TY - JOUR
T1 - Loss of Adipose Fatty Acid Oxidation Does Not Potentiate Obesity at Thermoneutrality
AU - Lee, Jieun
AU - Choi, Joseph
AU - Aja, Susan
AU - Scafidi, Susanna
AU - Wolfgang, Michael J.
N1 - Funding Information:
This work was supported in part by American Diabetes Association grant 1-16-IBS-313 and National Institutes of Health grants R01NS072241 to M.J.W. and K08NS069815 to S.S. J.L. was supported in part by National Institutes of Health grant T32GM007445.
Funding Information:
This work was supported in part by American Diabetes Association grant 1-16-IBS-313 and National Institutes of Health grants R01NS072241 to M.J.W. and K08NS069815 to S.S. J.L. was supported in part by National Institutes of Health grant T32GM007445.
Publisher Copyright:
© 2016 The Authors.
PY - 2016/2/16
Y1 - 2016/2/16
N2 - 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 (Cpt2A-/-) 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 Cpt2A-/- 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 Cpt2A-/- 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 Cpt2A-/- mice in response to a high-fat diet, even when mice were housed at thermoneutrality.
AB - 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 (Cpt2A-/-) 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 Cpt2A-/- 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 Cpt2A-/- 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 Cpt2A-/- mice in response to a high-fat diet, even when mice were housed at thermoneutrality.
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U2 - 10.1016/j.celrep.2016.01.029
DO - 10.1016/j.celrep.2016.01.029
M3 - Article
C2 - 26854223
AN - SCOPUS:84958121188
SN - 2211-1247
VL - 14
SP - 1308
EP - 1316
JO - Cell Reports
JF - Cell Reports
IS - 6
ER -