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      α/β-Hydrolase Domain 6 Deletion Induces Adipose Browning and Prevents Obesity and Type 2 Diabetes.

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          Abstract

          Suppression of α/β-domain hydrolase-6 (ABHD6), a monoacylglycerol (MAG) hydrolase, promotes glucose-stimulated insulin secretion by pancreatic β cells. We report here that high-fat-diet-fed ABHD6-KO mice show modestly reduced food intake, decreased body weight gain and glycemia, improved glucose tolerance and insulin sensitivity, and enhanced locomotor activity. ABHD6-KO mice also show increased energy expenditure, cold-induced thermogenesis, brown adipose UCP1 expression, fatty acid oxidation, and white adipose browning. Adipose browning and cold-induced thermogenesis are replicated by the ABHD6 inhibitor WWL70 and by antisense oligonucleotides targeting ABHD6. Our evidence suggests that one mechanism by which the lipolysis derived 1-MAG signals intrinsic and cell-autonomous adipose browning is via PPARα and PPARγ activation, and that ABHD6 regulates adipose browning by controlling signal competent 1-MAG levels. Thus, ABHD6 regulates energy homeostasis, brown adipose function, and white adipose browning and is a potential therapeutic target for obesity and type 2 diabetes.

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          Author and article information

          Journal
          Cell Rep
          Cell reports
          Elsevier BV
          2211-1247
          Mar 29 2016
          : 14
          : 12
          Affiliations
          [1 ] Departments of Nutrition and Biochemistry and Montreal Diabetes Research Center, CRCHUM and Université de Montréal, Montréal, QC H1W 4A4, Canada.
          [2 ] Metanome Incorporated, Houston, TX 77046, USA.
          [3 ] Department of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195, USA.
          [4 ] Departments of Nutrition and Biochemistry and Montreal Diabetes Research Center, CRCHUM and Université de Montréal, Montréal, QC H1W 4A4, Canada. Electronic address: murthy.madiraju@crchum.qc.ca.
          [5 ] Departments of Nutrition and Biochemistry and Montreal Diabetes Research Center, CRCHUM and Université de Montréal, Montréal, QC H1W 4A4, Canada. Electronic address: marc.prentki@umontreal.ca.
          Article
          S2211-1247(16)30211-X
          10.1016/j.celrep.2016.02.076
          26997277
          4318a940-146a-4b5b-bf5f-605d00634ca7
          History

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