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Article Publish Status: FREE
Abstract Title:

Mitochondrial CoQ deficiency is a common driver of mitochondrial oxidants and insulin resistance.

Abstract Source:

Elife. 2018 Feb 6 ;7. Epub 2018 Feb 6. PMID: 29402381

Abstract Author(s):

Daniel J Fazakerley, Rima Chaudhuri, Pengyi Yang, Ghassan J Maghzal, Kristen C Thomas, James R Krycer, Sean J Humphrey, Benjamin L Parker, Kelsey H Fisher-Wellman, Christopher C Meoli, Nolan J Hoffman, Ciana Diskin, James G Burchfield, Mark J Cowley, Warren Kaplan, Zora Modrusan, Ganesh Kolumam, Jean Yh Yang, Daniel L Chen, Dorit Samocha-Bonet, Jerry R Greenfield, Kyle L Hoehn, Roland Stocker, David E James

Article Affiliation:

Daniel J Fazakerley

Abstract:

Insulin resistance in muscle, adipocytes and liver is a gateway to a number of metabolic diseases. Here, we show a selective deficiency in mitochondrial coenzyme Q (CoQ) in insulin-resistant adipose and muscle tissue. This defect was observed in a range of in vitro insulin resistance models and adipose tissue from insulin-resistant humans and was concomitant with lower expression of mevalonate/CoQ biosynthesis pathway proteins in most models. Pharmacologic or genetic manipulations that decreased mitochondrial CoQ triggered mitochondrial oxidants and insulin resistance while CoQ supplementation in either insulin-resistant cell models or mice restored normal insulin sensitivity. Specifically, lowering of mitochondrial CoQ caused insulin resistance in adipocytes as a result of increased superoxide/hydrogen peroxide production via complex II. These data suggest that mitochondrial CoQ is a proximal driver of mitochondrial oxidants and insulin resistance, and that mechanisms that restore mitochondrial CoQ may be effective therapeutic targets for treating insulin resistance.

Study Type : Human In Vitro

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