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Relevant bibliographies by topics / Adipose tissue; Fat storage

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Academic literature on the topic 'Adipose tissue; Fat storage'

Author: Grafiati

Published: 4 June 2021

Last updated: 4 February 2022

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Journal articles on the topic "Adipose tissue; Fat storage"

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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Dissertations / Theses on the topic "Adipose tissue; Fat storage"

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Samra, Jaswinder Singh. "Regulation of fat mobilisation in normal subjects in the post-absorptive state : role of hormones." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.319044.

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Farré, Guasch Elisabet. "Adipose Stem Cells from Buccal Fat Pad and Abdominal Adipose Tissue for Bone tissue Engineering." Doctoral thesis, Universitat Internacional de Catalunya, 2011. http://hdl.handle.net/10803/31987.

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ABSTRACT Background and Objective: Stem cells offer an interesting tool for tissue engineering, but the clinical applications are limited by donor site morbidity and low cell number upon harvest. Recent studies have identified an abundant source of stem cells in subcutaneous adipose tissue. These adipose stem cells (ASC), are able to differentiate to several lineages and express multiple growth factors, which makes them suitable for clinical application. Buccal fat pad (BFP), an adipose encapsulated mass in the oral cavity, could represent an easy access source for dentists and oral surgeons. Biosynthetic substitutes such as β-tricalcium phosphate (β-TCP), hydroxyapatite (HA), and mixtures of HA/β-TCP (biphasic calcium phosphate; BCP) have been successfully used as bone graft biomaterials. Growth factors stimulating osteogenic differentiation are also interesting for bone tissue engineering applications. We aimed to investigate whether BFP is a rich source of ASC, and whether ASC triggered for only 15 min with bone morphogenetic protein-2 (BMP-2), and seeded onto different calcium phosphate scaffolds composed of β-TCP alone or mixtures of HA/β-TCP, could stimulate bone formation. Materials & Methods: ASC obtained from subcutaneous abdominal adipose tissue and BFP were counted and analyzed by flow cytometry, to determine ASC cell number, phenotype and percentage. At two weeks of culture, the multipotent differentiation potential of ASC from BFP was analyzed. Furthermore, fresh ASC either or not stimulated with 10ng/ml BMP-2 for 15min were seeded on different calcium phosphate scaffolds. ASC attachment, proliferation and osteogenic differentiation was analyzed and compared. Results: BFP contained ~30% of ASC. The ASC number obtained per gram of adipose tissue from BFP at one week of culture was 2-fold higher than in subcutaneous abdominal adipose tissue. Angiogenic marker expression was also higher, and ASC showed multipotent differentiation potential as well. Fifteen min BMP-2 treatment increased ASC cell proliferation and osteogenic differentiation on BCP composed of 60% HA and 40% β-TCP, but not on other scaffolds containing less percentage of HA. Conclusions: Buccal fat pad is a rich alternative source of ASC suitable for bone tissue engineering. Short stimulation of only 15 minutes with BMP-2 is enough to stimulate ASC proliferation and osteogenic differentiation. Therefore ASC could be treated shortly with BMP-2 and seeded on BCP with 60% HA to improve bone regeneration.

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Ojha, Shalini. "Pericardial fat is a nutritionally regulated depot of brown adipose tissue." Thesis, University of Nottingham, 2015. http://eprints.nottingham.ac.uk/30678/.

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Introduction: Obesity and related cardio-metabolic complications have acquired global epidemic proportions. Suboptimal nutritional environment in early life induces adaptations in energy homeostasis, metabolism and adipose tissue development that may confer short-term survival advantages but are detrimental in later life, particularly if nutrient supply is restored. Brown adipose tissue (BAT) has a unique role in energy homeostasis because it can provide a potential compensatory mechanism against excess weight gain via cold or diet-induced adaptive thermogenesis. Brown adipocytes also have a potential role in lipid and glucose metabolism and BAT activation can increase clearance of lipids and glucose from the circulation. Pericardial fat, particularly epicardial adipose tissue (fat present between the myocardium and the visceral layer of the pericardium), is anatomically and clinically related to cardiac morphology and function and is believed to be a metabolically active organ that affects cardiac function and the evolution of cardiac pathologies. High expression of mRNA for uncoupling protein (UCP) 1 in adult human epicardial adipose tissue suggests that this may be a depot of BAT. Hypotheses: In my thesis, I hypothesised that pericardial adipose tissue is a depot of brown fat in humans and sheep. I also hypothesised that suboptimal nutrition in early life will affect adiposity and development of BAT in this depot. Methods: UCP1 mRNA expression and protein abundance and other BAT and white adipose tissue related genes were studied in pericardial adipose tissue. In the first study, pericardial fat was sampled from newborn and 30 day old sheep born to mothers fed with 100% or 60% of their total metabolisable energy (ME) requirement from 110 day gestation to term. In the second study, pericardial fat was sampled from near-term (140 day gestation) fetuses delivered to mothers fed 100% or 60% of total ME requirement from 28 to 80 days and then fed ad libitum. Gene expression was measured by reverse transcription-polymerase chain reaction and protein abundance by Western blotting and immunohistochemistry. To confirm the presence of BAT in the human epicardial fat depot, relative abundance of UCP1 was measured by Western Blotting in epicardial, paracardial, and subcutaneous fat samples taken from adults. In the final study, epicardial fat samples were collected from 63 children (0-18 years of age) undergoing cardiac surgery and gene expression of UCP1 and other BAT and WAT related genes identified by microarray. The presence of UCP1 was confirmed by immunohistochemistry. Results: Pericardial adipose tissue is a depot of BAT in fetal and newborn sheep. Suboptimal maternal nutrition in late gestation reduces the abundance of UCP1 and downregulates other BAT related genes whilst suboptimal maternal nutrition in early-to-mid gestation followed by ad libitum feeding to term, increases adiposity, enhances UCP1 abundance and upregulates genes involved in brown and white adipogenesis. Epicardial fat from newborn infants, children, adolescents and older adults contains UCP1 confirming that it is a BAT depot in humans. UCP1 gene expression in infancy and early childhood in humans is downregulated in children with poor nutritional states. Conclusions: I have shown that adipose tissue depots present around the heart are a repository of brown fat, at least in humans and sheep. In view of the potential role of BAT in regulation of lipid and glucose metabolism, this may have therapeutic implications for treatment of cardiovascular complications of obesity. Suboptimal nutrition in utero and during early life compromises BAT development. Although the exact mechanism of how these changes affect the propensity towards obesity and metabolic dysregulation remains to be elucidated, a reduction in thermogenesis presents a plausible mechanism for the increased metabolic efficiency associated with nutritional deprivation in early life. BAT persists beyond the neonatal period in to adult life and, therefore, presents a potential target for long lasting nutritional manipulations to promote better health.

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Wiklund, Peder. "Adipose tissue, the skeleton and cardiovascular disease." Doctoral thesis, Umeå universitet, Geriatrik, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-42083.

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Cardiovascular disease (CVD) is the leading cause of death in the Western World, although the incidence of myocardial infarction (MI) has declined over the last decades. However, obesity, which is one of the most important risk factors for CVD, is increasingly common. Osteoporosis is also on the rise because of an aging population. Based on considerable overlap in the prevalence of CVD and osteoporosis, a shared etiology has been proposed. Furthermore, the possibility of interplay between the skeleton and adipose tissue has received increasing attention the last few years with the discovery that leptin can influence bone metabolism and that osteocalcin can influence adipose tissue. A main aim of this thesis was to investigate the effects of fat mass distribution and bone mineral density on the risk of MI. Using dual-energy x-ray absorptiometry (DEXA) we measured 592 men and women for regional fat mass in study I. In study II this was expanded to include 3258 men and women. In study III 6872 men and women had their bone mineral density measured in the total hip and femoral neck using DEXA. We found that a fat mass distribution with a higher proportion of abdominal fat mass was associated with both an adverse risk factor profile and an increased risk of MI. In contrast, a higher gynoid fat mass distribution was associated with a more favorable risk factor profile and a decreased risk of MI, highlighting the different properties of abdominal and gynoid fat depots (study I-II). In study III, we investigated the association of bone mineral density and risk factors shared between CVD and osteoporosis, and risk of MI. We found that lower bone mineral density was associated with hypertension, and also tended to be associated to other CVD risk factors. Low bone mineral density was associated with an increased risk of MI in both men and women, apparently independently of the risk factors studied (study III). In study IV, we investigated 50 healthy, young men to determine if a high-impact loading intervention in the form of a series of jumps would lead to changes in glucose and lipid metabolism. We found that the intervention group had significantly lowered serum glucose levels compared to the control group. Changes in all metabolic parameters favored the intervention group with an increase in lipolysis from baseline and a decrease in cholesterol. In summary, the proportion of abdominal and gynoid fat mass displayed contrasting associations to both CVD risk factors and MI risk. Abdominal fat mass was associated with a higher risk while a high proportion of gynoid fat mass was associated with a lower risk. Bone mineral density displayed an inverse association with MI risk, seemingly independently of CVD risk factors, suggesting other explanations to a shared pathogenesis. Finally, high impact loading on the skeleton in young, healthy men decreased serum glucose levels and tended to improve other metabolic parameters, suggesting that the skeleton can affect energy metabolism.

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Axelsson, Jonas. "Fat tissue, adipokines and clinical complications of chronic kidney disease /." Stockholm : Department of Clinical Science, Intervention and Technology, Divisions of Renal Medicine and Baxter Novum, Karolinska institutet, 2006. http://diss.kib.ki.se/2006/91-7140-653-0/.

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Thapar, Divya. "Osteopontin knockout abates high fat diet-induced insulin resistance and adipose tissue inflammation." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2008. http://wwwlib.umi.com/cr/ucsd/fullcit?p1459910.

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Thesis (M.S.)--University of California, San Diego, 2008.
Title from first page of PDF file (viewed January 5, 2009). Available via ProQuest Digital Dissertations. Includes bibliographical references (p. 43-46).

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Nnodim, J. O. "Morphological studies on the development and the control mechanisms of brown adipose tissue." Thesis, Bucks New University, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.356211.

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Dziubajlo, Maria. "Factors affecting the composition and physical properties of pig adipose tissue triacylglycerols." Thesis, Imperial College London, 1991. http://hdl.handle.net/10044/1/46754.

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Manolopoulos, Konstantinos. "Adrenergic regulation of regional fat metabolism." Thesis, University of Oxford, 2011. http://ora.ox.ac.uk/objects/uuid:31dfdca3-e3df-41a6-bf27-74f6ccdcf0a7.

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Introduction: An increased gluteofemoral adipose tissue (AT) mass is associated with a protective cardiovascular and metabolic risk profile, and effective fatty acid retention in femoral AT has been proposed as a possible mechanism. Catecholamines are important regulators of AT lipolysis and blood flow (ATBF). The aim of the thesis was to investigate regional differences in the adrenergic regulation of fatty acid release and ATBF between abdominal and femoral AT in vivo. Furthermore, in vivo regional fatty acid trafficking was studied in a physiological setting over 24 h. Methods: Regional fatty acid trafficking, along with the measurement of ATBF, was studied with the arterio-venous difference technique and stable isotope tracers in healthy volunteers. Adrenergic agonists (isoprenaline, adrenaline) were infused either locally by microinfusion, or systemically. Local microinfusion of adrenoreceptor antagonists (propranolol, phentolamine) was used to characterize specific adrenoreceptor subtype effects. The trafficking of dietary fatty acids was studied over a 24 h period involving three meals containing stable isotope-labelled fatty acids along with intravenous infusions of another labelled fatty acid. Results: Femoral ATBF and lipolysis was less responsive to adrenergic stimulation with adrenaline compared to abdominal AT. This was due to increased femoral α-adrenoreceptor responsiveness. When studied over 24 h, femoral AT showed a lower lipolysis rate compared to abdominal AT, while dietary fatty acids were extracted more avidly by abdominal AT. Uptake of non-dietary fatty acids (derived from very-low-density lipoproteins or unbound non-esterified fatty acids) was comparable between abdominal and femoral AT. Conclusion: There are fundamental differences in response to adrenergic stimuli between abdominal and gluteofemoral tissues and the ability of femoral AT to trap non-dietary fatty acids may provide protection of other tissues from ectopic fatty acid deposition.

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Zieger, Konstanze, Juliane Weiner, Anne Kunath, Martin Gericke, Kerstin Krause, Matthias Kern, Michael Stumvoll, Nora Klöting, Matthias Blüher, and John T. Heiker. "Ablation of kallikrein 7 (KLK7) in adipose tissue ameliorates metabolic consequences of high fat diet-induced obesity by counteracting adipose tissue inflammation in vivo." Springer, 2018. https://ul.qucosa.de/id/qucosa%3A33207.

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Vaspin is an adipokine which improves glucose metabolism and insulin sensitivity in obesity. Kallikrein 7 (KLK7) is the first known protease target inhibited by vaspin and a potential target for the treatment of metabolic disorders. Here, we tested the hypothesis that inhibition of KLK7 in adipose tissue may beneficially affect glucose metabolism and adipose tissue function. Therefore, we have inactivated the Klk7 gene in adipose tissue using conditional gene-targeting strategies in mice. Klk7-deficient mice (ATKlk7 −/−) exhibited less weight gain, predominant expansion of subcutaneous adipose tissue and improved whole body insulin sensitivity under a high fat diet (HFD). ATKlk7 −/− mice displayed higher energy expenditure and food intake, most likely due to altered adipokine secretion including lower circulating leptin. Pro-inflammatory cytokine expression was significantly reduced in combination with an increased percentage of alternatively activated (anti-inflammatory) M2 macrophages in epigonadal adipose tissue of ATKlk7 −/−. Taken together, by attenuating adipose tissue inflammation, altering adipokine secretion and epigonadal adipose tissue expansion, Klk7 deficiency in adipose tissue partially ameliorates the adverse effects of HFD-induced obesity. In summary, we provide first evidence for a previously unrecognized role of KLK7 in adipose tissue with effects on whole body energy expenditure and insulin sensitivity.

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Books on the topic "Adipose tissue; Fat storage"

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Avram, Mathew M. Fat removal: Invasive and non-invasive body contouring. Chichester, West Sussex: John Wiley & Sons Inc., 2015.

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Liposuction surgery and autologous fat transplantation. Norwalk, Conn: Appleton & Lange, 1988.

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Bienertová-Vašků, Julie. Body fat: Composition, measurements, and reduction procedures. Hauppauge, N.Y: Nova Science, 2011.

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The good fat revoultion: A 30-day plan that triggers brown fat---the secret to losing weight and living healthier. New York: St. Martin's Press, 2009.

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Structural fat grafting. St. Louis, Mo: Quality Medical Pub., 2004.

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Fat management: The thermogenic factor. Lehi, Utah: Victory Publications, 1994.

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Wood, Philip A. How fat works. Cambridge, MA: Harvard University Press, 2005.

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How fat works. Cambridge, Mass: Harvard University Press, 2006.

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Goldberg, David J., and Alexander L. Berlin. Disorders of fat and cellulite: Advances in diagnosis and treatment. New York: Informa Healthcare, 2011.

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The missing piece to the weight loss puzzle. [England?]: Bedford Kennsington, 1995.

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Book chapters on the topic "Adipose tissue; Fat storage"

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Imam, Syed Khalid. "White Adipose Tissue: Beyond Fat Storage." In Obesity, 1–12. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-19821-7_1.

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Magalon, Guy, and Jeremy Magalon. "Biology of Adipose Tissue." In Gluteal Fat Augmentation, 9–14. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-58945-5_2.

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Kazak, Lawrence. "Bioenergetic Analyses in Adipose Tissue." In Thermogenic Fat, 125–34. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6820-6_12.

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Veilleux, Alain, and André Tchernof. "Sex Differences in Body Fat Distribution." In Adipose Tissue Biology, 123–66. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4614-0965-6_5.

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Mansour, Mohamed Fouad, Chon-Wai Jeremy Chan, Sofia Laforest, Alain Veilleux, and André Tchernof. "Sex Differences in Body Fat Distribution." In Adipose Tissue Biology, 257–300. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-52031-5_8.

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Zulet, María A., María J. Moreno-Aliaga, and J. Alfredo Martínez. "Dietary Determinants of Fat Mass and Body Composition." In Adipose Tissue Biology, 271–315. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4614-0965-6_9.

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Zulet, María A., María J. Moreno-Aliaga, and J. Alfredo Martínez. "Dietary Determinants of Fat Mass and Body Composition." In Adipose Tissue Biology, 319–82. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-52031-5_10.

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Reverte-Salisa, Laia, Abhishek Sanyal, and Alexander Pfeifer. "Role of cAMP and cGMP Signaling in Brown Fat." In Brown Adipose Tissue, 161–82. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/164_2018_117.

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Yoneshiro, Takeshi, Mami Matsushita, and Masayuki Saito. "Translational Aspects of Brown Fat Activation by Food-Derived Stimulants." In Brown Adipose Tissue, 359–79. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/164_2018_159.

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Chondronikola, Maria, Craig Porter, John O. Ogunbileje, and Labros S. Sidossis. "Identification and Quantification of Human Brown Adipose Tissue." In Thermogenic Fat, 159–76. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6820-6_16.

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Conference papers on the topic "Adipose tissue; Fat storage"

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Schipper, H. "SP0034 Adipose tissue inflammation: once fat was fat and that was that." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.7652.

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Ahmed, Sumaya, and Nasser Rizk. "The Expression of Bile Acid Receptor TGR5 in Adipose Tissue in Diet-Induced Obese Mice." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0212.

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Bile acids are significant physiological factors for digestion, solubilization, absorption, toxic metabolites and xenobiotics. In addition, bile acids are responsible of signal transduction as well as metabolic regulation that activate several receptors such as farnesoid X receptor (FXR) and the membrane G-protein receptor 5 (TGR5). Activation of TGR5 by bile acids is associated with prevention of obesity as well as ameliorating the resistance to insulin via increasing energy expenditure. The objective of this research is to investigate TGR5 gene expression level in different fat depots including visceral or epididymal adipose tissue (eWAT), brown adipose tissue and inguinal adipose tissue (iWAT) and to study the response of TGR5 gene expression to the antiobesity treatment (SFN). Three groups of male CD1 mice were used in this study; lean group fed with SCD, DIO mice on HFD and DIO obese mice treated with anti-obesity treatment. Body weight (BW) and phenotype data were evaluated by weekly including blood samples for analysis of glucose, insulin, leptin, triglycerides (TG). Total RNA was extracted from different fat depots and RT-PCR profiler array technology was used to in order to assess the mRNA expression of TGR5 and leptin. There was significant downregulation of TGR5 gene expression level in obese (DIO) mice and remarkable upregulation of TGR5 gene expression after successful weight loss in DIO mice treated with SFN in time dependent manner at 1 weeks and 4 weeks of ip applications. In conclusion, obesity is associated with decrease in expression of TGR5 in different fat depots and treatment with anti-obesity drug (Sulforaphane) causes stepwise upregulation of TGR5 gene expression in epididymal white adipose tissue parallel stepwise decrease in body weight. Increase of expression of TGR5 in DIO mice in eWAT is accompanied by improvement in glucose homeostasis and insulin action.

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Pivovarova, O., K. Kessler, K. Jürchott, S. Hornemann, C. Sticht, M. Kemper, N. Gretz, N. Rudovich, A. Kramer, and AFH Pfeiffer. "Effects of the diurnal distribution of carbohydrates and fat on the adipose tissue transcriptome in humans." In Diabetes Kongress 2018 – 53. Jahrestagung der DDG. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1641788.

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Troyanova-Wood, Maria, Cassidy Gobbell, Zhaokai Meng, and Vladislav V. Yakovlev. "Assessing the effect of a high-fat diet on rodents' adipose tissue using Brillouin and Raman spectroscopy." In SPIE BiOS, edited by Robert R. Alfano and Stavros G. Demos. SPIE, 2016. http://dx.doi.org/10.1117/12.2213525.

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Geerligs, M., G. W. M. Peters, C. W. J. Oomens, P. Ackermans, and F. P. T. Baaijens. "Mechanical Behaviour of the Subcutaneous Fat Layer." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176364.

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A very important function of the human subcutaneous fat layer is to act as a mechanical cushion. However, prolonged loading may result in damage such as pressure ulcers. Depending on the severity and origin of the ulcer, skin, subcutaneous fat and muscle can be affected. The aetiology of pressure ulcers is still poorly understood; it is not even clear whether wounds start to develop in skin, in the fat layer or even in deeper layers [1]. One of the tools used to better understand the way mechanical loading affects tissues is mechanical modeling. The success of a mechanical model strongly depends on the constitutive equations that are used to describe the mechanical properties obtained with experimental work. For skin and muscle much is already known, but a tremendous lack of data is found regarding the properties of adipose tissue. In the case of the subcutaneous fat tissue, very few of the mechanical properties have been determined experimentally.

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Castelo Branco Ramos Nakandakari, Susana, DENNYS ESPER CORREA CINTRA, Patrica Brito Rodrigues, Marcella Ramos Sant'ana, RAFAEL C. GASPAR, Vitor Rosetto MuÑoz, Camilla Bertuzzo Veiga, et al. "Mesenteric adipose tissue inflammatory profile of C57BL/6J mice in acute consumption of high-fat diet and flaxseed oil." In XXV Congresso de Iniciação Cientifica da Unicamp. Campinas - SP, Brazil: Galoa, 2017. http://dx.doi.org/10.19146/pibic-2017-78662.

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Tsuji, T., AM Houghton, AS Leme, and SD Shapiro. "Cigarette Smoke Exposure Leads to Adipose Tissue Inflammation with MMP-12-Mediated Inhibition of Angiogenesis and Fat Wasting in Mice." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5882.

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Ong, Henry H., Corey D. Webb, Marnie L. Gruen, Alyssa H. Hasty, John C. Gore, and E. B. Welch. "Fat-water MRI is sensitive to local adipose tissue inflammatory changes in a diet-induced obesity mouse model at 15T." In SPIE Medical Imaging, edited by Barjor Gimi and Robert C. Molthen. SPIE, 2015. http://dx.doi.org/10.1117/12.2082333.

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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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Khadge, Saraswoti, Geoffrey M. Thiele, John Graham Sharp, Lynell W. Klassen, Timothy R. McGuire, Michael J. Duryee, Holly C. Britton, et al. "Abstract 245: Dietary long-chain omega-3 fatty acids reduce adipose inflammation in mammary tissue of mice fed moderate fat-isocaloric diets." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-245.

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