Abstract:
:"Beige" adipocytes reside in white adipose tissue (WAT) and dissipate energy as heat. Several studies have shown that cold temperature can activate pro-opiomelanocortin-expressing (POMC) neurons and increase sympathetic neuronal tone to regulate WAT beiging. WAT, however, is traditionally known to be sparsely innervated. Details regarding the neuronal innervation and, more importantly, the propagation of the signal within the population of "beige" adipocytes are sparse. Here, we demonstrate that beige adipocytes display an increased cell-to-cell coupling via connexin 43 (Cx43) gap junction channels. Blocking of Cx43 channels by 18α-glycyrrhetinic acid decreases POMC-activation-induced adipose tissue beiging. Adipocyte-specific deletion of Cx43 reduces WAT beiging to a level similar to that observed in denervated fat pads. In contrast, overexpression of Cx43 is sufficient to promote beiging even with mild cold stimuli. These data reveal the importance of cell-to-cell communication, effective in cold-induced WAT beiging, for the propagation of limited neuronal inputs in adipose tissue.
journal_name
Cell Metabjournal_title
Cell metabolismauthors
Zhu Y,Gao Y,Tao C,Shao M,Zhao S,Huang W,Yao T,Johnson JA,Liu T,Cypess AM,Gupta O,Holland WL,Gupta RK,Spray DC,Tanowitz HB,Cao L,Lynes MD,Tseng YH,Elmquist JK,Williams KW,Lin HV,Scherer PEdoi
10.1016/j.cmet.2016.08.005subject
Has Abstractpub_date
2016-09-13 00:00:00pages
420-433issue
3eissn
1550-4131issn
1932-7420pii
S1550-4131(16)30421-1journal_volume
24pub_type
杂志文章相关文献
Cell Metabolism文献大全abstract::The AMPK (AMP-activated protein kinase) and TOR (target-of-rapamycin) pathways are interlinked, opposing signaling pathways involved in sensing availability of nutrients and energy and regulation of cell growth. AMPK (Yin, or the "dark side") is switched on by lack of energy or nutrients and inhibits cell growth, whil...
journal_title:Cell metabolism
pub_type: 杂志文章,评审
doi:10.1016/j.cmet.2020.01.015
更新日期:2020-03-03 00:00:00
abstract::Fibrosis is increasingly appreciated as a major player in adipose tissue dysfunction. In rapidly expanding adipose tissue, pervasive hypoxia leads to an induction of HIF1α that in turn leads to a potent profibrotic transcriptional program. The pathophysiological impact of adipose tissue fibrosis is likely to play an e...
journal_title:Cell metabolism
pub_type: 杂志文章,评审
doi:10.1016/j.cmet.2013.06.016
更新日期:2013-10-01 00:00:00
abstract::The polarization of adipose tissue-resident macrophages toward the alternatively activated, anti-inflammatory M2 phenotype is believed to improve insulin sensitivity. However, the mechanisms controlling tissue macrophage activation remain unclear. Here we show that adipocytes are a source of Th2 cytokines, including I...
journal_title:Cell metabolism
pub_type: 杂志文章
doi:10.1016/j.cmet.2008.04.002
更新日期:2008-06-01 00:00:00
abstract::The fat mass and obesity-associated (FTO) gene was placed center stage when common intronic variants within the gene were robustly associated with human obesity. Murine models of perturbed Fto expression have shown effects on body weight and composition. However, a clear understanding of the link between FTO intronic ...
journal_title:Cell metabolism
pub_type: 杂志文章,评审
doi:10.1016/j.cmet.2014.09.010
更新日期:2014-11-04 00:00:00
abstract::The conversion of lipolysis-derived fatty acids into ketone bodies (ketogenesis) is a crucial metabolic adaptation to prolonged periods of food scarcity. The process occurs primarily in liver mitochondria and is initiated by fatty-acid-mediated stimulation of the ligand-operated transcription factor, peroxisome prolif...
journal_title:Cell metabolism
pub_type: 杂志文章
doi:10.1016/j.cmet.2018.09.014
更新日期:2019-01-08 00:00:00
abstract::AMPK is a kinase involved in cell energy homeostasis. In this issue of Cell Metabolism, Chopra and colleagues (2011) reveal a new function of AMPK in stimulating fat absorption. AMPK enhances the expression of the bile acid transporter, BSEP, by activating the coactivator SRC-2, thus promoting bile acid secretion. ...
journal_title:Cell metabolism
pub_type: 评论,杂志文章
doi:10.1016/j.cmet.2010.12.009
更新日期:2011-01-05 00:00:00
abstract::Common variants in WNT pathway genes have been associated with bone mass and fat distribution, the latter predicting diabetes and cardiovascular disease risk. Rare mutations in the WNT co-receptors LRP5 and LRP6 are similarly associated with bone and cardiometabolic disorders. We investigated the role of LRP5 in human...
journal_title:Cell metabolism
pub_type: 杂志文章
doi:10.1016/j.cmet.2015.01.009
更新日期:2015-02-03 00:00:00
abstract::Precise control of the thyroid hormone (T3)-dependent transcriptional program is required by multiple cell systems, including muscle stem cells. Deciphering how this is achieved and how the T3 signal is controlled in stem cell niches is essentially unknown. We report that in response to proliferative stimuli such as a...
journal_title:Cell metabolism
pub_type: 杂志文章
doi:10.1016/j.cmet.2014.10.009
更新日期:2014-12-02 00:00:00
abstract::Resveratrol induces mitochondrial biogenesis and protects against metabolic decline, but whether SIRT1 mediates these benefits is the subject of debate. To circumvent the developmental defects of germline SIRT1 knockouts, we have developed an inducible system that permits whole-body deletion of SIRT1 in adult mice. Mi...
journal_title:Cell metabolism
pub_type: 杂志文章
doi:10.1016/j.cmet.2012.04.003
更新日期:2012-05-02 00:00:00
abstract::Peroxisome proliferator-activated receptor δ (PPARδ) is a critical regulator of energy metabolism in the heart. Here, we propose a mechanism that integrates two deleterious characteristics of heart failure, hypoxia and a metabolic shift toward glycolysis, involving the microRNA cluster miR-199a∼214 and PPARδ. We demon...
journal_title:Cell metabolism
pub_type: 杂志文章
doi:10.1016/j.cmet.2013.08.009
更新日期:2013-09-03 00:00:00
abstract::For many years, mitochondria were viewed as semiautonomous organelles, required only for cellular energetics. This view has been largely supplanted by the concept that mitochondria are fully integrated into the cell and that mitochondrial stresses rapidly activate cytosolic signaling pathways that ultimately alter nuc...
journal_title:Cell metabolism
pub_type: 杂志文章,评审
doi:10.1016/j.cmet.2014.01.011
更新日期:2014-05-06 00:00:00
abstract::The mechanistic target of rapamycin complex 1 (mTORC1) coordinates nutrient availability with cell growth. Recent reports by Sabatini and coworkers (Saxton et al., 2016; Wolfson et al., 2016) characterize a cytoplasmic amino acid receptor that couples the binding of leucine to the activation of mTORC1. ...
journal_title:Cell metabolism
pub_type: 杂志文章
doi:10.1016/j.cmet.2016.02.012
更新日期:2016-03-08 00:00:00
abstract::Polg mtDNA mutator mice are important models for investigating the role of acquired mtDNA mutations in aging. Despite extensive study, there remains little consensus on either the etiology of the progeroid phenotype or the mtDNA mutation spectrum induced by disrupted polymerase-γ function. To investigate the latter, w...
journal_title:Cell metabolism
pub_type: 杂志文章
doi:10.1016/j.cmet.2010.11.012
更新日期:2010-12-01 00:00:00
abstract::Impaired angiogenesis has been implicated in adipose tissue dysfunction and the development of obesity and associated metabolic disorders. Here, we report the unexpected finding that vascular endothelial growth factor B (VEGFB) gene transduction into mice inhibits obesity-associated inflammation and improves metabolic...
journal_title:Cell metabolism
pub_type: 杂志文章
doi:10.1016/j.cmet.2016.03.004
更新日期:2016-04-12 00:00:00
abstract::Advances in neuro-technology for mapping, manipulating, and monitoring molecularly defined cell types are rapidly advancing insight into neural circuits that regulate appetite. Here, we review these important tools and their applications in circuits that control food seeking and consumption. Technical capabilities pro...
journal_title:Cell metabolism
pub_type: 杂志文章,评审
doi:10.1016/j.cmet.2015.12.002
更新日期:2016-02-09 00:00:00
abstract::Over the past years, plenty of evidence has emerged illustrating how metabolism supports many aspects of cellular function and how metabolic reprogramming can drive cell differentiation and fate. Here, we present a method to assess the metabolic configuration of single cells within their native tissue microenvironment...
journal_title:Cell metabolism
pub_type: 杂志文章
doi:10.1016/j.cmet.2017.08.014
更新日期:2017-11-07 00:00:00
abstract::Diabetes is a growing epidemic, and many patients depend on insulin injections to control the disease and minimize long-term complications. In a recent manuscript published in Science, Xie et al. (2016) generate insulin-producing cells from a somatic embryonic kidney cell line through minimal genetic modification capa...
journal_title:Cell metabolism
pub_type: 评论,杂志文章
doi:10.1016/j.cmet.2017.01.018
更新日期:2017-02-07 00:00:00
abstract::The brain is the most cholesterol-rich organ in the body, most of which comes from in situ synthesis. Here we demonstrate that in insulin-deficient diabetic mice, there is a reduction in expression of the major transcriptional regulator of cholesterol metabolism, SREBP-2, and its downstream genes in the hypothalamus a...
journal_title:Cell metabolism
pub_type: 杂志文章
doi:10.1016/j.cmet.2010.11.006
更新日期:2010-12-01 00:00:00
abstract::Suppressor of cytokine signaling-3 (Socs-3) negatively regulates the action of various cytokines, as well as the metabolic hormones leptin and insulin. Mice with haploinsufficiency of Socs-3, or those with neuronal deletion of Socs-3, are lean and more leptin and insulin sensitive. To examine the role of Socs-3 within...
journal_title:Cell metabolism
pub_type: 杂志文章
doi:10.1016/j.cmet.2006.06.010
更新日期:2006-08-01 00:00:00
abstract::SIRT1 regulates energy homeostasis by controlling the acetylation status and activity of a number of enzymes and transcriptional regulators. The fact that NAD(+) levels control SIRT1 activity confers a hypothetical basis for the design of new strategies to activate SIRT1 by increasing NAD(+) availability. Here we show...
journal_title:Cell metabolism
pub_type: 杂志文章
doi:10.1016/j.cmet.2011.03.004
更新日期:2011-04-06 00:00:00
abstract::Cannabinoid signaling by CB1 receptors drives fibrogenesis and fat accumulation in liver. A report in this issue of Cell Metabolism (Jeong et al., 2008) now links hepatic stellate cells, a resident liver fibrogenic cell type, to the generation of steatosis through production of the endocannabinoid 2-arachidonoylglycer...
journal_title:Cell metabolism
pub_type: 评论,杂志文章
doi:10.1016/j.cmet.2008.02.002
更新日期:2008-03-01 00:00:00
abstract::Obesity-related morbidity and mortality are related to fat accumulation and fat distribution in humans. Two large-scale meta-analyses recently published in Nature by Shungin et al. (2015) and Locke et al. (2015) report novel genetic associations for central and overall obesity; these greatly advance our understanding ...
journal_title:Cell metabolism
pub_type: 评论,杂志文章
doi:10.1016/j.cmet.2015.03.016
更新日期:2015-04-07 00:00:00
abstract::Cholesterol levels in mammalian cells are controlled by an intricate mechanism in which the transcription factor SREBP plays a key role. Work in this issue (Radhakrishnan et al., 2008) employing direct measurement of endoplasmic reticulum cholesterol levels offers insights into the "switch" that controls this system w...
journal_title:Cell metabolism
pub_type: 评论,杂志文章
doi:10.1016/j.cmet.2008.11.006
更新日期:2008-12-01 00:00:00
abstract::Cholesteryl ester accumulation by macrophages is a critical early event in atherogenesis. To test the hypothesis that sterol loading promotes foam cell formation and vascular disease by perturbing a network of interacting proteins, we used a global approach to identify proteins that are differentially expressed when m...
journal_title:Cell metabolism
pub_type: 杂志文章
doi:10.1016/j.cmet.2010.01.003
更新日期:2010-02-03 00:00:00
abstract::T cells promote inflammation in obesity, but how metabolic stress associated with obesity alters T cell responses remains unclear. In this issue of Cell Metabolism,Mauro et al. (2017) demonstrate that saturated fatty acids directly increase effector-memory T cell formation by amplifying T cell antigen-receptor-induced...
journal_title:Cell metabolism
pub_type: 评论,杂志文章
doi:10.1016/j.cmet.2017.02.012
更新日期:2017-03-07 00:00:00
abstract::Silent information regulator 2 (Sir2) proteins, or sirtuins, are protein deacetylases/mono-ADP-ribosyltransferases found in organisms ranging from bacteria to humans. Their dependence on nicotinamide adenine dinucleotide (NAD+) links their activity to cellular metabolic status. In bacteria, the sirtuin CobB regulates ...
journal_title:Cell metabolism
pub_type: 杂志文章,评审
doi:10.1016/j.cmet.2007.11.006
更新日期:2008-02-01 00:00:00
abstract::Genome-wide association studies (GWAS) have identified multiple chronic kidney disease (CKD)-associated single-nucleotide polymorphisms (SNPs) mainly localized to non-coding genomic regions. To understand which genes and which cell types are affected by these genetic variants, compartment-specific transcriptome, genom...
journal_title:Cell metabolism
pub_type: 评论,杂志文章
doi:10.1016/j.cmet.2018.12.009
更新日期:2019-01-08 00:00:00
abstract::Leptin activates the long form of the leptin receptor (LRb) to control feeding and neuroendocrine function and thus regulate adiposity. While adiposity influences insulin sensitivity, leptin also regulates glucose homeostasis independently of energy balance. Disruption of the LRb/STAT3 signal in s/s mice results in hy...
journal_title:Cell metabolism
pub_type: 杂志文章
doi:10.1016/j.cmet.2005.02.001
更新日期:2005-03-01 00:00:00
abstract::The Saccharomyces cerevisiae chromatin silencing factor Sir2 suppresses genomic instability and extends replicative life span. In contrast, we find that mouse embryonic fibroblasts (MEFs) deficient for SIRT1, a mammalian Sir2 homolog, have dramatically increased resistance to replicative senescence. Extended replicati...
journal_title:Cell metabolism
pub_type: 杂志文章
doi:10.1016/j.cmet.2005.06.007
更新日期:2005-07-01 00:00:00
abstract::Despite the prevalence of obesity and its related diseases, the signaling pathways for appetite control and satiety are not clearly understood. Here we report C. elegans quiescence behavior, a cessation of food intake and movement that is possibly a result of satiety. C. elegans quiescence shares several characteristi...
journal_title:Cell metabolism
pub_type: 杂志文章
doi:10.1016/j.cmet.2008.01.005
更新日期:2008-03-01 00:00:00