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FGF21 regulates PGC-1a and browning of white adipose tissues in adaptive thermogenesis.

Authors: Fisher, Ffolliott M  Kleiner, Sandra  Douris, Nicholas  Fox, Elliott C  Mepani, Rina J  Verdeguer, Francisco  Wu, Jun  Kharitonenkov, Alexei  Flier, Jeffrey S  Maratos-Flier, Eleftheria  Spiegelman, Bruce M 
Citation: Fisher FM, etal., Genes Dev. 2012 Feb 1;26(3):271-81. doi: 10.1101/gad.177857.111.
Pubmed: (View Article at PubMed) PMID:22302939
DOI: Full-text: DOI:10.1101/gad.177857.111

Certain white adipose tissue (WAT) depots are readily able to convert to a "brown-like" state with prolonged cold exposure or exposure to ß-adrenergic compounds. This process is characterized by the appearance of pockets of uncoupling protein 1 (UCP1)-positive, multilocular adipocytes and serves to increase the thermogenic capacity of the organism. We show here that fibroblast growth factor 21 (FGF21) plays a physiologic role in this thermogenic recruitment of WATs. In fact, mice deficient in FGF21 display an impaired ability to adapt to chronic cold exposure, with diminished browning of WAT. Adipose-derived FGF21 acts in an autocrine/paracrine manner to increase expression of UCP1 and other thermogenic genes in fat tissues. FGF21 regulates this process, at least in part, by enhancing adipose tissue PGC-1α protein levels independently of mRNA expression. We conclude that FGF21 acts to activate and expand the thermogenic machinery in vivo to provide a robust defense against hypothermia.


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RGD Object Information
RGD ID: 13673850
Created: 2018-06-23
Species: All species
Last Modified: 2018-06-23
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.