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Adipose fatty acid oxidation is required for thermogenesis and potentiates oxidative stress-induced inflammation.

Authors: Lee, Jieun  Ellis, Jessica M  Wolfgang, Michael J 
Citation: Lee J, etal., Cell Rep. 2015 Jan 13;10(2):266-79. doi: 10.1016/j.celrep.2014.12.023. Epub 2015 Jan 8.
Pubmed: (View Article at PubMed) PMID:25578732
DOI: Full-text: DOI:10.1016/j.celrep.2014.12.023

To understand the contribution of adipose tissue fatty acid oxidation to whole-body metabolism, we generated mice with an adipose-specific knockout of carnitine palmitoyltransferase 2 (CPT2(A-/-)), an obligate step in mitochondrial long-chain fatty acid oxidation. CPT2(A-/-) mice became hypothermic after an acute cold challenge, and CPT2(A-/-) brown adipose tissue (BAT) failed to upregulate thermogenic genes in response to agonist-induced stimulation. The adipose-specific loss of CPT2 resulted in diet-dependent changes in adiposity but did not result in changes in body weight on low- or high-fat diets. Additionally, CPT2(A-/-) mice had suppressed high-fat diet-induced oxidative stress and inflammation in visceral white adipose tissue (WAT); however, high-fat diet-induced glucose intolerance was not improved. These data show that fatty acid oxidation is required for cold-induced thermogenesis in BAT and high-fat diet-induced oxidative stress and inflammation in WAT.

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RGD Object Information
RGD ID: 13673835
Created: 2018-06-23
Species: All species
Last Modified: 2018-06-23
Status: ACTIVE



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