Loss of Adipose Fatty Acid Oxidation Does Not Potentiate Obesity at Thermoneutrality

Publication date: Available online 4 February 2016
Source:Cell Reports
Author(s): Jieun Lee, Joseph Choi, Susan Aja, Susanna Scafidi, Michael J. Wolfgang
Ambient temperature affects energy intake and expenditure to maintain homeostasis in a continuously fluctuating environment. Here, mice with an adipose-specific defect in fatty acid oxidation (Cpt2^A−/−) were subjected to varying temperatures to determine the role of adipose bioenergetics in environmental adaptation and body weight regulation. Microarray analysis of mice acclimatized to thermoneutrality revealed that Cpt2^A−/− interscapular brown adipose tissue (BAT) failed to induce the expression of thermogenic genes such as Ucp1 and Pgc1α in response to adrenergic stimulation, and increasing ambient temperature exacerbated these defects. Furthermore, thermoneutral housing induced mtDNA stress in Cpt2^A−/− BAT and ultimately resulted in a loss of interscapular BAT. Although the loss of adipose fatty acid oxidation resulted in clear molecular, cellular, and physiologic deficits in BAT, body weight gain and glucose tolerance were similar in control and Cpt2^A−/− mice in response to a high-fat diet, even when mice were housed at thermoneutrality.

Graphical abstract

Teaser

Lee et al. show that a loss of adipose fatty acid oxidation (FAO) at thermoneutrality results in defective induction of thermogenic genes and mtDNA stress in BAT. Long-term housing of FAO-deficient mice results in a loss of interscapular BAT; however, body weight gain and glucose tolerance were unaffected.


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