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Publication
Ablation of PRDM16 and beige adipose causes metabolic dysfunction and a
subcutaneous to visceral fat switch.
Authors Cohen P, Levy JD, Zhang Y, Frontini A, Kolodin DP, Svensson KJ, Lo JC, Zeng X,
Ye L, Khandekar MJ, Wu J, Gunawardana SC, Banks AS, Camporez JP, Jurczak MJ,
Kajimura S, Piston DW, Mathis D, Cinti S, Shulman GI, Seale P, Spiegelman BM
Submitted By Submitted Externally on 11/10/2015
Status Published
Journal Cell
Year 2014
Date Published 1/1/2014
Volume : Pages 156 : 304 - 16
PubMed Reference 24439384
Abstract A clear relationship exists between visceral obesity and type 2 diabetes,
whereas subcutaneous obesity is comparatively benign. Here, we show that
adipocyte-specific deletion of the coregulatory protein PRDM16 caused minimal
effects on classical brown fat but markedly inhibited beige adipocyte function
in subcutaneous fat following cold exposure or ß3-agonist treatment. These
animals developed obesity on a high-fat diet, with severe insulin resistance and
hepatic steatosis. They also showed altered fat distribution with markedly
increased subcutaneous adiposity. Subcutaneous adipose tissue in mutant mice
acquired many key properties of visceral fat, including decreased thermogenic
and increased inflammatory gene expression and increased macrophage
accumulation. Transplantation of subcutaneous fat into mice with diet-induced
obesity showed a loss of metabolic benefit when tissues were derived from PRDM16
mutant animals. These findings indicate that PRDM16 and beige adipocytes are
required for the "browning" of white fat and the healthful effects of
subcutaneous adipose tissue.








Genes
SymbolDescription
Prdm16PR domain containing 16
Adipoqadiponectin, C1Q and collagen domain containing

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