Please use this identifier to cite or link to this item: https://hdl.handle.net/2440/118443
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Type: Journal article
Title: Oxidative modifications of mitochondrial complex II are associated with insulin resistance of visceral fat in obesity
Author: Ngo, D.
Sverdlov, A.
Karki, S.
Macartney-Coxson, D.
Stubbs, R.
Farb, M.
Carmine, B.
Hess, D.
Colucci, W.
Gokce, N.
Citation: American Journal of Physiology: Endocrinology and Metabolism, 2019; 316(2):E177-E177
Publisher: American Physiological Society
Issue Date: 2019
ISSN: 0193-1849
1522-1555
Statement of
Responsibility: 
Doan T. M. Ngo, Aaron L. Sverdlov, Shakun Karki, Donia Macartney-Coxson, Richard S. Stubbs, Melissa G. Farb, Brian Carmine, Donald T. Hess, Wilson S. Colucci and Noyan Gokce
Abstract: Obesity, particularly visceral adiposity, has been linked to mitochondrial dysfunction and increased oxidative stress, which have been suggested as mechanisms of insulin resistance. The mechanism(s) behind this remains incompletely understood. In this study, we hypothesized that mitochondrial complex II dysfunction plays a role in impaired insulin sensitivity in visceral adipose tissue of subjects with obesity. We obtained subcutaneous and visceral adipose tissue biopsies from 43 subjects with obesity (body mass index ≥ 30 kg/m2) during planned bariatric surgery. Compared with subcutaneous adipose tissue, visceral adipose tissue exhibited decreased complex II activity, which was restored with the reducing agent dithiothreitol (5 mM) ( P < 0.01). A biotin switch assay identified that cysteine oxidative posttranslational modifications (OPTM) in complex II subunit A (succinate dehydrogenase A) were increased in visceral vs. subcutaneous fat ( P < 0.05). Insulin treatment (100 nM) stimulated complex II activity in subcutaneous fat ( P < 0.05). In contrast, insulin treatment of visceral fat led to a decrease in complex II activity ( P < 0.01), which was restored with addition of the mitochondria-specific oxidant scavenger mito-TEMPO (10 µM). In a cohort of 10 subjects with severe obesity, surgical weight loss decreased OPTM and restored complex II activity, exclusively in the visceral depot. Mitochondrial complex II may be an unrecognized and novel mediator of insulin resistance associated with visceral adiposity. The activity of complex II is improved by weight loss, which may contribute to metabolic improvements associated with bariatric surgery.
Keywords: Adipose tissue
insulin resistance
mitochondrial complex II
mitochondrial function
obesity
succinate dehydrogenase
Rights: © 2019 the American Physiological Society
DOI: 10.1152/ajpendo.00227.2018
Grant ID: http://purl.org/au-research/grants/nhmrc/1037603
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