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Increased obesity resistance and insulin sensitivity in mice lacking the isocitrate dehydrogenase 2 gene

Authors
Lee, Su JeongKim, Sung HwanPark, Kwon MooLee, Jin HyupPark, Jeen-Woo
Issue Date
10월-2016
Publisher
ELSEVIER SCIENCE INC
Keywords
Reactive oxygen species; Isocitrate dehydrogenase 2; Obesity
Citation
FREE RADICAL BIOLOGY AND MEDICINE, v.99, pp.179 - 188
Indexed
SCIE
SCOPUS
Journal Title
FREE RADICAL BIOLOGY AND MEDICINE
Volume
99
Start Page
179
End Page
188
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/87406
DOI
10.1016/j.freeradbiomed.2016.08.011
ISSN
0891-5849
Abstract
Reactive oxygen species (ROS) are a byproduct of normal metabolism and play important roles in cell signaling and homeostasis. Mitochondria, the main organelles involved in intracellular ROS production, play central roles in modulating redox-dependent cellular processes such as metabolism and apoptosis. We recently reported an important role for mitochondrial NADP(+)-dependent isocitrate dehydrogenase (IDH2) in cellular redox regulation. Here, we show that mice with targeted disruption of IDH2 exhibit resistance to obesity, with lower body weight and reduced visceral fat, and increased insulin sensitivity accompanied by enhanced energy expenditure relative to controls. This function of IDH2 is linked to its capacity to suppress lipogenesis in visceral adipose tissue, partly via transcriptional repression of SREBPI, and to increase thermogenesis in adipocytes by transcriptional activation of UCP1 via activation of the p38 signaling axis. Our results highlight the importance of redox balance in the regulation of metabolism and demonstrate that IDH2 plays a major role in modulating both insulin sensitivity and fuel metabolism, thereby establishing this protein as a potential therapeutic target in the treatment of type 2 diabetes and obesity. (C) 2016 Elsevier Inc. All rights reserved.
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