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Rigshospitalet - a part of Copenhagen University Hospital
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Gamma-Aminobutyric Acid Signaling in Brown Adipose Tissue Promotes Systemic Metabolic Derangement in Obesity

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  1. ERG Controls B Cell Development by Promoting Igh V-to-DJ Recombination

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  2. Single mRNP Analysis Reveals that Small Cytoplasmic mRNP Granules Represent mRNA Singletons

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  1. Isolation and Characterization of Human Brown Adipocytes

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  2. Altered brown fat thermoregulation and enhanced cold-induced thermogenesis in young, healthy, winter-swimming men

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  3. Lipolysis drives expression of the constitutively active receptor GPR3 to induce adipose thermogenesis

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  4. VPS39-deficiency observed in type 2 diabetes impairs muscle stem cell differentiation via altered autophagy and epigenetics

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  5. Endogenous Fatty Acid Synthesis Drives Brown Adipose Tissue Involution

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Brown adipose tissue (BAT) is a metabolically active organ that contributes to the maintenance of systemic metabolism. The sympathetic nervous system plays important roles in the homeostasis of BAT and promotes its browning and activation. However, the role of other neurotransmitters in BAT homeostasis remains largely unknown. Our metabolomic analyses reveal that gamma-aminobutyric acid (GABA) levels are increased in the interscapular BAT of mice with dietary obesity. We also found a significant increase in GABA-type B receptor subunit 1 (GABA-BR1) in the cell membranes of brown adipocytes of dietary obese mice. When administered to obese mice, GABA induces BAT dysfunction together with systemic metabolic disorder. Conversely, the genetic inactivation or inhibition of GABA-BR1 leads to the re-browning of BAT under conditions of metabolic stress and ameliorated systemic glucose intolerance. These results indicate that the constitutive activation of GABA/GABA-BR1 signaling in obesity promotes BAT dysfunction and systemic metabolic derangement.

Original languageEnglish
JournalCell Reports
Volume24
Issue number11
Pages (from-to)2827-2837.e5
DOIs
Publication statusPublished - 11 Sep 2018

ID: 56585794