Coenzyme Q10 supplementation lowers hepatic oxidative stress and inflammation associated with diet-induced obesity in mice

Abstract

Please cite this article as: Sohet FM, Neyrinck AM, Pachikian BD, de Backer FC, Bindels LB, Niklowitz P, Menke T, Cani PD, Delzenne NM, Coenzyme Q10 supplementation lowers hepatic oxidative stress and inflammation associated with diet-induced obesity in mice, Biochemical Pharmacology (2008Pharmacology ( ), doi:10.1016Pharmacology ( /j.bcp.2009 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Aims:The aim of the study is to investigate the effect of the antioxidant coenzyme Q10 (CoQ10) on hepatic metabolic and inflammatory disorders associated with diet-induced obesity and glucose intolerance.Methods: C57bl6/j mice were fed for 8 weeks, either a control diet (CT) or a high fat diet plus 21% fructose in the drinking water (HFF). CoQ10 supplementation was performed in this later condition (HFFQ).Results HFF mice exhibit increased energy consumption, fat mass development, fasting glycemia and insulinemia and impaired glucose tolerance. HFF treatment promoted the expression of genes involved in reactive oxygen species production (NADPH oxidase), inflammation (CRP, STAMP-2) and metabolism (CPT1) in the liver. CoQ10 supplementation decreased the global hepatic mRNA expression of inflammatory and metabolic stresses markers without changing obesity and tissue lipid peroxides compared to HFF mice. HFF diets paradoxically decreased TBARS (reflecting lipid peroxides) levels in liver, muscle and adipose tissue versus CT group, an effect related to vitamin E content of the diet. Conclusion:In conclusion, HFF model promotes glucose intolerance and obesity by a mechanism independent on the level of tissue peroxides. CoQ10 tends to decrease hepatic stress gene expression, independently of any modulation of lipid peroxidation, which is classically considered as its most relevant effect.

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“…In another study, CoQ10 supplementation significantly reduced the IL-6 protein and TGF-b1 and Lep mRNA levels [6]. In addition, our study was in agreement with findings in cardiac tissue [23], and CoQ10 is known to have anti-inflammatory properties in mouse liver [24] and human plasma [25]. Also, gene expression of TNF-a were significantly decreased following CoQ10 intake in an experimental model of multiple sclerosis for three weeks [26].…”

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“…Recently, a randomized human clinical trial documented a significant improvement in NASH in nondiabetic subjects after long-term vitamin E administration compared to pioglitazone (186). Additionally, the observation of reduced systemic coenzyme Q10 levels in patients with NAFLD (223) has lead to limited investigation of the effects of dietary supplementation of coenzyme Q. Coenzyme Q10 supplementation has been observed to lower oxidative stress and markers of inflammation in a mouse, without modulating lipid peroxidation or improving systemic insulin resistance (195). Additionally, coenzyme Q9 monomethyl ether administration increased VLDL assembly in rats with high-fat-diet-induced steatosis (22,182), with no observed improvement in NAFLD or systemic insulin resistance (182).…”