Forgot your password?
New user?
New Window Opens on the Secret Life of Microbes: Scientists Develop First Microbial Profiles of Ecosystems
CAS announces the release of SciFinder Scholar for Mac OS X
Press Releases
Press Releases
| Check out our New Publishers' Select for Free Articles |
BBA - Molecular and Cell Biology of Lipids (v.1831, #5)
White and brown adipose stem cells: From signaling to clinical implications by Carolyn Algire; Dasa Medrikova; Stephan Herzig (pp. 896-904).
Epidemiological studies estimate that by the year 2030, 2.16billion people worldwide will be overweight and 1.12billion will be obese [1]. Besides its now established function as an endocrine organ, adipose tissue plays a fundamental role as an energy storage compartment. As such, adipose tissue is capable of extensive expansion or retraction depending on the energy balance or disease state of the host, a plasticity that is unparalleled in other organs and – under conditions of excessive energy intake – significantly contributes to the afore mentioned obesity pandemic. Expansion of adipose tissue is driven by both hypertrophy and hyperplasia of adipocytes, which can renew frequently to compensate for cell death. This underlines the importance of adipocyte progenitor cells within the distinct adipose tissue depots to control both energy storage and endocrine functions of adipose tissue. Here we summarize recent findings on the identity and plasticity of adipose stem cells, the involved signaling cascades, and potential clinical implications of these cells for the treatment of metabolic dysfunction in obesity. This article is part of a Special Issue entitled Brown and White Fat: From Signaling to Disease.► Adipocyte progenitors derive from pluripotent mesenchymal stem cells. ► Brown and white adipocytes develop from distinct cell lineages. ► Inducible brown adipocytes arise from progenitor differentiation or white adipocyte trans-differentiation. ► Recruitment of brown adipose tissue in humans may provide a novel approach to anti-obesity therapies.
Keywords: Adipose tissue; Progenitor cell; Obesity; Signaling
In vitro brown and “brite”/“beige” adipogenesis: Human cellular models and molecular aspects by Guillaume E. Beranger; Michael Karbiener; Valentin Barquissau; Didier F. Pisani; Marcel Scheideler; Dominique Langin; Ez-Zoubir Amri (pp. 905-914).
Brown adipose tissue (BAT) has long been thought to be absent or very scarce in human adults so that its contribution to energy expenditure was not considered as relevant. The recent discovery of thermogenic BAT in human adults opened the field for innovative strategies to combat overweight/obesity and associated diseases. This energy-dissipating function of BAT is responsible for adaptive thermogenesis in response to cold stimulation. In this context, adipocytes can be converted, within white adipose tissue (WAT), into multilocular adipocytes expressing UCP1, a mitochondrial protein that plays a key role in heat production by uncoupling the activity of the respiratory chain from ATP synthesis. These adipocytes have been named “brite” or “beige” adipocytes. Whereas BAT has been studied for a long time in murine models both in vivo and in vitro, there is now a strong demand for human cellular models to validate and/or identify critical factors involved in the induction of a thermogenic program within adipocytes. In this review we will discuss the different human cellular models described in the literature and what is known regarding the regulation of their differentiation and/or activation process. In addition, the role of microRNAs as novel regulators of brown/“brite” adipocyte differentiation and conversion will be depicted. Finally, investigation of both the conversion and the metabolism of white-to-brown converted adipocytes is required for the development of therapeutic strategies targeting overweight/obesity and associated diseases. This article is part of a Special Issue entitled Brown and White Fat: From Signaling to Disease.► Human adults possess thermogenic BAT whose activation can lead to weight loss. ► White adipocytes can be converted into “brite” (brown-in-white) adipocytes. ► Human cell models are needed to decipher the molecular events of brite formation. ► miRNAs are novel regulators of adipogenesis towards white, brite/brown adipocytes.
Keywords: Brite; White and brown adipocyte; Gene expression; Adipogenesis; MicroRNA
Bone morphogenic proteins signaling in adipogenesis and energy homeostasis by Salvatore Modica; Christian Wolfrum (pp. 915-923).
A great deal is known about the molecular mechanisms regulating terminal differentiation of pre-adipocytes into mature adipocytes. In contrast, the knowledge about pathways that trigger commitment of mesenchymal stem cells into the adipocyte lineage is fragmented. In recent years, the role of members of the bone morphogenic protein family in regulating the early steps of adipogenesis has been the focus of research. Findings based on these studies have also highlighted an unexpected role for some bone morphogenic protein in energy homeostasis via regulation of adipocyte development and function. This review summarizes the knowledge about bone morphogenic proteins and their role in adipocyte commitment and regulation of whole body energy homeostasis. This article is part of a Special Issue entitled Brown and White Fat: From Signaling to Disease.► BMPs serve as regulators of stem cell commitment. ► BMPs regulate mature brown and white adipose tissue function. ► BMPs control energy homeostasis by central regulation of energy homeostasis.
Keywords: Abbreviations; WAT; white adipose tissue; BAT; brown adipose tissue; MSC; mesenchymal stem cell; UCP1; uncoupling protein 1; PRDM16; PR domain containing 16; PPARγ; peroxisome proliferator-activated receptor gamma; BMP; bone morphogenic protein; PGC1; peroxisome proliferator-activated receptor gamma coactivator 1; CtBP; C-terminal-binding protein; SMAD; small mother against decapentaplegic; TGF-β; tumor growth factor-β; ALK; activin receptor-like kinase; BMPR; bone morphogenic receptor; ActR; activin receptor; GDF; grown/differentiation factor; FGF; fibroblast growth factor; WNT; wingless; Rb; retinoblastoma; Pref-1; pre-adipocyte factor-1; C/EBP; CCAAT/enhancer binding protein; RIP140; receptor-interacting protein 140; PG; prostaglandin; HSL; hormone sensitive lipase; CNS; central nervous system; SNS; sympathetic nervous system; VMH; ventromedial hypothalamus; hPSCs; human pluripotent stem cellsBone morphogenic proteins; Mesenchymal stem cells; Adipogenesis; Brown adipocyte; White adipocyte; Energy homeostasis
Dynamic changes in lipid droplet-associated proteins in the “browning” of white adipose tissues by David Barneda; Andrea Frontini; Saverio Cinti; Mark Christian (pp. 924-933).
The morphological and functional differences between lipid droplets (LDs) in brown (BAT) and white (WAT) adipose tissues will largely be determined by their associated proteins. Analysing mRNA expression in mice fat depots we have found that most LD protein genes are expressed at higher levels in BAT, with the greatest differences observed for Cidea and Plin5. Prolonged cold exposure, which induces the appearance of brown-like adipocytes in mice WAT depots, was accompanied with the potentiation of the lipolytic machinery, with changes in ATGL, CGI-58 and G0S2 gene expression. However the major change detected in WAT was the enhancement of Cidea mRNA. Together with the increase in Cidec, it indicates that LD enlargement through LD–LD transference of fat is an important process during WAT browning. To study the dynamics of this phenotypic change, we have applied 4D confocal microscopy in differentiated 3T3-L1 cells under sustained β-adrenergic stimulation. Under these conditions the cells experienced a LD remodelling cycle, with progressive reduction on the LD size by lipolysis, followed by the formation of new LDs, which were subjected to an enlargement process, likely to be CIDE-triggered, until the cell returned to the basal state. This transformation would be triggered by the activation of a thermogenic futile cycle of lipolysis/lipogenesis and could facilitate the molecular mechanism for the unilocular to multilocular transformation during WAT browning. This article is part of a Special Issue entitled Brown and White Fat: From Signaling to Disease.Display Omitted► Lipid droplet proteins are more highly expressed in BAT than WAT. ► Cold acclimatization induces Cidea, Gyk and pro-lipolytic proteins in WAT. ► β-adrenergic induction of lipid droplet formation and growth by lipid transfer ► Thermogenic potential of the futile cycle of TAG hydrolysis and re-synthesis ► Role of lipid droplet remodelling in unilocular to multilocular adipocyte transition
Keywords: Abbreviations; LD; lipid droplet; BAT; brown adipose tissue; scWAT; subcutaneous white adipose tissue; gonWAT; periovarian white adipose tissue; mesWAT; mesenteric white adipose tissue; FAs; fatty acids; TAG; triacylglycerol; IBMX; isobutylmethylxanthine; PKA; protein kinase A; NLSD-I; neutral lipid storage disease with ichthyosis; ER; endoplasmic reticulum; ROS; reactive oxygen speciesLipid droplets; Adipose tissue; Thermogenesis; Transdifferentiation; Lipolysis; CIDEA
Effects of adipocyte lipoprotein lipase on de novo lipogenesis and white adipose tissue browning by Alexander Bartelt; Clara Weigelt; M. Lisa Cherradi; Andreas Niemeier; Todter Klaus Tödter; Joerg Heeren; Ludger Scheja (pp. 934-942).
Efficient storage of dietary and endogenous fatty acids is a prerequisite for a healthy adipose tissue function. Lipoprotein lipase (LPL) is the master regulator of fatty acid uptake from triglyceride-rich lipoproteins. In addition to LPL-mediated fatty acid uptake, adipocytes are able to synthesize fatty acids from non-lipid precursor, a process called de novo lipogenesis (DNL). As the physiological relevance of fatty acid uptake versus DNL for brown and white adipocyte function remains unclear, we studied the role of adipocyte LPL using adipocyte-specific LPL knockout animals (aLKO). ALKO mice displayed a profound increase in DNL-fatty acids, especially palmitoleate and myristoleate in brown adipose tissue (BAT) and white adipose tissue (WAT) depots while essential dietary fatty acids were markedly decreased. Consequently, we found increased expression in adipose tissues of genes encoding DNL enzymes ( Fasn, Scd1, and Elovl6) as well as the lipogenic transcription factor carbohydrate response element binding protein-β. In a high-fat diet (HFD) study aLKO mice were characterized by reduced adiposity and improved plasma insulin and adipokines. However, neither glucose tolerance nor inflammatory markers were ameliorated in aLKO mice compared to controls. No signs of increased BAT activation or WAT browning were detected in aLKO mice either on HFD or after 1week of β3-adrenergic stimulation using CL316,243. We conclude that despite a profound increase in DNL-derived fatty acids, proposed to be metabolically favorable, aLKO mice are not protected from metabolic disease per se. In addition, induction of DNL alone is not sufficient to promote browning of WAT. This article is part of a Special Issue entitled Brown and White Fat: From Signaling to Disease.► In a new model lacking lipoprotein lipase (LPL) selectively in adipocytes, ► the absence of LPL leads to increased de novo lipogenesis in adipose tissue, ► the production of the anti-inflammatory fatty acid palmitoleate and ► mild metabolic improvements which are independent of white adipose tissue browning.
Keywords: Abbreviations; Acaca; acetyl CoA carboxylase-α; aLKO; adipocyte LPL knockout; BAT; brown adipose tissue; Dio2; type 2 thyroid hormone deiodinase; ChREBP; carbohydrate response element binding protein; COX-2; cyclooxygenase-2; DNL; de novo; lipogenesis; Elovl; fatty acid elongase; Fasn; fatty acid synthase; FPLC; fast performance liquid chromatography; Glut4; glucose transporter 4; LPL; lipoprotein lipase; GPIHBP1; glycosylphosphatidylinositol-anchored high-density lipoprotein-binding protein 1; HFD; high-fat diet; Pgc1a; peroxisome proliferator activator receptors gamma coactivator-1-α; PUFA; polyunsaturated fatty acids; Scd1; stearoyl CoA desaturase-1; SEM; standard error of mean; SREBP1c; sterol regulatory element binding protein 1c; Tbp; TATA box binding protein; TG; triglycerides; TRL; triglyceride-rich lipoproteins; WT; wild type; WAT; white adipose tissue; iWAT; inguinal WAT; gWAT; gonadal WAT; Ucp1; uncoupling protein 1Lipoprotein lipase; Fatty acid; De novo; lipogenesis; Brown adipose tissue; Obesity; Insulin resistance
UCP1 mRNA does not produce heat by Jan Nedergaard; Barbara Cannon (pp. 943-949).
Because of the possible role of brown adipose tissue and UCP1 in metabolic regulation, even in adult humans, there is presently considerable interest in quantifying, from in-vitro data, the thermogenic capacities of brown and brite/beige adipose tissues. An important issue is therefore to establish which parameters are the most adequate for this. A particularly important issue is the relevance of UCP1 mRNA levels as estimates of the degree of recruitment and of the thermogenic capacity resulting from differences in physiological conditions and from experimental manipulations. By solely following UCP1 mRNA levels in brown adipose tissue, the conclusion would be made that the tissue's highest activation occurs after only 6h in the cold and then successively decreases to being only some 50% elevated after 1month in the cold. However, measurement of total UCP1 protein levels per depot ("mouse") reveals that the maximal thermogenic capacity estimated in this way is reached first after 1month but represents an approx. 10-fold increase in thermogenic capacity. Since this in-vitro measure correlates quantitatively and temporally with the acquisition of nonshivering thermogenesis, this must be considered the most physiologically relevant parameter. Similarly, observations that cold acclimation barely increases UCP1 mRNA levels in classical brown adipose tissue but leads to a 200-fold increase in UCP1 mRNA levels in brite/beige adipose tissue depots may overemphasise the physiological significance of these depots, as the high fold-increases are due to very low initial levels, and the UCP1 mRNA levels reached are at least an order of magnitude lower than in brown adipose tissue; furthermore, based on total UCP1 protein amounts, the brite/beige depots attain only about 10% of the thermogenic capacity of the classical brown adipose tissue depots. Consequently, inadequate conclusions may be reached if UCP1 mRNA levels are used as a proxy for the metabolic significance of recruited versus non-recruited brown adipose tissue and for estimating the metabolic significance of brown versus brite/beige adipose tissues. This article is part of a Special Issue entitled Brown and White Fat: From Signaling to Disease.Display Omitted► We discuss molecular and biochemical parameters of recruitment of brown and brite fat. ► UCP1 mRNA levels yield confounding indications of the degree of recruitment. ► Similarly, specific UCP1 protein levels (i.e. per mg protein) are not adequates. ► Only total UCP1 protein per depot/animal correlates with thermogenic capacity. ► Relative UCP1 mRNA increases in brite fat are extremely high but thermogenic capacity comparatively low.
Keywords: Brown adipose tissue; Brite adipose tissue; Beige adipose tissue; White adipose tissue; UCP1; Nonshivering thermogenesis; Diet-induced thermogenesis
White-to-brown transdifferentiation of omental adipocytes in patients affected by pheochromocytoma by Andrea Frontini; Alessandra Vitali; Jessica Perugini; Incoronata Murano; Chiara Romiti; Daniel Ricquier; Mario Guerrieri; Saverio Cinti (pp. 950-959).
In all mammals, white adipose tissue (WAT) and brown adipose tissue (BAT) are found together in several fat depots, forming a multi-depot organ. Adrenergic stimulation induces an increase in BAT usually referred to as “browning”. This phenomenon is important because of its potential use in curbing obesity and related disorders; thus, understanding its cellular mechanisms in humans may be useful for the development of new therapeutic strategies. Data in rodents have supported the direct transformation of white into brown adipocytes. Biopsies of pure white omental fat were collected from 12 patients affected by the catecholamine-secreting tumor pheochromocytoma (pheo-patients) and compared with biopsies from controls. Half of the omental fat samples from pheo-patients contained uncoupling protein 1 (UCP1)-immunoreactive-(ir) multilocular cells that were often arranged in a BAT-like pattern endowed with noradrenergic fibers and dense capillary network. Many UCP1-ir adipocytes showed the characteristic morphology of paucilocular cells, which we have been described as cytological marker of transdifferentiation. Electron microscopy showed increased mitochondrial density in multi- and paucilocular cells and disclosed the presence of perivascular brown adipocyte precursors. Brown fat genes, such as UCP1, PR domain containing 16 (PRDM16) and β3-adrenoreceptor, were highly expressed in the omentum of pheo-patients and in those cases without visible morphologic re-arrangement. Of note, the brown determinant PRDM16 was detected by immunohistochemistry only in nuclei of multi- and paucilocular adipocytes. Quantitative electron microscopy and immunohistochemistry for Ki67 suggest an unlikely contribution of proliferative events to the phenomenon. The data support the idea that, in adult humans, white adipocytes of pure white fat that are subjected to adrenergic stimulation are able to undergo a process of direct transformation into brown adipocytes. This article is part of a Special Issue entitled Brown and White Fat: From Signaling to Disease.► The omental fat of pheochromocytoma patients is subjected to a phenotypic switch toward BAT. ► PRDM16 is expressed by paucilocular adipocytes. ► Proliferation is a secondary, if present, contribution to tissue remodeling. ► White-to-brown adipocyte transdifferentiation seems to be the major phenomenon underlining the phenotypic change.
Keywords: Human; Pheochromocytoma; White adipose tissue; Brown adipose tissue; Browning; Morphology
Browning attenuates murine white adipose tissue expansion during postnatal development by D. Lasar; A. Julius; T. Fromme; M. Klingenspor (pp. 960-968).
During postnatal development of mice distinct white adipose tissue depots display a transient appearance of brown-like adipocytes. These brite (brown in white) adipocytes share characteristics with classical brown adipocytes including a multilocular appearance and the expression of the thermogenic protein uncoupling protein 1. In this study, we compared two inbred mouse strains 129S6sv/ev and C57BL6/N known for their different propensity to diet-induced obesity. We observed transient browning in retroperitoneal and inguinal adipose tissue depots of these two strains. From postnatal day 10 to 20 the increase in the abundance of multilocular adipocytes and uncoupling protein 1 expression was higher in 129S6sv/ev than in C57BL6/N pups. The parallel increase in the mass of the two fat depots was attenuated during this browning period. Conversely, epididymal white and interscapular brown adipose tissue displayed a steady increase in mass during the first 30days of life. In this period, 129S6sv/ev mice developed a significantly higher total body fat mass than C57BL6/N. Thus, while on a local depot level a high number of brite cells is associated with the attenuation of adipose tissue expansion the strain comparison reveals no support for a systemic impact on energy balance. This article is part of a Special Issue entitled Brown and White Fat: From Signaling to Disease.► Mouse adipose tissue depots undergo a postnatal browning phenomenon. ► The magnitude of this phenomenon is mouse strain specific. ► A mouse strain with more pronounced browning displays less body and fat mass gain. ► During the recruitment of brown adipocytes, fat depot growth is attenuated.
Keywords: Postnatal development; Strain difference; Brite cell recruitment; Retroperitoneal white adipose tissue; Brite cell
Pharmacological and nutritional agents promoting browning of white adipose tissue by M. Luisa Bonet; Paula Oliver; Andreu Palou (pp. 969-985).
The role of brown adipose tissue in the regulation of energy balance and maintenance of body weight is well known in rodents. Recently, interest in this tissue has re-emerged due to the realization of active brown-like adipose tissue in adult humans and inducible brown-like adipocytes in white adipose tissue depots in response to appropriate stimuli (“browning process”). Brown-like adipocytes that appear in white fat depots have been called “brite” (from brown-in-white) or “beige” adipocytes and have characteristics similar to brown adipocytes, in particular the capacity for uncoupled respiration. There is controversy as to the origin of these brite/beige adipocytes, but regardless of this, induction of the browning of white fat represents an attractive potential strategy for the management and treatment of obesity and related complications. Here, the different physiological, pharmacological and dietary determinants that have been linked to white-to-brown fat remodeling and the molecular mechanisms involved are reviewed in detail. In the light of available data, interesting therapeutic perspectives can be expected from the use of specific drugs or food compounds able to induce a program of brown fat differentiation including uncoupling protein 1 expression and enhancing oxidative metabolism in white adipose cells. However, additional research is needed, mainly focused on the physiological relevance of browning and its dietary control, where the use of ferrets and other non-rodent animal models with a more similar adipose tissue organization and metabolism to humans could be of much help. This article is part of a Special Issue entitled Brown and White Fat: From Signaling to Disease.► Brown fat has a clear therapeutic potential for obesity management. ► Browning implies the acquisition of brown-fat properties in white adipose tissue. ► White adipose tissue browning has been related to decreased adiposity in animal models. ► Specific drugs and food compounds are able to induce white adipose tissue browning. ► The physiological relevance of browning in humans needs further investigation.
Keywords: Brown adipose tissue; White adipose tissue browning; Brite/beige adipocytes; Thermogenesis; Obesity
Stimulation of mitochondrial oxidative capacity in white fat independent of UCP1: A key to lean phenotype by Pavel Flachs; Martin Rossmeisl; Ondrej Kuda; Jan Kopecky (pp. 986-1003).
We are facing a revival of the strategy to counteract obesity and associated metabolic disorders by inducing thermogenesis mediated by mitochondrial uncoupling protein-1 (UCP1). Thus, the main focus is on the adaptive non-shivering thermogenesis occurring both in the typical depots of brown adipose tissue (BAT) and in UCP1-containing cells that could be induced in white adipose tissue (WAT). Because contribution of WAT to resting metabolic rate is relatively small, the possibility to reduce adiposity by enhancing energy expenditure in classical white adipocytes is largely neglected. However, several pieces of evidence support a notion that induction of energy expenditure based on oxidation of fatty acids (FA) in WAT may be beneficial for health, namely: (i) studies in both humans and rodents document negative association between oxidative capacity of mitochondria in WAT and obesity; (ii) pharmacological activation of AMPK in rats as well as cold-acclimation of UCP1-ablated mice results in obesity resistance associated with increased oxidative capacity in WAT; and (iii) combined intervention using long-chain n-3 polyunsaturated FA (omega 3) and mild calorie restriction exerted synergism in the prevention of obesity in mice fed a high-fat diet; this was associated with strong hypolipidemic and insulin-sensitizing effects, as well as prevention of inflammation, and synergistic induction of mitochondrial oxidative phosphorylation (OXPHOS) and FA oxidation, specifically in epididymal WAT. Importantly, these changes occurred without induction of UCP1 and suggested the involvement of: (i) futile substrate cycle in white adipocytes, which is based on lipolysis of intracellular triacylglycerols and re-esterification of FA, in association with the induction of mitochondrial OXPHOS capacity, β-oxidation, and energy expenditure; (ii) endogenous lipid mediators (namely endocannabinoids, eicosanoids, prostanoids, resolvins, and protectins) and their cognate receptors; and (iii) AMP-activated protein kinase in WAT. Quantitatively, the strong induction of FA oxidation in WAT in response to the combined intervention is similar to that observed in the transgenic mice rendered resistant to obesity by ectopic expression of UCP1 in WAT. The induction of UCP1-independent FA oxidation and energy expenditure in WAT in response to the above physiological stimuli could underlie the amelioration of obesity and low-grade WAT inflammation, and it could reduce the release of FA from adipose tissue and counteract harmful consequences of lipid accumulation in other tissues. In this respect, new combination treatments may be designed using naturally occurring micronutrients (e.g. omega 3), reduced calorie intake or pharmaceuticals, exerting synergism in the induction of the mitochondrial OXPHOS capacity and stimulation of lipid catabolism in white adipocytes, and improving metabolic flexibility of WAT. The role of mutual interactions between adipocytes and immune cells contained in WAT in tissue metabolism should be better characterised. This article is part of a Special Issue entitled Brown and White Fat: From Signaling to Disease.► Mitochondrial oxidative capacity in white fat correlates negatively with adiposity. ► Energy is required for futile fatty acid cycling (TAG/FA cycle) in adipocytes. ► Stimulation of TAG/FA cycle is associated with the induction of β-oxidation in adipocytes. ► TAG/FA-mediated energy expenditure (EE) may reduce adiposity and lipotoxicity. ► Physiological interventions may induce UCP1-independent EE in white fat.
Keywords: Abbreviations; ACC; acetyl-CoA carboxylase; AMPK; AMP-activated protein kinase; aP2-; Ucp1; mice; transgenic mice expressing UCP1 gene from the aP2 gene promoter; AA; arachidonic acid; ATM; adipose tissue macrophages; BAT; brown adipose tissue; BCAA; branched-chain amino acids; CB1; cannabinoid type-1 receptor; CR; calorie restriction; CTRP3; adiponectin paralog C1q/TNF-related protein 3; DHA; docosahexaenoic acid; EPA; eicosapentaenoic acid; FAT/CD36; fatty acid translocase/CD36; FA; fatty acids; FAS; fatty acid synthase; FGF-21; fibroblast growth factor-21; HF; high-fat; HSL; hormone-sensitive lipase; LPS; lipopolysaccharide; omega 3; long-chain; n; -3 polyunsaturated fatty acids; mtDNA; mitochondrial DNA; MCP-1; monocyte chemoattractant protein-1; OXPHOS; oxidative phosphorylation; PC; pyruvate carboxylase; PDK4; pyruvate dehydrogenase kinase 4; PEPCK; phosphoenolpyruvate carboxykinase; PD1; protectin D1; PGC-1; the PPARγ coactivator 1; PPAR; peroxisome proliferator-activated receptor; SIRT1; NAD; +; -dependent deacetylase sirtuin 1; SREBP-1c; sterol regulatory element-binding protein-1c; TAG; triacylglycerols; TAG/FA cycle; futile substrate cycle based on lipolysis of intracellular triacylglycerols and re-esterification of fatty acids; TZD; thiazolidinedione; UCP1; mitochondrial uncoupling protein 1; WAT; white adipose tissue; 15d-PGJ2; 15-deoxy-Δ12,14-prostaglandin J2Fatty acid re-esterification; Futile substrate cycle; PPARγ; Adipose tissue; Lipid mediator; Obesity
Brown adipose tissue functions in humans by Kirsi A. Virtanen; Wouter D. van Marken Lichtenbelt; Pirjo Nuutila (pp. 1004-1008).
Human adults have functionally active BAT. The metabolic function can be reliably measured in vivo using modern imaging modalities (namely PET/CT). Cold seems to be one of the most potent stimulators of BAT metabolic activity but other stimulators (for example insulin) are actively studied. Obesity is related to lower metabolic activity of BAT but it may be reversed after successful weight reduction such as after bariatric surgery. This article is part of a Special Issue entitled Brown and White Fat: From Signaling to Disease.► Function of BAT can be measured using PET technique. ► Functional activity of BAT is increased during stimulation, e.g. during cold exposure. ► BAT is an insulin-sensitive tissue type. ► Intracellular lipid storage is the primary energy source in BAT during stimulation. ► In obesity metabolic balance and BAT functional activity seem to be related.
Keywords: Brown adipose tissue; PET; Cold; Insulin; Human