Loss of Adipose Fatty Acid Oxidation Does Not Potentiate Obesity at Thermoneutrality
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 environm...
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doaj-5012fca1c60945c5a65e1792603719402020-11-25T01:40:28ZengElsevierCell Reports2211-12472016-02-011461308131610.1016/j.celrep.2016.01.029Loss of Adipose Fatty Acid Oxidation Does Not Potentiate Obesity at ThermoneutralityJieun Lee0Joseph Choi1Susan Aja2Susanna Scafidi3Michael J. Wolfgang4Department of Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USADepartment of Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USADepartment of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USADepartment of Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USADepartment of Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USAAmbient 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.http://www.sciencedirect.com/science/article/pii/S2211124716000504 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Jieun Lee Joseph Choi Susan Aja Susanna Scafidi Michael J. Wolfgang |
spellingShingle |
Jieun Lee Joseph Choi Susan Aja Susanna Scafidi Michael J. Wolfgang Loss of Adipose Fatty Acid Oxidation Does Not Potentiate Obesity at Thermoneutrality Cell Reports |
author_facet |
Jieun Lee Joseph Choi Susan Aja Susanna Scafidi Michael J. Wolfgang |
author_sort |
Jieun Lee |
title |
Loss of Adipose Fatty Acid Oxidation Does Not Potentiate Obesity at Thermoneutrality |
title_short |
Loss of Adipose Fatty Acid Oxidation Does Not Potentiate Obesity at Thermoneutrality |
title_full |
Loss of Adipose Fatty Acid Oxidation Does Not Potentiate Obesity at Thermoneutrality |
title_fullStr |
Loss of Adipose Fatty Acid Oxidation Does Not Potentiate Obesity at Thermoneutrality |
title_full_unstemmed |
Loss of Adipose Fatty Acid Oxidation Does Not Potentiate Obesity at Thermoneutrality |
title_sort |
loss of adipose fatty acid oxidation does not potentiate obesity at thermoneutrality |
publisher |
Elsevier |
series |
Cell Reports |
issn |
2211-1247 |
publishDate |
2016-02-01 |
description |
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. |
url |
http://www.sciencedirect.com/science/article/pii/S2211124716000504 |
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