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Unknown actor in adipose tissue metabolism hiding in plain sight.
Collins S
(2019) Proc Natl Acad Sci U S A 116: 17145-17146
MeSH Terms: Adipose Tissue, Thermogenesis
Added July 22, 2020
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1 Members
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MeSH Terms
HDAC11 suppresses the thermogenic program of adipose tissue via BRD2.
Bagchi RA, Ferguson BS, Stratton MS, Hu T, Cavasin MA, Sun L, Lin YH, Liu D, Londono P, Song K, Pino MF, Sparks LM, Smith SR, Scherer PE, Collins S, Seto E, McKinsey TA
(2018) JCI Insight 3:
MeSH Terms: Adipose Tissue, Brown, Adipose Tissue, White, Adult, Aged, Aged, 80 and over, Animals, Diet, High-Fat, Disease Models, Animal, Energy Metabolism, Epigenesis, Genetic, Fatty Liver, Female, Gene Expression Regulation, Histone Deacetylases, Humans, Insulin Resistance, Male, Mice, Mice, Knockout, Middle Aged, Obesity, Thermogenesis, Transcription Factors
Show Abstract · Added July 22, 2020
Little is known about the biological function of histone deacetylase 11 (HDAC11), which is the lone class IV HDAC. Here, we demonstrate that deletion of HDAC11 in mice stimulates brown adipose tissue (BAT) formation and beiging of white adipose tissue (WAT). Consequently, HDAC11-deficient mice exhibit enhanced thermogenic potential and, in response to high-fat feeding, attenuated obesity, improved insulin sensitivity, and reduced hepatic steatosis. Ex vivo and cell-based assays revealed that HDAC11 catalytic activity suppresses the BAT transcriptional program, in both the basal state and in response to β-adrenergic receptor signaling, through a mechanism that is dependent on physical association with BRD2, a bromodomain and extraterminal (BET) acetyl-histone-binding protein. These findings define an epigenetic pathway for the regulation of energy homeostasis and suggest the potential for HDAC11-selective inhibitors for the treatment of obesity and diabetes.
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CalR: A Web-Based Analysis Tool for Indirect Calorimetry Experiments.
Mina AI, LeClair RA, LeClair KB, Cohen DE, Lantier L, Banks AS
(2018) Cell Metab 28: 656-666.e1
MeSH Terms: Analysis of Variance, Animals, Calorimetry, Indirect, Cloud Computing, Data Visualization, Energy Metabolism, Humans, Linear Models, Mice, Obesity, Pulmonary Gas Exchange, Reproducibility of Results, Thermogenesis, Web Browser, Weight Loss, Workflow
Show Abstract · Added May 16, 2019
We report a web-based tool for analysis of experiments using indirect calorimetry to measure physiological energy balance. CalR simplifies the process to import raw data files, generate plots, and determine the most appropriate statistical tests for interpretation. Analysis using the generalized linear model (which includes ANOVA and ANCOVA) allows for flexibility in interpreting diverse experimental designs, including those of obesity and thermogenesis. Users also may produce standardized output files for an experiment that can be shared and subsequently re-evaluated using CalR. This framework will provide the transparency necessary to enhance consistency, rigor, and reproducibility. The CalR analysis software will greatly increase the speed and efficiency with which metabolic experiments can be organized, analyzed per accepted norms, and reproduced and will likely become a standard tool for the field. CalR is accessible at https://CalRapp.org/.
Copyright © 2018 Elsevier Inc. All rights reserved.
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16 MeSH Terms
Second messenger signaling mechanisms of the brown adipocyte thermogenic program: an integrative perspective.
Shi F, Collins S
(2017) Horm Mol Biol Clin Investig 31:
MeSH Terms: Adipocytes, Beige, Adipocytes, Brown, Animals, Cyclic AMP-Dependent Protein Kinases, Cyclic GMP-Dependent Protein Kinases, Energy Metabolism, Gene Expression Regulation, Humans, Intracellular Space, Mechanistic Target of Rapamycin Complex 1, MicroRNAs, Natriuretic Agents, RNA, Long Noncoding, Receptors, Adrenergic, beta, Second Messenger Systems, Signal Transduction, Thermogenesis, Uncoupling Protein 1
Show Abstract · Added September 26, 2018
β-adrenergic receptors (βARs) are well established for conveying the signal from catecholamines to adipocytes. Acting through the second messenger cyclic adenosine monophosphate (cAMP) they stimulate lipolysis and also increase the activity of brown adipocytes and the 'browning' of adipocytes within white fat depots (so-called 'brite' or 'beige' adipocytes). Brown adipose tissue mitochondria are enriched with uncoupling protein 1 (UCP1), which is a regulated proton channel that allows the dissipation of chemical energy in the form of heat. The discovery of functional brown adipocytes in humans and inducible brown-like ('beige' or 'brite') adipocytes in rodents have suggested that recruitment and activation of these thermogenic adipocytes could be a promising strategy to increase energy expenditure for obesity therapy. More recently, the cardiac natriuretic peptides and their second messenger cyclic guanosine monophosphate (cGMP) have gained attention as a parallel signaling pathway in adipocytes, with some unique features. In this review, we begin with some important historical work that touches upon the regulation of brown adipocyte development and physiology. We then provide a synopsis of some recent advances in the signaling cascades from β-adrenergic agonists and natriuretic peptides to drive thermogenic gene expression in the adipocytes and how these two pathways converge at a number of unexpected points. Finally, moving from the physiologic hormonal signaling, we discuss yet another level of control downstream of these signals: the growing appreciation of the emerging roles of non-coding RNAs as important regulators of brown adipocyte formation and function. In this review, we discuss new developments in our understanding of the signaling mechanisms and factors including new secreted proteins and novel non-coding RNAs that control the function as well as the plasticity of the brown/beige adipose tissue as it responds to the energy needs and environmental conditions of the organism.
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Characterizing active and inactive brown adipose tissue in adult humans using PET-CT and MR imaging.
Gifford A, Towse TF, Walker RC, Avison MJ, Welch EB
(2016) Am J Physiol Endocrinol Metab 311: E95-E104
MeSH Terms: Adipose Tissue, Brown, Adult, Cold Temperature, Female, Fluorodeoxyglucose F18, Humans, Image Processing, Computer-Assisted, Magnetic Resonance Imaging, Male, Positron Emission Tomography Computed Tomography, Radiopharmaceuticals, Thermogenesis, Thoracic Wall, Young Adult
Show Abstract · Added May 24, 2016
Activated brown adipose tissue (BAT) plays an important role in thermogenesis and whole body metabolism in mammals. Positron emission tomography (PET)-computed tomography (CT) imaging has identified depots of BAT in adult humans, igniting scientific interest. The purpose of this study is to characterize both active and inactive supraclavicular BAT in adults and compare the values to those of subcutaneous white adipose tissue (WAT). We obtained [(18)F]fluorodeoxyglucose ([(18)F]FDG) PET-CT and magnetic resonance imaging (MRI) scans of 25 healthy adults. Unlike [(18)F]FDG PET, which can detect only active BAT, MRI is capable of detecting both active and inactive BAT. The MRI-derived fat signal fraction (FSF) of active BAT was significantly lower than that of inactive BAT (means ± SD; 60.2 ± 7.6 vs. 62.4 ± 6.8%, respectively). This change in tissue morphology was also reflected as a significant increase in Hounsfield units (HU; -69.4 ± 11.5 vs. -74.5 ± 9.7 HU, respectively). Additionally, the CT HU, MRI FSF, and MRI R2* values are significantly different between BAT and WAT, regardless of the activation status of BAT. To the best of our knowledge, this is the first study to quantify PET-CT and MRI FSF measurements and utilize a semiautomated algorithm to identify inactive and active BAT in the same adult subjects. Our findings support the use of these metrics to characterize and distinguish between BAT and WAT and lay the foundation for future MRI analysis with the hope that some day MRI-based delineation of BAT can stand on its own.
1 Communities
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14 MeSH Terms
Sustained Brown Fat Stimulation and Insulin Sensitization by a Humanized Bispecific Antibody Agonist for Fibroblast Growth Factor Receptor 1/βKlotho Complex.
Kolumam G, Chen MZ, Tong R, Zavala-Solorio J, Kates L, van Bruggen N, Ross J, Wyatt SK, Gandham VD, Carano RA, Dunshee DR, Wu AL, Haley B, Anderson K, Warming S, Rairdan XY, Lewin-Koh N, Zhang Y, Gutierrez J, Baruch A, Gelzleichter TR, Stevens D, Rajan S, Bainbridge TW, Vernes JM, Meng YG, Ziai J, Soriano RH, Brauer MJ, Chen Y, Stawicki S, Kim HS, Comps-Agrar L, Luis E, Spiess C, Wu Y, Ernst JA, McGuinness OP, Peterson AS, Sonoda J
(2015) EBioMedicine 2: 730-43
MeSH Terms: Adiponectin, Adipose Tissue, Brown, Animals, Antibodies, Bispecific, Cell Line, Energy Metabolism, Fibroblast Growth Factors, HEK293 Cells, Humans, Insulin, Macaca fascicularis, Male, Membrane Proteins, Mice, Inbred BALB C, Mice, Inbred C57BL, Mice, Obese, Protein Binding, Receptor, Fibroblast Growth Factor, Type 1, Thermogenesis, Weight Loss
Show Abstract · Added September 10, 2015
Dissipating excess calories as heat through therapeutic stimulation of brown adipose tissues (BAT) has been proposed as a potential treatment for obesity-linked disorders. Here, we describe the generation of a humanized effector-less bispecific antibody that activates fibroblast growth factor receptor (FGFR) 1/βKlotho complex, a common receptor for FGF21 and FGF19. Using this molecule, we show that antibody-mediated activation of FGFR1/βKlotho complex in mice induces sustained energy expenditure in BAT, browning of white adipose tissue, weight loss, and improvements in obesity-associated metabolic derangements including insulin resistance, hyperglycemia, dyslipidemia and hepatosteatosis. In mice and cynomolgus monkeys, FGFR1/βKlotho activation increased serum high-molecular-weight adiponectin, which appears to contribute over time by enhancing the amplitude of the metabolic benefits. At the same time, insulin sensitization by FGFR1/βKlotho activation occurs even before the onset of weight loss in a manner that is independent of adiponectin. Together, selective activation of FGFR1/βKlotho complex with a long acting therapeutic antibody represents an attractive approach for the treatment of type 2 diabetes and other obesity-linked disorders through enhanced energy expenditure, insulin sensitization and induction of high-molecular-weight adiponectin.
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20 MeSH Terms
A heart-adipose tissue connection in the regulation of energy metabolism.
Collins S
(2014) Nat Rev Endocrinol 10: 157-63
MeSH Terms: Adipocytes, Adipose Tissue, Energy Metabolism, Humans, Myocardium, Natriuretic Peptides, Obesity, Sympathetic Nervous System, Thermogenesis
Show Abstract · Added July 22, 2020
Almost 20 years ago, the protein encoded by the ob locus in mice was identified as an adipocyte-secreted hormone, now termed leptin, which functions as a peripheral signal to communicate the organism's energy reserve--and thereby protects against starvation due to insufficient caloric resources. Additional peripheral factors have since been identified that coordinate interorgan crosstalk to manage energy resources. The heart is included in this network through its regulated release of natriuretic peptides A and B--cardiac hormones originally identified as important in blood pressure control. Emerging evidence that natriuretic peptide receptors are expressed in adipose tissue, and that circulating levels of these peptides are decreased in animals and humans with obesity, could imply that natriuretic peptides are also involved in the regulation of energy metabolism. The natriuretic peptides stimulate triglyceride lipolysis in adipocytes, a process also regulated by the sympathetic nervous system. In addition, these two pathways promote uncoupling of mitochondrial respiration and thermogenesis in brown adipocytes. This Review focuses on the roles of the natriuretic peptides and the sympathetic nervous system in regulating adipocyte metabolism. The potential for manipulating the natriuretic peptide pathway to increase energy expenditure in obesity and manage the complications of cardiometabolic disease is also discussed.
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p62 links β-adrenergic input to mitochondrial function and thermogenesis.
Müller TD, Lee SJ, Jastroch M, Kabra D, Stemmer K, Aichler M, Abplanalp B, Ananthakrishnan G, Bhardwaj N, Collins S, Divanovic S, Endele M, Finan B, Gao Y, Habegger KM, Hembree J, Heppner KM, Hofmann S, Holland J, Küchler D, Kutschke M, Krishna R, Lehti M, Oelkrug R, Ottaway N, Perez-Tilve D, Raver C, Walch AK, Schriever SC, Speakman J, Tseng YH, Diaz-Meco M, Pfluger PT, Moscat J, Tschöp MH
(2013) J Clin Invest 123: 469-78
MeSH Terms: Adaptor Proteins, Signal Transducing, Adipocytes, Brown, Adipose Tissue, Brown, Animals, Cells, Cultured, Heat-Shock Proteins, MAP Kinase Signaling System, Mice, Mice, Knockout, Mitochondria, Mitochondrial Proteins, Organ Specificity, Sequestosome-1 Protein, Thermogenesis, Transcription Factors, p38 Mitogen-Activated Protein Kinases
Show Abstract · Added July 22, 2020
The scaffold protein p62 (sequestosome 1; SQSTM1) is an emerging key molecular link among the metabolic, immune, and proliferative processes of the cell. Here, we report that adipocyte-specific, but not CNS-, liver-, muscle-, or myeloid-specific p62-deficient mice are obese and exhibit a decreased metabolic rate caused by impaired nonshivering thermogenesis. Our results show that p62 regulates energy metabolism via control of mitochondrial function in brown adipose tissue (BAT). Accordingly, adipocyte-specific p62 deficiency led to impaired mitochondrial function, causing BAT to become unresponsive to β-adrenergic stimuli. Ablation of p62 leads to decreased activation of p38 targets, affecting signaling molecules that control mitochondrial function, such as ATF2, CREB, PGC1α, DIO2, NRF1, CYTC, COX2, ATP5β, and UCP1. p62 ablation in HIB1B and BAT primary cells demonstrated that p62 controls thermogenesis in a cell-autonomous manner, independently of brown adipocyte development or differentiation. Together, our data identify p62 as a novel regulator of mitochondrial function and brown fat thermogenesis.
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Energy expenditure in obese children with pseudohypoparathyroidism type 1a.
Shoemaker AH, Lomenick JP, Saville BR, Wang W, Buchowski MS, Cone RD
(2013) Int J Obes (Lond) 37: 1147-53
MeSH Terms: Absorptiometry, Photon, Adolescent, Age of Onset, Basal Metabolism, Blood Glucose, Body Composition, Calorimetry, Indirect, Child, Disease Susceptibility, Energy Metabolism, Female, Glycated Hemoglobin A, Humans, Insulin, Pediatric Obesity, Phenotype, Polymorphism, Single Nucleotide, Postprandial Period, Pseudohypoparathyroidism, Rest, Thermogenesis, United States, Weight Gain
Show Abstract · Added December 10, 2013
CONTEXT - Patients with pseudohypoparathyroidism type 1a (PHP-1a) develop early-onset obesity. The abnormality in energy expenditure and/or energy intake responsible for this weight gain is unknown.
OBJECTIVE - The aim of this study was to evaluate energy expenditure in children with PHP-1a compared with obese controls.
PATIENTS - We studied 6 obese females with PHP-1a and 17 obese female controls. Patients were recruited from a single academic center.
MEASUREMENTS - Resting energy expenditure (REE) and thermogenic effect of a high fat meal were measured using whole room indirect calorimetry. Body composition was assessed using whole body dual energy x-ray absorptiometry. Fasting glucose, insulin, and hemoglobin A1C were measured.
RESULTS - Children with PHP-1a had decreased REE compared with obese controls (P<0.01). After adjustment for fat-free mass, the PHP-1a group's REE was 346.4 kcals day(-1) less than obese controls (95% CI (-585.5--106.9), P<0.01). The thermogenic effect of food (TEF), expressed as percent increase in postprandial energy expenditure over REE, was lower in PHP-1a patients than obese controls, but did not reach statistical significance (absolute reduction of 5.9%, 95% CI (-12.2-0.3%), P=0.06).
CONCLUSIONS - Our data indicate that children with PHP-1a have decreased REE compared with the obese controls, and that may contribute to the development of obesity in these children. These patients may also have abnormal diet-induced thermogenesis in response to a high-fat meal. Understanding the causes of obesity in PHP-1a may allow for targeted nutritional or pharmacologic treatments in the future.
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3 Members
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23 MeSH Terms
Impaired thermogenesis and adipose tissue development in mice with fat-specific disruption of insulin and IGF-1 signalling.
Boucher J, Mori MA, Lee KY, Smyth G, Liew CW, Macotela Y, Rourk M, Bluher M, Russell SJ, Kahn CR
(2012) Nat Commun 3: 902
MeSH Terms: Adipocytes, Adipose Tissue, Animals, Body Composition, Cells, Cultured, Energy Metabolism, Insulin, Insulin-Like Growth Factor I, Male, Mice, Mice, Knockout, Temperature, Thermogenesis
Show Abstract · Added July 21, 2014
Insulin and insulin-like growth factor 1 (IGF-1) have important roles in adipocyte differentiation, glucose tolerance and insulin sensitivity. Here to assess how these pathways can compensate for each other, we created mice with a double tissue-specific knockout of insulin and IGF-1 receptors to eliminate all insulin/IGF-1 signalling in fat. These FIGIRKO mice had markedly decreased white and brown fat mass and were completely resistant to high fat diet-induced obesity and age- and high fat diet-induced glucose intolerance. Energy expenditure was increased in FIGIRKO mice despite a >85% reduction in brown fat mass. However, FIGIRKO mice were unable to maintain body temperature when placed at 4 °C. Brown fat activity was markedly decreased in FIGIRKO mice but was responsive to β3-receptor stimulation. Thus, insulin/IGF-1 signalling has a crucial role in the control of brown and white fat development, and, when disrupted, leads to defective thermogenesis and a paradoxical increase in basal metabolic rate.
1 Communities
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13 MeSH Terms