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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Main Authors: Jieun Lee, Joseph Choi, Susan Aja, Susanna Scafidi, Michael J. Wolfgang
Format: Article
Language:English
Published: Elsevier 2016-02-01
Series:Cell Reports
Online Access:http://www.sciencedirect.com/science/article/pii/S2211124716000504
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spelling 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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