of functions beyond simple fat storage.
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Hageman, Rachael S., Asja Wagener, Claudia Hantschel, Karen L. Svenson, Gary A. Churchill, and Gudrun A. Brockmann. "High-fat diet leads to tissue-specific changes reflecting risk factors for diseases in DBA/2J mice." Physiological Genomics 42, no. 1 (June 2010): 55–66. http://dx.doi.org/10.1152/physiolgenomics.00072.2009.
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The aim of this study was to characterize the responses of individual tissues to high-fat feeding as a function of mass, fat composition, and transcript abundance. We examined a panel of eight tissues [5 white adipose tissues (WAT), brown adipose tissue (BAT), liver, muscle] obtained from DBA/2J mice on either a standard breeding diet (SBD) or a high-fat diet (HFD). HFD led to weight gain, decreased insulin sensitivity, and tissue-specific responses, including inflammation, in these mice. The dietary fatty acids were partially metabolized and converted in both liver and fat tissues. Saturated fatty acids (SFA) were converted in the liver to monounsaturated fatty acids (MUFA) and polyunsaturated fatty acids (PUFA), and oleic acid (C18:1) was the preferred MUFA for storage of excess energy in all tissues of HFD-fed mice. Transcriptional changes largely reflected the tissue-specific fat deposition. SFA were negatively correlated with genes in the collagen family and processes involving the extracellular matrix. We propose a novel role of the tryptophan hydroxylase 2 (Tph2) gene in adipose tissues of diet-induced obesity. Tissue-specific responses to HFD were identified. Liver steatosis was evident in HFD-fed mice. Gonadal, retroperitoneal and subcutaneous adipose tissue and BAT exhibited severe inflammatory and immune responses. Mesenteric adipose tissue was the most metabolically active adipose tissue. Gluteal adipose tissue had the highest mass gain but was sluggish in its metabolism. In HFD conditions, BAT functioned largely like WAT in its role as a depot for excess energy, whereas WAT played a role in thermogenesis.
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Meiliana, Anna, and Andi Wijaya. "Hypertrophic Obesity and Subcutaneous Adipose Tissue Dysfunction." Indonesian Biomedical Journal 6, no. 2 (August 1, 2014): 79. http://dx.doi.org/10.18585/inabj.v6i2.33.
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BACKGROUND: Over the past 50 years, scientists have recognized that not all adipose tissue is alike, and that health risk is associated with the location as well as the amount of body fat. Different depots are sufficiently distinct with respect to fatty-acid storage and release as to probably play unique roles in human physiology. Whether fat redistribution causes metabolic disease or whether it is a marker of underlying processes that are primarily responsible is an open question.CONTENT: The limited expandability of the subcutaneous adipose tissue leads to inappropriate adipose cell expansion (hypertrophic obesity) with local inflammation and a dysregulated and insulin-resistant adipose tissue. The inability to store excess fat in the subcutaneous adipose tissue is a likely key mechanism for promoting ectopic fat accumulation in tissues and areas where fat can be stored, including the intra-abdominal and visceral areas, in the liver, epi/pericardial area, around vessels, in the myocardium, and in the skeletal muscles. Many studies have implicated ectopic fat accumulation and the associated lipotoxicity as the major determinant of the metabolic complications of obesity driving systemic insulin resistance, inflammation, hepatic glucose production, and dyslipidemia.SUMMARY: In summary, hypertrophic obesity is due to an impaired ability to recruit and differentiate available adipose precursor cells in the subcutaneous adipose tissue. Thus, the subcutaneous adipose tissue may be particular in its limited ability in certain individuals to undergo adipogenesis during weight increase. Inability to promote subcutaneous adipogenesis under periods of affluence would favor lipid overlow and ectopic fat accumulation with negative metabolic consequences.KEYWORDS: obesity, adipogenesis, subcutaneous adipose tissue, visceral adipose tissue, adipocyte dysfunction
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Tchernof, André, and Jean-Pierre Després. "Pathophysiology of Human Visceral Obesity: An Update." Physiological Reviews 93, no. 1 (January 2013): 359–404. http://dx.doi.org/10.1152/physrev.00033.2011.
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Excess intra-abdominal adipose tissue accumulation, often termed visceral obesity, is part of a phenotype including dysfunctional subcutaneous adipose tissue expansion and ectopic triglyceride storage closely related to clustering cardiometabolic risk factors. Hypertriglyceridemia; increased free fatty acid availability; adipose tissue release of proinflammatory cytokines; liver insulin resistance and inflammation; increased liver VLDL synthesis and secretion; reduced clearance of triglyceride-rich lipoproteins; presence of small, dense LDL particles; and reduced HDL cholesterol levels are among the many metabolic alterations closely related to this condition. Age, gender, genetics, and ethnicity are broad etiological factors contributing to variation in visceral adipose tissue accumulation. Specific mechanisms responsible for proportionally increased visceral fat storage when facing positive energy balance and weight gain may involve sex hormones, local cortisol production in abdominal adipose tissues, endocannabinoids, growth hormone, and dietary fructose. Physiological characteristics of abdominal adipose tissues such as adipocyte size and number, lipolytic responsiveness, lipid storage capacity, and inflammatory cytokine production are significant correlates and even possible determinants of the increased cardiometabolic risk associated with visceral obesity. Thiazolidinediones, estrogen replacement in postmenopausal women, and testosterone replacement in androgen-deficient men have been shown to favorably modulate body fat distribution and cardiometabolic risk to various degrees. However, some of these therapies must now be considered in the context of their serious side effects. Lifestyle interventions leading to weight loss generally induce preferential mobilization of visceral fat. In clinical practice, measuring waist circumference in addition to the body mass index could be helpful for the identification and management of a subgroup of overweight or obese patients at high cardiometabolic risk.
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Cao, Yanli, Nicola Gathaiya, Qiaojun Han, Bradley J. Kemp, and Michael D. Jensen. "Subcutaneous adipose tissue free fatty acid uptake measured using positron emission tomography and adipose biopsies in humans." American Journal of Physiology-Endocrinology and Metabolism 317, no. 2 (August 1, 2019): E194—E199. http://dx.doi.org/10.1152/ajpendo.00030.2019.
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Positron emission tomography (PET) radiopharmaceuticals can noninvasively measure free fatty acid (FFA) uptake into adipose tissue. We studied 29 volunteers to test whether abdominal and femoral subcutaneous adipose tissue FFA uptake measured using [1-11C]palmitate PET agrees with FFA storage rates measured using an intravenous bolus of [1-14C]palmitate and adipose biopsies. The dynamic left ventricular cavity PET images combined with blood sample radioactivity corrected for the 11CO2 content were used to create the blood time activity curve (TAC), and the constant ( Ki) was determined using Patlak analysis of the TACs generated for regions of interest in abdominal subcutaneous fat. These data were used to calculate palmitate uptake rates in abdominal subcutaneous adipose tissue (µmol·kg−1·min−1). Immediately after the dynamic imaging, a static image of the thigh was taken to measure the standardized uptake value (SUV) in thigh adipose tissue, which was scaled to each participant’s abdominal adipose tissue SUV to calculate thigh adipose palmitate uptake rates. Abdominal adipose palmitate uptake using PET [1-11C]palmitate was correlated with, but significantly ( P < 0.001) greater than, FFA storage measured using [1-14C]palmitate and adipose biopsy. Thigh adipose palmitate measured using PET calculation was positively correlated ( R2 = 0.44, P < 0.0001) with and not different from the biopsy approach. The relative differences between PET measured abdominal subcutaneous adipose tissue palmitate uptake and biopsy-measured palmitate storage were positively correlated ( P = 0.03) with abdominal subcutaneous fat. We conclude that abdominal adipose tissue FFA uptake measured using PET does not equate to adipose FFA storage measured using biopsy techniques.
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Bederman, Ilya, Alex DiScenna, Leigh Henderson, Aura Perez, Jeannie Klavanian, Daniel Kovtun, Olivia Collins, et al. "Small adipose stores in cystic fibrosis mice are characterized by reduced cell volume, not cell number." American Journal of Physiology-Gastrointestinal and Liver Physiology 315, no. 6 (December 1, 2018): G943—G953. http://dx.doi.org/10.1152/ajpgi.00096.2017.
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Cystic fibrosis (CF) is a lethal genetic disorder that affects many organ systems of the body, including various endocrine and exocrine tissues. Health and survival positively associate with body mass, and as a consequence, CF clinical care includes high-fat, high-calorie diets to maintain and increase adipose tissue stores. Such strategies have been implemented without a clear understanding of the cause and effect relationship between body mass and patients’ health. Here, we used CF mouse models, which display small adipose stores, to begin examining body fat as a prelude into mechanistic studies of low body growth in CF, so that optimal therapeutic strategies could be developed. We reasoned that low adiposity must result from reduced number and/or volume of adipocytes. To determine relative contribution of either mechanism, we quantified volume of intraperitoneal and subcutaneous adipocytes. We found smaller, but not fewer, adipocytes in CF compared with wild-type (WT) animals. Specifically, intraperitoneal CF adipocytes were one-half the volume of WT cells, whereas subcutaneous cells were less affected by the Cftr genotype. No differences were found in cell types between CF and WT adipose tissues. Adipose tissue CFTR mRNA was detected, and we found greater CFTR expression in intraperitoneal depots as compared with subcutaneous samples. RNA sequencing revealed that CF adipose tissue exhibited lower expression of several key genes of adipocyte function ( Lep, Pck1, Fas, Jun), consistent with low triglyceride storage. The data indicate that CF adipocytes contain fewer triglycerides than WT cells, and a role for CFTR in these cells is proposed. NEW & NOTEWORTHY Adipocytes in cystic fibrosis mice exhibit smaller size due to low triglyceride storage. Adipocyte cell number per fat pad is similar, implying triglyceride storage problem. The absence of CFTR function in adipose tissue has been proposed as a direct link to low triglyceride storage in cystic fibrosis.
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Mundi, Manpreet S., Chistina Koutsari, and Michael D. Jensen. "Effects of Increased Free Fatty Acid Availability on Adipose Tissue Fatty Acid Storage in Men." Journal of Clinical Endocrinology & Metabolism 99, no. 12 (December 1, 2014): E2635—E2642. http://dx.doi.org/10.1210/jc.2014-2690.
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Context: A portion of free fatty acids (FFA) released from adipose tissue lipolysis are re-stored in adipocytes via direct uptake. Rates of direct adipose tissue FFA storage are much greater in women than men, but women also have greater systemic FFA flux and more body fat. Objective: We tested the hypotheses that experimental increases in FFA in men would equalize the rates of direct adipose tissue FFA storage in men and women. Design: We used a lipid emulsion infusion to raise FFA in men to levels seen in post-absorptive women. Direct FFA storage (μmol·kg fat−1·min−1) rates in abdominal and femoral fat was assessed using stable isotope tracer infusions to measure FFA disappearance rates and an iv FFA radiotracer bolus/timed biopsy. Setting: These studies were performed in a Clinical Research Center. Participants: Data from 13 non-obese women was compared with that from eight obese and eight non-obese men. Intervention: The men received a lipid emulsion infusion to raise FFA. Main Outcome Measures: We measured the rates of direct FFA storage in abdominal and femoral adipose tissue. Results: The three groups were similar in age and FFA flux by design; obese men had similar body fat percentage as non-obese women. Despite matching for FFA concentrations and flux, FFA storage per kg abdominal (P < .01) and femoral (P < .001) fat was less in both lean and obese men than in non-obese women. Abdominal FFA storage rates were correlated with proteins/enzymes in the FFA uptake/triglyceride synthesis pathway in men. Conclusion: The lesser rates of direct FFA adipose tissue in men compared with women cannot be explained by reduced FFA availability.
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Frayn, Keith N., Peter Arner, and Hannele Yki-Järvinen. "Fatty acid metabolism in adipose tissue, muscle and liver in health and disease." Essays in Biochemistry 42 (November 27, 2006): 89–103. http://dx.doi.org/10.1042/bse0420089.
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Fat is the largest energy reserve in mammals. Most tissues are involved in fatty acid metabolism, but three are quantitatively more important than others: adipose tissue, skeletal muscle and liver. Each of these tissues has a store of triacylglycerol that can be hydrolysed (mobilized) in a regulated way to release fatty acids. In the case of adipose tissue, these fatty acids may be released into the circulation for delivery to other tissues, whereas in muscle they are a substrate for oxidation and in liver they are a substrate for re-esterification within the endoplasmic reticulum to make triacylglycerol that will be secreted as very-low-density lipoprotein. These pathways are regulated, most clearly in the case of adipose tissue. Adipose tissue fat storage is stimulated, and fat mobilization suppressed, by insulin, leading to a drive to store energy in the fed state. Muscle fatty acid metabolism is more sensitive to physical activity, during which fatty acid utilization from extracellular and intracellular sources may increase enormously. The uptake of fat by the liver seems to depend mainly upon delivery in the plasma, but the secretion of very-low-density lipoprotein triacylglycerol is suppressed by insulin. There is clearly cooperation amongst the tissues, so that, for instance, adipose tissue fat mobilization increases to meet the demands of skeletal muscle during exercise. When triacylglycerol accumulates excessively in skeletal muscle and liver, sometimes called ectopic fat deposition, then the condition of insulin resistance arises. This may reflect a lack of exercise and an excess of fat intake.
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Chen, Yang, Mingyue Zhao, Chenhao Wang, Huaizhen Wen, Yuntao Zhang, Mingxu Lu, Salah Adlat, et al. "Adipose vascular endothelial growth factor B is a major regulator of energy metabolism." Journal of Endocrinology 244, no. 3 (March 2020): 511–21. http://dx.doi.org/10.1530/joe-19-0341.
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Excessive fat accumulation causes obesity and many diseases. Previous study demonstrates VEGFB universal knockout induces obese phenotypes including expansion of white adipose tissue, whitening of brown adipose tissue, increase of fat accumulation and reduction in energy consumption. However, roles of VEGFB in adipose tissues are not clear. In this study, we have generated a mouse model with adipose-specific VEGFB repression using CRISPR/dCas9 system (Vegfb AdipoDown ) and investigated the roles of VEGFB in adipose development and energy metabolism. VEGFB repression induced significant changes in adipose tissue structure and function. Vegfb AdipoDown mice have larger body sizes, larger volume of white adipose tissues than its wild type littermates. Adipose-specific VEGFB repression induced morphological and functional transformation of adipose tissues toward white adipose for energy storage. Metabolic processes are broadly changed in Vegfb AdipoDown adipose tissues including carbohydrate metabolism, lipid metabolism, nucleotide metabolism and amino acid metabolism. We have demonstrated that adipose VEGFB repression can recapitulate most of the phenotypes of the whole body VEGFB knockout mouse. Intriguingly, approximately 50% VEGFB repression in adipose tissues can almost completely mimic the effects of universal Vegfb deletion, suggesting adipose VEGFB is a major regulator of energy metabolism and may be important in prevention and treatment of obesity.
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Søndergaard, E., L. C. Gormsen, B. Nellemann, M. D. Jensen, and S. Nielsen. "Body composition determines direct FFA storage pattern in overweight women." American Journal of Physiology-Endocrinology and Metabolism 302, no. 12 (June 15, 2012): E1599—E1604. http://dx.doi.org/10.1152/ajpendo.00015.2012.
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Direct FFA storage in adipose tissue is a recently appreciated pathway for postabsorptive lipid storage. We evaluated the effect of body fat distribution on direct FFA storage in women with different obesity phenotypes. Twenty-eight women [10 upper body overweight/obese (UBO; WHR >0.85, BMI >28 kg/m2), 11 lower body overweight/obese (LBO; WHR <0.80, BMI >28 kg/m2), and 7 lean (BMI <25 kg/m2)] received an intravenous bolus dose of [9,10-3H]palmitate- and [1-14C]triolein-labeled VLDL tracer followed by upper body subcutaneous (UBSQ) and lower body subcutaneous (LBSQ) fat biopsies. Regional fat mass was assessed by combining DEXA and CT scanning. We report greater fractional storage of FFA in UBSQ fat in UBO women compared with lean women ( P < 0.01). The LBO women had greater storage per 106 fat cells in LBSQ adipocytes compared with UBSQ adipocytes ( P = 0.04), whereas the other groups had comparable storage in UBSQ and LBSQ adipocytes. Fractional FFA storage was significantly associated with fractional VLDL-TG storage in both UBSQ ( P < 0.01) and LBSQ ( P = 0.03) adipose tissue. In conclusion, UBO women store a greater proportion of FFA in the UBSQ depot compared with lean women. In addition, LBO women store FFA more efficiently in LBSQ fat cells compared with UBSQ fat cells, which may play a role in development of their LBO phenotype. Finally, direct FFA storage and VLDL-TG fatty acid storage are correlated, indicating they may share a common rate-limiting pathway for fatty acid storage in adipose tissue.
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Wang, Hong-Hui, Qian Cui, Teng Zhang, Lei Guo, Ming-Zhe Dong, Yi Hou, Zhen-Bo Wang, Wei Shen, Jun-Yu Ma, and Qing-Yuan Sun. "Removal of mouse ovary fat pad affects sex hormones, folliculogenesis and fertility." Journal of Endocrinology 232, no. 2 (February 2017): 155–64. http://dx.doi.org/10.1530/joe-16-0174.
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As a fat storage organ, adipose tissue is distributed widely all over the body and is important for energy supply, body temperature maintenance, organ protection, immune regulation and so on. In humans, both underweight and overweight women find it hard to become pregnant, which suggests that appropriate fat storage can guarantee the female reproductive capacity. In fact, a large mass of adipose tissue distributes around the reproductive system both in the male and female. However, the functions of ovary fat pad (the nearest adipose tissue to ovary) are not known. In our study, we found that the ovary fat pad-removed female mice showed decreased fertility and less ovulated mature eggs. We further identified that only a small proportion of follicles developed to antral follicle, and many follicles were blocked at the secondary follicle stage. The overall secretion levels of estrogen and FSH were lower in the whole estrus cycle (especially at proestrus); however, the LH level was higher in ovary fat pad-removed mice than that in control groups. Moreover, the estrus cycle of ovary fat pad-removed mice showed significant disorder. Besides, the expression of FSH receptor decreased, but the LH receptor increased in ovary fat pad-removed mice. These results suggest that ovary fat pad is important for mouse reproduction.
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Schulz, Tim J., and Yu-Hua Tseng. "Brown adipose tissue: development, metabolism and beyond." Biochemical Journal 453, no. 2 (June 28, 2013): 167–78. http://dx.doi.org/10.1042/bj20130457.
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Obesity represents a major risk factor for the development of several of our most common medical conditions, including Type 2 diabetes, dyslipidaemia, non-alcoholic fatty liver, cardiovascular disease and even some cancers. Although increased fat mass is the main feature of obesity, not all fat depots are created equal. Adipocytes found in white adipose tissue contain a single large lipid droplet and play well-known roles in energy storage. By contrast, brown adipose tissue is specialized for thermogenic energy expenditure. Owing to its significant capacity to dissipate energy and regulate triacylglycerol (triglyceride) and glucose metabolism, and its demonstrated presence in adult humans, brown fat could be a potential target for the treatment of obesity and metabolic syndrome. Undoubtedly, fundamental knowledge about the formation of brown fat and regulation of its activity is imperatively needed to make such therapeutics possible. In the present review, we integrate the recent advancements on the regulation of brown fat formation and activity by developmental and hormonal signals in relation to its metabolic function.
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Thompson, Dylan, Fredrik Karpe, Max Lafontan, and Keith Frayn. "Physical Activity and Exercise in the Regulation of Human Adipose Tissue Physiology." Physiological Reviews 92, no. 1 (January 2012): 157–91. http://dx.doi.org/10.1152/physrev.00012.2011.
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Physical activity and exercise are key components of energy expenditure and therefore of energy balance. Changes in energy balance alter fat mass. It is therefore reasonable to ask: What are the links between physical activity and adipose tissue function? There are many complexities. Physical activity is a multifaceted behavior of which exercise is just one component. Physical activity influences adipose tissue both acutely and in the longer term. A single bout of exercise stimulates adipose tissue blood flow and fat mobilization, resulting in delivery of fatty acids to skeletal muscles at a rate well-matched to metabolic requirements, except perhaps in vigorous intensity exercise. The stimuli include adrenergic and other circulating factors. There is a period following an exercise bout when fatty acids are directed away from adipose tissue to other tissues such as skeletal muscle, reducing dietary fat storage in adipose. With chronic exercise (training), there are changes in adipose tissue physiology, particularly an enhanced fat mobilization during acute exercise. It is difficult, however, to distinguish chronic “structural” changes from those associated with the last exercise bout. In addition, it is difficult to distinguish between the effects of training per se and negative energy balance. Epidemiological observations support the idea that physically active people have relatively low fat mass, and intervention studies tend to show that exercise training reduces fat mass. A much-discussed effect of exercise versus calorie restriction in preferentially reducing visceral fat is not borne out by meta-analyses. We conclude that, in addition to the regulation of fat mass, physical activity may contribute to metabolic health through beneficial dynamic changes within adipose tissue in response to each activity bout.
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Raclot, Thierry, and Hugues Oudart. "Selectivity of fatty acids on lipid metabolism and gene expression." Proceedings of the Nutrition Society 58, no. 3 (August 1999): 633–46. http://dx.doi.org/10.1017/s002966519900083x.
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Triacylglycerols represent the main form of storage for a wide spectrum of fatty acids. Their utilization first involves mobilization from adipose tissue through lipolysis. The release of individual fatty acids from adipose tissue is selective in vitro and in vivo in animal studies and also in human subjects. Generally, fatty acids are more readily mobilized from fat cells when they are short-chain and unsaturated. This selectivity could affect the storage of individual fatty acids in adipose tissue, and their subsequent supply to tissues. The nature of the dietary fats could affect lipid homeostasis and body fat deposition. Dietary fish oil influences adipose tissue development in a site-specific manner as a function of diet and feeding period. A diet high in n-3 polyunsaturated fatty acids (PUFA) results in a preferential partitioning of ingested energy towards oxidation at the expense of storage. Fatty acids are important mediators of gene expression in the liver. Indeed, genes encoding both glycolytic and lipogenic enzymes and key metabolic enzymes involved in fatty acid oxidation are regulated by dietary PUFA. White adipose tissue could also be a target for PUFA control of gene expression. The treatment of pre-adipose cells by fatty acids induces the expression of numerous genes that encode proteins involved in fatty acid metabolism. The mechanisms of PUFA-mediated repression of gene expression in adipocytes seem to be different, at least partly, from those described in liver. Tissue-specific and site-specific factors are possibly involved in the specific effect of PUFA on gene expression, although other mechanisms cannot be excluded.
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McGrattan, P. D., A. R. G. Wylie, and J. Nelson. "Tissue-specific differences in insulin binding affinity and insulin receptor concentrations in skeletal muscles, adipose tissue depots and liver of cattle and sheep." Animal Science 71, no. 3 (December 2000): 501–8. http://dx.doi.org/10.1017/s1357729800055466.
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AbstractDifferences in insulin binding affinity and in concentrations of insulin receptor, were found in a variety of tissues taken, at slaughter, from mature steers (701 (s.d. 23) kg) and growing lambs (47 (s.d. 2·1) kg). In both species, liver had lower insulin binding affinity than skeletal muscles m. pectineus m. longissimus dorsi and m. rectus capitis (all P < 0·001) and subcutaneous, omental and perirenal adipose depots (all P < 0·001). Site-specific differences in affinity for insulin existed between adipose depots (subcutaneous < omental, P < 0·05; subcutaneous < perirenal, P < 0·001) and between tissue-types (subcutaneous fat < m. pectineus skeletal muscle, P < 0·05; m. rectus capitis < perirenal fat, P < 0·05) in steers. In lambs also, receptor affinity for insulin differed between tissue-type (m. longissimus dorsi < perirenal fat, P < 0·05; m. rectus capitis < subcutaneous fat, P < 0·05 and m. rectus capitis < perirenal fat, P < 0·001) but lambs did not show the adipose depot-specific differences in insulin affinity observed in steers. Insulin receptor concentration differed between adipose depots (subcutaneous < omental, P < 0·05; subcutaneous < perirenal, P < 0·01) and between tissue-type (m. pectineus < perirenal fat P < 0·05) in steers and perirenal and subcutaneous adipose depots of lambs had higher receptor concentrations than m. longissimus dorsi and m. pectineusP < 0·001). This is the first study to demonstrate, in any species, differences in insulin receptor binding affinity and receptor concentration in a wide range of tissues (liver, skeletal muscles and adipose depots) from the same individual. Such differences in meat-producing animals could, through effects on tissue sensitivity and/or responsiveness to insulin, influence nutrient partitioning to tissues and affect overall rates of lipid storage and net protein synthesis.
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Morgan-Bathke, Maria, Liang Chen, Elisabeth Oberschneider, Debra Harteneck, and Michael D. Jensen. "Sex and depot differences in ex vivo adipose tissue fatty acid storage and glycerol-3-phosphate acyltransferase activity." American Journal of Physiology-Endocrinology and Metabolism 308, no. 9 (May 1, 2015): E830—E846. http://dx.doi.org/10.1152/ajpendo.00424.2014.
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Adipose tissue fatty acid storage varies according to sex, adipose tissue depot, and degree of fat gain. However, the mechanism(s) for these variations is not completely understood. We examined whether differences in adipose tissue glycerol-3-phosphate acyltransferase (GPAT) might play a role in these variations. We optimized an enzyme activity assay for total GPAT and GPAT1 activity in human adipose tissue and measured GPAT activity. Omental and subcutaneous adipose tissue was collected from obese and nonobese adults for measures of GPAT and GPAT1 activities, ex vivo palmitate storage, acyl-CoA synthetase (ACS) and diacylglycerol-acyltransferase (DGAT) activities, and CD36 protein. Total GPAT and GPAT1 activities decreased as a function of adipocyte size in both omental ( r = −0.71, P = 0.003) and subcutaneous ( r = −0.58, P = 0.04) fat. The relative contribution of GPAT1 to total GPAT activity increased as a function of adipocyte size, accounting for up to 60% of GPAT activity in those with the largest adipocytes. We found strong, positive correlations between ACS, GPAT, and DGAT activities for both sexes and depots ( r values 0.58–0.91) and between these storage factors and palmitate storage rates into TAG ( r values 0.55–0.90). We conclude that: 1) total GPAT activity decreases as a function of adipocyte size; 2) GPAT1 can account for over half of adipose GPAT activity in hypertrophic obesity; and 3) ACS, GPAT, and DGAT are coordinately regulated.
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Brøns, Charlotte, and Louise Groth Grunnet. "MECHANISMS IN ENDOCRINOLOGY: Skeletal muscle lipotoxicity in insulin resistance and type 2 diabetes: a causal mechanism or an innocent bystander?" European Journal of Endocrinology 176, no. 2 (February 2017): R67—R78. http://dx.doi.org/10.1530/eje-16-0488.
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Dysfunctional adipose tissue is associated with an increased risk of developing type 2 diabetes (T2D). One characteristic of a dysfunctional adipose tissue is the reduced expandability of the subcutaneous adipose tissue leading to ectopic storage of fat in organs and/or tissues involved in the pathogenesis of T2D that can cause lipotoxicity. Accumulation of lipids in the skeletal muscle is associated with insulin resistance, but the majority of previous studies do not prove any causality. Most studies agree that it is not the intramuscular lipids per se that causes insulin resistance, but rather lipid intermediates such as diacylglycerols, fatty acyl-CoAs and ceramides and that it is the localization, composition and turnover of these intermediates that play an important role in the development of insulin resistance and T2D. Adipose tissue is a more active tissue than previously thought, and future research should thus aim at examining the exact role of lipid composition, cellular localization and the dynamics of lipid turnover on the development of insulin resistance. In addition, ectopic storage of fat has differential impact on various organs in different phenotypes at risk of developing T2D; thus, understanding how adipogenesis is regulated, the interference with metabolic outcomes and what determines the capacity of adipose tissue expandability in distinct population groups is necessary. This study is a review of the current literature on the adipose tissue expandability hypothesis and how the following ectopic lipid accumulation as a consequence of a limited adipose tissue expandability may be associated with insulin resistance in muscle and liver.
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Votruba, Susanne B., and Michael D. Jensen. "Sex-specific differences in leg fat uptake are revealed with a high-fat meal." American Journal of Physiology-Endocrinology and Metabolism 291, no. 5 (November 2006): E1115—E1123. http://dx.doi.org/10.1152/ajpendo.00196.2006.
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The mechanism(s) by which sex specific differences in regional body fat distribution develop are not known. We assessed the effects of a high-fat (HF) meal on fatty acid oxidation and uptake into regional fat depots using isotopic tracers and adipose biopsies. Thirty men (BMI 23.6 ± 0.3 kg/m2) and 29 women (BMI 22.4 ± 0.3 kg/m2) received a meal containing [3H]triolein. Twelve of the men and 13 of the women received an additional 80 g of triolein in the meal (HF) and the remainder received a normal-fat (NF) meal. Adipose tissue lipoprotein lipase (LPL) activity was measured in the fed and fasted state. After 24 h, meal fatty acid uptake into subcutaneous adipose tissue was assessed. The efficiency of meal fat uptake into upper body subcutaneous fat was similar in both sexes, but women had a greater leg fat uptake, especially in response to a HF meal ( P < 0.0001). A correlation between fed-state LPL activity and meal fat uptake was found in both upper and lower body fat ( P < 0.0001, r = 0.69). These studies show that, in times of net fat storage, women preferentially increase uptake in leg adipose tissue, and this is likely mediated by fed-state LPL activity.
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Fernández-Quintela, Alfredo, Itziar Churruca, and Maria Puy Portillo. "The role of dietary fat in adipose tissue metabolism." Public Health Nutrition 10, no. 10A (October 2007): 1126–31. http://dx.doi.org/10.1017/s1368980007000602.
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AbstractEnergy intake and expenditure tend on average to remain adjusted to each other in order to maintain a stable body weight, which is only likely to be sustained if the fuel mix oxidised is equivalent to the nutrient content of the diet. Whereas protein and carbohydrate degradation and oxidation are closely adjusted to their intakes, fat balance regulation is less precise and that fat is more likely to be stored than oxidised.It has been demonstrated that dietary fatty acids have an influence not only on the fatty acid composition of membrane phospholipids, thus modulating several metabolic processes that take place in the adipocyte, but also on the composition and the quantity of different fatty acids in adipose tissue. Moreover, dietary fatty acids also modulate eicosanoid presence, which have hormone-like activities in lipid metabolism regulation in adipose tissue.Until recently, the adipocyte has been considered to be no more than a passive tissue for storage of excess energy. However, there is now compelling evidence that adipocytes have a role as endocrine secretory cells. Some of the adipokines produced by adipose tissue, such as leptin and adiponectin, act on adipose tissue in an autocrine/paracrine manner to regulate adipocyte metabolism. Furthermore, dietary fatty acids may influence the expression of adipokines.The nutrients are among the most influential of the environmental factors that determine the way adipose tissue genes are expressed by functioning as regulators of gene transcription. Therefore, not only dietary fat amount but also dietary fat composition influence adipose tissue metabolism.
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Santosa, Sylvia, Nikki C. Bush, and Michael D. Jensen. "Acute Testosterone Deficiency Alters Adipose Tissue Fatty Acid Storage." Journal of Clinical Endocrinology & Metabolism 102, no. 8 (June 21, 2017): 3056–64. http://dx.doi.org/10.1210/jc.2017-00757.
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AbstractContextAlthough the long-term effects of testosterone on adipose tissue lipid metabolism in men have been defined, the short-term regulation of these effects is not well understood.ObjectiveWe examined the effects of acute testosterone withdrawal on subcutaneous abdominal and femoral adipose tissue fatty acid (FA) storage and cellular mechanisms.DesignThis was a prospective, randomized trial.SettingMayo Clinic Clinical Research Unit.Patients or ParticipantsThirty-two male volunteers ages 18 to 50 participated in these studies.InterventionsVolunteers were randomized to receive (1) no treatment (control), (2) injections (7.5 mg) of Lupron®, or (3) Lupron and testosterone (L+T) replacement for 49 days, resulting in 4 weeks of sex steroid suppression in the Lupron group.Main Outcome MeasuresWe measured body composition, fat cell size, adipose tissue meal FA and direct free FA storage, lipoprotein lipase (LPL), acyl coenzyme A synthetase (ACS), diacylglycerol acyltransferase activities, and CD36 content.ResultsCompared with control and L+T groups, acute testosterone deficiency resulted in greater femoral adipose tissue meal FA storage rates, fasting and fed LPL activity, and ACS activity.ConclusionsThese results suggest that in men, testosterone plays a tonic role in restraining FA storage in femoral adipose tissue via suppression of LPL and ACS activities. FA storage mechanisms in men appear sensitive to short-term changes in testosterone concentrations.
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Bidar, Abdel Wahad, Karolina Ploj, Christopher Lelliott, Karin Nelander, Maria Sörhede Winzell, Gerhard Böttcher, Jan Oscarsson, Leonard Storlien, and Paul D. Hockings. "In vivo imaging of lipid storage and regression in diet-induced obesity during nutrition manipulation." American Journal of Physiology-Endocrinology and Metabolism 303, no. 11 (December 1, 2012): E1287—E1295. http://dx.doi.org/10.1152/ajpendo.00274.2012.
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Changes in adipose tissue distribution and ectopic fat storage in, liver and skeletal muscle tissue impact whole body insulin sensitivity in both humans and experimental animals. Numerous mouse models of obesity, insulin resistance, and diabetes exist; however, current methods to assess mouse phenotypes commonly involve direct harvesting of the tissues of interest, precluding the possibility of repeated measurements in the same animal. In this study, we demonstrate that whole body 3-D imaging of body fat composition can be used to analyze distribution as well as redistribution of fat after intervention by repeated assessment of intrahepatocellular lipids (IHCL), intra-abdominal, subcutaneous, and total adipose tissue (IAT, SAT, and TAT) and brown adipose tissue (BAT). C57BL/6J mice fed a cafeteria diet for 16 wk were compared with mice fed standard chow for 16 wk and mice switched from café diet to standard chow after 12 wk. MRI determinations were made at 9 and 15 wk, and autopsy was performed at 16 wk. There was a strong correlation between MRI-calculated weights in vivo at 15 wk and measured weights at 16 wk ex vivo for IAT ( r = 0.99), BAT ( r = 0.93), and IHCL ( r = 0.97). IHCL and plasma insulin increased steeply relative to body weight at body weights above 45 g. This study demonstrates that the use of 3-D imaging to assess body fat composition may allow substantial reductions in animal usage. The dietary interventions indicated that a marked metabolic deterioration occurred when the mice had gained a certain fat mass.
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Dilworth, Lowell, Aldeam Facey, and Felix Omoruyi. "Diabetes Mellitus and Its Metabolic Complications: The Role of Adipose Tissues." International Journal of Molecular Sciences 22, no. 14 (July 16, 2021): 7644. http://dx.doi.org/10.3390/ijms22147644.
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Many approaches have been used in the effective management of type 2 diabetes mellitus. A recent paradigm shift has focused on the role of adipose tissues in the development and treatment of the disease. Brown adipose tissues (BAT) and white adipose tissues (WAT) are the two main types of adipose tissues with beige subsets more recently identified. They play key roles in communication and insulin sensitivity. However, WAT has been shown to contribute significantly to endocrine function. WAT produces hormones and cytokines, collectively called adipocytokines, such as leptin and adiponectin. These adipocytokines have been proven to vary in conditions, such as metabolic dysfunction, type 2 diabetes, or inflammation. The regulation of fat storage, energy metabolism, satiety, and insulin release are all features of adipose tissues. As such, they are indicators that may provide insights on the development of metabolic dysfunction or type 2 diabetes and can be considered routes for therapeutic considerations. The essential roles of adipocytokines vis-a-vis satiety, appetite, regulation of fat storage and energy, glucose tolerance, and insulin release, solidifies adipose tissue role in the development and pathogenesis of diabetes mellitus and the complications associated with the disease.
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Cruz-Color, Lucía De la, Zamira Helena Hernández-Nazará, Montserrat Maldonado-González, Eliseo Navarro-Muñíz, José Alfredo Domínguez-Rosales, José Rodrigo Torres-Baranda, Elizabeth del Carmen Ruelas-Cinco, Sandra Margarita Ramírez-Meza, and Bertha Ruíz-Madrigal. "Association of the PNPLA2, SCD1 and Leptin Expression with Fat Distribution in Liver and Adipose Tissue From Obese Subjects." Experimental and Clinical Endocrinology & Diabetes 128, no. 11 (February 12, 2019): 715–22. http://dx.doi.org/10.1055/a-0829-6324.
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AbstractThe expansion of adipose tissue is regulated by insulin and leptin through sterol regulatory element-binding protein-1c (SREBP-1c), up-regulating lipogenesis in tissues by Stearoylcoenzyme A desaturase 1 (SCD1) enzyme, while adipose triglyceride lipase (ATGL) enzyme is key in lipolysis. The research objective was to evaluate the expression of Sterol Regulatory Element Binding Transcription Factor 1 (SREBF1), SCD1, Patatin Like Phospholipase Domain Containing 2 (PNPLA2), and leptin (LEP) genes in hepatic-adipose tissue, and related them with the increment and distribution of fat depots of individuals without insulin resistance. Thirty-eight subjects undergoing elective cholecystectomy with liver and adipose tissue biopsies (subcutaneous-omental) are included. Tissue gene expression was assessed by qPCR and biochemical parameters determined. Individuals are classified according to the body mass index, classified as lean (control group, n=12), overweight (n=11) and obesity (n=15). Abdominal adiposity was determined by anthropometric and histopathological study of the liver. Increased SCD1 expression in omental adipose tissue (p=0.005) and PNPLA2 in liver (p=0.01) were found in the obesity group. PNPLA2 decreased expression in subcutaneous adipose tissue was significant in individuals with abdominal adiposity (p=0.017). Anthropometric parameters positively correlated with liver PNPLA2 and the expression of liver PNPLA2 with serum leptin. SCD1 increased levels may represent lipid storage activity in omental adipose tissue. Liver PNPLA2 increased expression could function as a primary compensatory event of visceral fat deposits associated to the leptin hormone related to the increase of adipose tissue.
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Meiliana, Anna, and Andi Wijaya. "Brown and Beige Fat: Therapeutic Potential in Obesity." Indonesian Biomedical Journal 6, no. 2 (August 1, 2014): 65. http://dx.doi.org/10.18585/inabj.v6i2.32.
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BACKGROUND: The epidemic of obesity and type 2 diabetes presents a serious challenge to scientific and biomedical communities worldwide. There has been an upsurge of interest in the adipocyte coincident with the onset of the obesity epidemic and the realization that adipose tissue plays a major role in the regulation of metabolic function.CONTENT: Adipose tissue, best known for its role in fat storage, can also suppress weight gain and metabolic disease through the action of specialized, heat-producing adipocytes. Brown adipocytes are located in dedicated depots and express constitutively high levels of thermogenic genes, whereas inducible ‘brown-like’ adipocytes, also known as beige cells, develop in white fat in response to various activators. The activities of brown and beige fat cells reduce metabolic disease, including obesity, in mice and correlate with leanness in humans. Many genes and pathways that regulate brown and beige adipocyte biology have now been identified, providing a variety of promising therapeutic targets for metabolic disease.SUMMARY: The complexity of adipose tissue presents numerous challenges but also several opportunities for therapeutic intervention. There is persuasive evidence from animal models that enhancement of the function of brown adipocytes, beige adipocytes or both in humans could be very effective for treating type 2 diabetes and obesity. Moreover, there are now an extensive variety of factors and pathways that could potentially be targeted for therapeutic effects. In particular, the discoveries of circulating factors, such as irisin, fibroblast growth factor (FGF)21 and natriuretic peptides, that enhance brown and beige fat function in mice have garnered tremendous interest. Certainly, the next decade will see massive efforts to use beige and brown fat to ameliorate human metabolic disease.KEYWORDS: obesity, white adipose tissue, brown adipose tissue, beige adipose tissue, adipose organ, thermogenesis, energy expenditure
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Hermier, D., A. Quignard-Boulangé, I. Dugail, G. Guy, M. R. Salichon, L. Brigant, B. Ardouin, and B. Leclercq. "Evidence of Enhanced Storage Capacity in Adipose Tissue of Genetically Fat Chickens." Journal of Nutrition 119, no. 10 (October 1, 1989): 1369–75. http://dx.doi.org/10.1093/jn/119.10.1369.
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Bi, Junfeng, Wei Wang, Zhonghua Liu, Xiahe Huang, Qingqing Jiang, George Liu, Yingchun Wang, and Xun Huang. "Seipin Promotes Adipose Tissue Fat Storage through the ER Ca2+-ATPase SERCA." Cell Metabolism 19, no. 5 (May 2014): 861–71. http://dx.doi.org/10.1016/j.cmet.2014.03.028.
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Miegueu, Pierre, David H. St-Pierre, Marc Lapointe, Pegah Poursharifi, HuiLing Lu, Abhishek Gupta, and Katherine Cianflone. "Substance P decreases fat storage and increases adipocytokine production in 3T3-L1 adipocytes." American Journal of Physiology-Gastrointestinal and Liver Physiology 304, no. 4 (February 15, 2013): G420—G427. http://dx.doi.org/10.1152/ajpgi.00162.2012.
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Obesity, inflammation, and insulin resistance are closely linked. Substance P (SP), via its neurokinin 1 receptor (NK1R), mediates inflammatory and, possibly, neuroendocrine processes. We examined SP effects on lipid storage and cytokine production in 3T3-L1 adipocytes and adipose tissues. 3T3-L1 adipocytes and preadipocytes express NK1R, and 8 days of SP supplementation during differentiation to 3T3-L1 preadipocytes decreased lipid droplet accumulation. SP (10 nM, 24 h) increased lipolysis in primary adipocytes (138 ± 7%, P < 0.05) and reduced fatty acid uptake (−31 ± 7%, P < 0.05) and mRNA expression of the differentiation-related transcription factors peroxisome proliferator-activated receptor-γ type 2 (−64 ± 2%, P < 0.001) and CCAAT enhancer-binding protein (CEBP)-α (−65 ± 2%, P < 0.001) and the lipid storage genes fatty acid-binding protein type 4 (−59 ± 2%, P < 0.001) and diacylglycerol O-acyltransferase-1 (−45 ± 2%, P < 0.01) in 3T3-L1 adipocytes, while CD36, a fatty acid transporter (+82 ± 19%, P < 0.01), was augmented. SP increased secretion of complement C3 (148 ± 15%, P < 0.04), monocyte chemoattractant protein-1 (156 ± 16%, P < 0.03), and keratinocyte-derived chemokine (148 ± 18%, P = 0.045) in 3T3-L1 adipocytes and monocyte chemoattractant protein-1 (496 ± 142%, P < 0.02) and complement C3 (152 ± 25%, P < 0.04) in adipose tissue and primary adipocytes, respectively. These SP effects were accompanied by downregulation of insulin receptor substrate 1 (−82 ± 2%, P < 0.01) and GLUT4 (−76 ± 2%, P < 0.01) mRNA expression, and SP acutely blocked insulin-mediated stimulation of fatty acid uptake and Akt phosphorylation. Although adiponectin secretion was unchanged, mRNA expression was decreased (−86 ± 8%, P < 0.001). In humans, NK1R expression correlates positively with plasma insulin, fatty acid, and complement C3 and negatively with adiponectin, CEBPα, CEBPβ, and peroxisome proliferator-activated receptor-γ mRNA expression in omental, but not subcutaneous, adipose tissue. Our results suggest that, beyond its neuroendocrine and inflammatory effects, SP could also be involved in targeting adipose tissue and influencing insulin resistance.
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Vernon Rayner, D. "The sympathetic nervous system in white adipose tissue regulation." Proceedings of the Nutrition Society 60, no. 3 (August 2001): 357–64. http://dx.doi.org/10.1079/pns2001101.
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Sympathetic stimulation has long been recognized to mobilise fatty acids from white adipose tissue. However, it is now apparent that adipose tissue is not only concerned with energy storage as fat, but is a major endocrine and secretory organ. This change has resulted from the identification of leptin as a hormone of energy balance secreted by white adipose tissue. The sympathetic system is a key regulator of leptin production in white fat. Sympathomimetic amines, cold exposure or fasting (which lead to sympathetic stimulation of white fat), decrease ob gene expression in the tissue and leptin production. On the other hand, sympathetic blockade often increases circulating leptin and ob gene expression, and it is postulated that the sympathetic system has a tonic inhibitory action on leptin synthesis. In rodents this action is through stimulation of b3-adrenoceptors. The adrenal medulla (as opposed to the direct sympathetic innervation) has been thought to play only a minor role in the catecholaminergic regulation of white adipose tissue. However, in rodents responses of the leptin system to adrenergic blockade vary with the method used. Changes in leptin and ob gene expression are considerably less using methods of blockade that only effect the terminal adrenergic innervation, rather than medullary secretions as well. Stimulation of the leptin system increases sympathetic activity and hence metabolic activity in many tissues. As well as leptin, other (but not all) secretions from white adipose tissue are subject to sympathetic regulation. In obesity the sympathetic sensitivity of adipose tissue is reduced and this factor may underlie the dysregulation of leptin production and other adipose tissue secretions.
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Cox, Nehemiah, Lucile Crozet, Inge R. Holtman, Pierre-Louis Loyher, Tomi Lazarov, Jessica B. White, Elvira Mass, et al. "Diet-regulated production of PDGFcc by macrophages controls energy storage." Science 373, no. 6550 (July 1, 2021): eabe9383. http://dx.doi.org/10.1126/science.abe9383.
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The mechanisms by which macrophages regulate energy storage remain poorly understood. We identify in a genetic screen a platelet-derived growth factor (PDGF)/vascular endothelial growth factor (VEGF)–family ortholog, Pvf3, that is produced by macrophages and is required for lipid storage in fat-body cells of Drosophila larvae. Genetic and pharmacological experiments indicate that the mouse Pvf3 ortholog PDGFcc, produced by adipose tissue–resident macrophages, controls lipid storage in adipocytes in a leptin receptor– and C-C chemokine receptor type 2–independent manner. PDGFcc production is regulated by diet and acts in a paracrine manner to control lipid storage in adipose tissues of newborn and adult mice. At the organismal level upon PDGFcc blockade, excess lipids are redirected toward thermogenesis in brown fat. These data identify a macrophage-dependent mechanism, conducive to the design of pharmacological interventions, that controls energy storage in metazoans.
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Lu, Xiaodan, Yan Ji, Luqing Zhang, Yuntao Zhang, Shuzhi Zhang, Yao An, Peng Liu, and Yaowu Zheng. "Resistance to Obesity by Repression of VEGF Gene Expression through Induction of Brown-Like Adipocyte Differentiation." Endocrinology 153, no. 7 (May 16, 2012): 3123–32. http://dx.doi.org/10.1210/en.2012-1151.
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Adipose tissues are classified into white adipose tissue (WAT) and brown adipose tissue (BAT). WAT is responsible for energy storage, and malfunction is associated with obesity. BAT, on the contrary, consumes fat to generate heat through uncoupling mitochondrial respiration and is important in body weight control. Vascular endothelial growth factor (VEGF)-A is the founding member of the VEGF family and has been found highly expressed in adipose tissue. A genetic mouse model of an inducible VEGF (VEGF-A) repression system was used to study VEGF-regulated energy metabolism in WAT. VEGF-repressed mice demonstrated lower food efficiency, lower body weight, and resistance to high-fat diet-induced obesity. Repression of VEGF expression caused morphological and molecular changes in adipose tissues. VEGF repression induced brown-like adipocyte development in WAT, up-regulation of BAT-specific genes including PRDM16, GATA-1, BMP-7, CIDEA, and UCP-1 and down-regulation of leptin, a WAT-specific gene. VEGF repression up-regulated expression of VEGF-B and its downstream fatty acid transport proteins. Relative levels of VEGF/VEGF-B may be important switches in energy metabolism and of pharmaceutical significances.
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Okuno, Senji. "Significance of Adipose Tissue Maintenance in Patients Undergoing Hemodialysis." Nutrients 13, no. 6 (May 31, 2021): 1895. http://dx.doi.org/10.3390/nu13061895.
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In the general population, obesity is known to be associated with adverse outcomes, including mortality. In contrast, high body mass index (BMI) may provide a survival advantage for hemodialysis patients, which is known as the obesity paradox. Although BMI is the most commonly used measure for the assessment of obesity, it does not distinguish between fat and lean mass. Fat mass is considered to serve as an energy reserve against a catabolic condition, while the capacity to survive starvation is also thought to be dependent on its amount. Thus, fat mass is used as a nutritional marker. For example, improvement of nutritional status by nutritional intervention or initiation of hemodialysis is associated with an increase in fat mass. Several studies have shown that higher levels of fat mass were associated with better survival in hemodialysis patients. Based on body distribution, fat mass is classified into subcutaneous and visceral fat. Visceral fat is metabolically more active and associated with metabolic abnormalities and inflammation, and it is thus considered to be a risk factor for cardiovascular disease and mortality. On the other hand, subcutaneous fat has not been consistently linked to adverse phenomena and may reflect nutritional status as a type of energy storage. Visceral and subcutaneous adipose tissues have different metabolic and inflammatory characteristics and may have opposing influences on various outcomes, including mortality. Results showing an association between increased subcutaneous fat and better survival, along with other conditions, such as cancer or cirrhosis, in hemodialysis patients have been reported. This evidence suggests that fat mass distribution (i.e., visceral fat and subcutaneous fat) plays a more important role for these beneficial effects in hemodialysis patients.
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Le Lay, S., P. Ferré, and I. Dugail. "Adipocyte cholesterol balance in obesity." Biochemical Society Transactions 32, no. 1 (February 1, 2004): 103–6. http://dx.doi.org/10.1042/bst0320103.
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Adipose tissue is specialized in the storage of energy in the form of triacylglycerol. Within the fat cell, triacylglycerols are found in a well-defined structural compartment called the lipid droplet, which occupies the vast majority of the fat cell volume. However, many other lipids are present in the lipid droplet. These include sterols, carotenoids, cholecalciferol and lipophilic toxic pollutants of the environment such as dioxins and tocopherols. The topic of this article is the role of fat cell cholesterol in adipose tissue physiology and its potential implication in pathological states such as obesity.
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Garcia-Arcos, Itsaso, Yaeko Hiyama, Konstantinos Drosatos, Kalyani G. Bharadwaj, Yunying Hu, Ni Huiping Son, Sheila M. O'Byrne, et al. "Adipose-specific Lipoprotein Lipase Deficiency More Profoundly Affects Brown than White Fat Biology." Journal of Biological Chemistry 288, no. 20 (March 31, 2013): 14046–58. http://dx.doi.org/10.1074/jbc.m113.469270.
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Adipose fat storage is thought to require uptake of circulating triglyceride (TG)-derived fatty acids via lipoprotein lipase (LpL). To determine how LpL affects the biology of adipose tissue, we created adipose-specific LpL knock-out (ATLO) mice, and we compared them with whole body LpL knock-out mice rescued with muscle LpL expression (MCK/L0) and wild type (WT) mice. ATLO LpL mRNA and activity were reduced, respectively, 75 and 70% in gonadal adipose tissue (GAT), 90 and 80% in subcutaneous tissue, and 84 and 85% in brown adipose tissue (BAT). ATLO mice had increased plasma TG levels associated with reduced chylomicron TG uptake into BAT and lung. ATLO BAT, but not GAT, had altered TG composition. GAT from MCK/L0 was smaller and contained less polyunsaturated fatty acids in TG, although GAT from ATLO was normal unless LpL was overexpressed in muscle. High fat diet feeding led to less adipose in MCK/L0 mice but TG acyl composition in subcutaneous tissue and BAT reverted to that of WT. Therefore, adipocyte LpL in BAT modulates plasma lipoprotein clearance, and the greater metabolic activity of this depot makes its lipid composition more dependent on LpL-mediated uptake. Loss of adipose LpL reduces fat accumulation only if accompanied by greater LpL activity in muscle. These data support the role of LpL as the “gatekeeper” for tissue lipid distribution.
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Chitraju, Chandramohan, Tobias C. Walther, and Robert V. Farese. "The triglyceride synthesis enzymes DGAT1 and DGAT2 have distinct and overlapping functions in adipocytes." Journal of Lipid Research 60, no. 6 (April 1, 2019): 1112–20. http://dx.doi.org/10.1194/jlr.m093112.
Full textAbstract:
Mammals store metabolic energy as triacylglycerols (TGs) in adipose tissue. TG synthesis is catalyzed by the evolutionarily unrelated acyl-CoA:diacylglycerol acyltransferase (DGAT) enzymes DGAT1 and DGAT2, which catalyze the same reaction and account for nearly all TG synthesis. The reasons for their convergent evolution to synthesize TGs remain unclear. Mice lacking DGAT1 are viable with reduced fat stores of TGs, whereas DGAT2 KO mice die postnatally just after birth with >90% reduction of TGs, suggesting that DGAT2 is the predominant enzyme for TG storage. To better understand the functional differences between the DGATs, we studied mice fed chow or high-fat diets lacking either enzyme in adipose tissue. Unexpectedly, mice lacking DGAT2 in adipocytes have normal TG storage and glucose metabolism on regular or high-fat diets, indicating DGAT2 is not essential for fat storage. In contrast, mice lacking DGAT1 in adipocytes have normal TG storage on a chow diet but moderately decreased body fat accompanied by glucose intolerance when challenged with a high-fat diet. The latter changes were associated with the activation of ER stress pathways. We conclude that DGAT1 and DGAT2 can largely compensate for each other for TG storage but that DGAT1 uniquely has an important role in protecting the ER from the lipotoxic effects of high-fat diets.
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Faraj, May, Hui Ling Lu, and Katherine Cianflone. "Diabetes, lipids, and adipocyte secretagogues." Biochemistry and Cell Biology 82, no. 1 (February 1, 2004): 170–90. http://dx.doi.org/10.1139/o03-078.
Full textAbstract:
That obesity is associated with insulin resistance and type II diabetes mellitus is well accepted. Overloading of white adipose tissue beyond its storage capacity leads to lipid disorders in non-adipose tissues, namely skeletal and cardiac muscles, pancreas, and liver, effects that are often mediated through increased non-esterified fatty acid fluxes. This in turn leads to a tissue-specific disordered insulin response and increased lipid deposition and lipotoxicity, coupled to abnormal plasma metabolic and (or) lipoprotein profiles. Thus, the importance of functional adipocytes is crucial, as highlighted by the disorders seen in both "too much" (obesity) and "too little" (lipodystrophy) white adipose tissue. However, beyond its capacity for fat storage, white adipose tissue is now well recognised as an endocrine tissue producing multiple hormones whose plasma levels are altered in obese, insulin-resistant, and diabetic subjects. The consequence of these hormonal alterations with respect to both glucose and lipid metabolism in insulin target tissues is just beginning to be understood. The present review will focus on a number of these hormones: acylation-stimulating protein, leptin, adiponectin, tumour necrosis factor α, interleukin-6, and resistin, defining their changes induced in obesity and diabetes mellitus and highlighting their functional properties that may protect or worsen lipid metabolism.Key words: C3adesarg, fatty acid trapping, lipolysis, lipogenesis.
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Vaitkus, Janina A., and Francesco S. Celi. "The role of adipose tissue in cancer-associated cachexia." Experimental Biology and Medicine 242, no. 5 (December 8, 2016): 473–81. http://dx.doi.org/10.1177/1535370216683282.
Full textAbstract:
Adipose tissue (fat) is a heterogeneous organ, both in function and histology, distributed throughout the body. White adipose tissue, responsible for energy storage and more recently found to have endocrine and inflammation-modulatory activities, was historically thought to be the only type of fat present in adult humans. The recent demonstration of functional brown adipose tissue in adults, which is highly metabolic, shifted this paradigm. Additionally, recent studies demonstrate the ability of white adipose tissue to be induced toward the brown adipose phenotype – “beige” or “brite” adipose tissue – in a process referred to as “browning.” While these adipose tissue depots are under investigation in the context of obesity, new evidence suggests a maladaptive role in other metabolic disturbances including cancer-associated cachexia, which is the topic of this review. This syndrome is multifactorial in nature and is an independent factor associated with poor prognosis. Here, we review the contributions of all three adipose depots – white, brown, and beige – to the development and progression of cancer-associated cachexia. Specifically, we focus on the local and systemic processes involving these adipose tissues that lead to increased energy expenditure and sustained negative energy balance. We highlight key findings from both animal and human studies and discuss areas within the field that need further exploration. Impact statement Cancer-associated cachexia (CAC) is a complex, multifactorial syndrome that negatively impacts patient quality of live and prognosis. This work reviews a component of CAC that lacks prior discussion: adipose tissue contributions. Uniquely, it discusses all three types of adipose tissue, white, beige, and brown, their interactions, and their contributions to the development and progression of CAC. Summarizing key bench and clinical studies, it provides information that will be useful to both basic and clinical researchers in designing experiments, studies, and clinical trials.
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Villarroya, Joan, Rubén Cereijo, and Francesc Villarroya. "An endocrine role for brown adipose tissue?" American Journal of Physiology-Endocrinology and Metabolism 305, no. 5 (September 1, 2013): E567—E572. http://dx.doi.org/10.1152/ajpendo.00250.2013.
Full textAbstract:
White adipose tissue is recognized as both a site of energy storage and an endocrine organ that produces a myriad of endocrine factors called adipokines. Brown adipose tissue (BAT) is the main site of nonshivering thermogenesis in mammals. The amount and activity of brown adipocytes are associated with protection against obesity and associated metabolic alterations. These effects of BAT are traditionally attributed to its capacity for the oxidation of fatty acids and glucose to sustain thermogenesis. However, recent data suggest that the beneficial effects of BAT could involve a previously unrecognized endocrine role through the release of endocrine factors. Several signaling molecules with endocrine properties have been found to be released by brown fat, especially under conditions of thermogenic activation. Moreover, experimental BAT transplantation has been shown to improve glucose tolerance and insulin sensitivity mainly by influencing hepatic and cardiac function. It has been proposed that these effects are due to the release of endocrine factors by brown fat, such as insulin-like growth factor I, interleukin-6, or fibroblast growth factor-21. Further research is needed to determine whether brown fat plays an endocrine role and, if so, to comprehensively identify which endocrine factors are released by BAT. Such research may reveal novel clues for the observed association between brown adipocyte activity and a healthy metabolic profile, and it could also enlarge a current view of potential therapeutic tools for obesity and associated metabolic diseases.
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Romanski, Susan A., Rita M. Nelson, and Michael D. Jensen. "Meal fatty acid uptake in adipose tissue: gender effects in nonobese humans." American Journal of Physiology-Endocrinology and Metabolism 279, no. 2 (August 1, 2000): E455—E462. http://dx.doi.org/10.1152/ajpendo.2000.279.2.e455.
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We tested for gender differences in dietary fatty acid metabolism in 12 nonobese men and 12 nonobese women using the meal fatty acid tracer/adipose tissue biopsy study design. In addition to determining body composition, measurements of regional adipose tissue lipoprotein lipase activity, blood flow, and fat cell size were performed to place the meal fatty acid kinetic studies in perspective. Twenty-four hours after ingesting the test meal, the concentration of meal fatty acids was greater ( P < 0.05) in abdominal subcutaneous than in thigh adipose tissue in both men (0.61 ± 0.12 vs. 0.45 ± 0.09 mg/g) and women (0.59 ± 0.10 vs. 0.43 ± 0.05) but was not different between men and women. A greater percentage of dietary fat was stored in subcutaneous adipose tissue in women than in men (38 ± 3 vs. 24 ± 3%, respectively, P < 0.05), and a greater portion of meal fatty acid disposal was unaccounted for in men. Significant gender differences in regional adipose tissue blood flow after meal ingestion were noted; the differences were in the direction that could support greater nutrient storage in lower body fat in women.
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Andersen, Iben R., Esben Søndergaard, Lars P. Sørensen, Birgitte Nellemann, Lars C. Gormsen, Michael D. Jensen, and Søren Nielsen. "Increased VLDL-TG Fatty Acid Storage in Skeletal Muscle in Men With Type 2 Diabetes." Journal of Clinical Endocrinology & Metabolism 102, no. 3 (November 29, 2016): 831–39. http://dx.doi.org/10.1210/jc.2016-2979.
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AbstractContext:Lipoprotein lipase (LPL) activity is considered the rate-limiting step of very-low-density-lipoprotein triglycerides (VLDL-TG) tissue storage, and has been suggested to relate to the development of obesity as well as insulin resistance and type 2 diabetes.Objective:The objective of the study was to assess the relationship between the quantitative storage of VLDL-TG fatty acids and LPL activity and other storage factors in muscle and adipose tissue. In addition, we examine whether such relations were influenced by type 2 diabetes.Design:We recruited 23 men (12 with type 2 diabetes, 11 nondiabetic) matched for age and body mass index. Postabsorptive VLDL-TG muscle and subcutaneous adipose tissue (abdominal and leg) quantitative storage was measured using tissue biopsies in combination with a primed-constant infusion of ex vivo triolein labeled [1-14C]VLDL-TG and a bolus infusion of ex vivo triolein labeled [9,10-3H]VLDL-TG. Biopsies were analyzed for LPL activity and cellular storage factors.Results:VLDL-TG storage rate was significantly greater in men with type 2 diabetes compared with nondiabetic men in muscle tissue (P = 0.02). We found no significant relationship between VLDL-TG storage rate and LPL activity or other storage factors in muscle or adipose tissue. However, LPL activity correlated with fractional VLDL-TG storage in abdominal fat (P = 0.04).Conclusions:Men with type 2 diabetes have increased VLDL-TG storage in muscle tissue, potentially contributing to increased intramyocellular triglyceride and ectopic lipid deposition. Neither muscle nor adipose tissue storage rates were related to LPL activity. This argues against LPL as a rate-limiting step in the postabsorptive quantitative storage of VLDL-TG.
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Duncan, S., M. McCann, G. Qiang, V. Gil, H. Whang Kong, and C. Liew. "ID: 87: TRANSCRIPTION FACTOR CREB3L3 IS A NOVEL REGULATOR FOR ADIPOCYTE BIOLOGY AND METABOLISM." Journal of Investigative Medicine 64, no. 4 (March 22, 2016): 930.2–931. http://dx.doi.org/10.1136/jim-2016-000120.41.
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The presence of differential metabolic risks between the metabolically-protective subcutaneous adipose tissue (SAT) and the disease-associated visceral adipose tissue (VAT) is well established, but the mechanisms that cause these differences are not well understood. Cyclic AMP responsive element binding protein 3-like 3 (CREB3L3), a previously characterized liver-specific ER-bound transcription factor, was found to be expressed in murine SAT and VAT. In obese human subjects and an obese mouse model, we found that CREB3L3 is downregulated in SAT, but not in VAT. To examine the role of CREB3L3 in adipocyte biology and metabolism, we created a fat-specific CREB3L3 knockout (KO) mouse using the AdipoQ-Cre mouse. To establish a potential role for CREB3L3 in adipocytes, we examined in vitro differentiated adipocytes from isolated WT and KO primary stromal vascular fraction. We observed that ablation of CREB3L3 in SAT adipocytes significantly upregulated expression of both lipogenic and lipolytic markers. At the same time, we also observed significantly increased expression of thermogenic markers like PGC1α and Cox8b. Taken together our data suggest potential upregulation of the fat futile cycle in SAT upon deletion of CREB3L3. Surprisingly, we found that CREB3L3 KO tends to downregulate expression of markers of both lipogenesis and lipolysis in VAT adipocytes. This observation could potentially be contributed by the tendency of CREB3l3 KO VAT to have inhibited differentiation. To investigate the in vivo function of CREB3L3, we challenged WT and KO mice with high fat diet with weekly body weight assessment. We observed that CREB3L3 ablation in adipose tissues promotes significant weight gain in mice on HFD. Unexpectedly, despite being heavier, the KO mice are not more glucose intolerant or insulin resistant. These data together suggest that ablation of CREB3L3 could potentially promote fat storage in adipose tissues to prevent metabolic diseases caused by ectopic fat deposition.
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Fargali, Samira, Thomas Scherer, Andrew C. Shin, Masato Sadahiro, Christoph Buettner, and Stephen R. Salton. "Germline ablation of VGF increases lipolysis in white adipose tissue." Journal of Endocrinology 215, no. 2 (August 31, 2012): 313–22. http://dx.doi.org/10.1530/joe-12-0172.
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Targeted deletion of VGF, a neuronal and endocrine secreted protein and neuropeptide precursor, produces a lean, hypermetabolic mouse that is resistant to diet-, lesion-, and genetically induced obesity and diabetes. We hypothesized that increased sympathetic nervous system activity in Vgf−/Vgf− knockout mice is responsible for increased energy expenditure and decreased fat storage and that increased β-adrenergic receptor stimulation induces lipolysis in white adipose tissue (WAT) of Vgf−/Vgf− mice. We found that fat mass was markedly reduced in Vgf−/Vgf− mice. Within knockout WAT, phosphorylation of protein kinase A substrate increased in males and females, phosphorylation of hormone-sensitive lipase (HSL) (ser563) increased in females, and levels of adipose triglyceride lipase, comparative gene identification-58, and phospho-perilipin were higher in male Vgf−/Vgf− WAT compared with wild-type, consistent with increased lipolysis. The phosphorylation of AMP-activated protein kinase (AMPK) (Thr172) and levels of the AMPK kinase, transforming growth factor β-activated kinase 1, were decreased. This was associated with a decrease in HSL ser565 phosphorylation, the site phosphorylated by AMPK, in both male and female Vgf−/Vgf− WAT. No significant differences in phosphorylation of CREB or the p42/44 MAPK were noted. Despite this evidence supporting increased cAMP signaling and lipolysis, lipogenesis as assessed by fatty acid synthase protein expression and phosphorylated acetyl-CoA carboxylase was not decreased. Our data suggest that the VGF precursor or selected VGF-derived peptides dampen sympathetic outflow pathway activity to WAT to regulate fat storage and lipolysis.
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Rosell, Meritxell, Myrsini Kaforou, Andrea Frontini, Anthony Okolo, Yi-Wah Chan, Evanthia Nikolopoulou, Steven Millership, et al. "Brown and white adipose tissues: intrinsic differences in gene expression and response to cold exposure in mice." American Journal of Physiology-Endocrinology and Metabolism 306, no. 8 (April 15, 2014): E945—E964. http://dx.doi.org/10.1152/ajpendo.00473.2013.
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Brown adipocytes dissipate energy, whereas white adipocytes are an energy storage site. We explored the plasticity of different white adipose tissue depots in acquiring a brown phenotype by cold exposure. By comparing cold-induced genes in white fat to those enriched in brown compared with white fat, at thermoneutrality we defined a “brite” transcription signature. We identified the genes, pathways, and promoter regulatory motifs associated with “browning,” as these represent novel targets for understanding this process. For example, neuregulin 4 was more highly expressed in brown adipose tissue and upregulated in white fat upon cold exposure, and cell studies showed that it is a neurite outgrowth-promoting adipokine, indicative of a role in increasing adipose tissue innervation in response to cold. A cell culture system that allows us to reproduce the differential properties of the discrete adipose depots was developed to study depot-specific differences at an in vitro level. The key transcriptional events underpinning white adipose tissue to brown transition are important, as they represent an attractive proposition to overcome the detrimental effects associated with metabolic disorders, including obesity and type 2 diabetes.