Sohet Florence M, Neyrinck Audrey M, Pachikian Barbara D, de Backer Fabienne C, Bindels Laure B, Niklowitz Petra, Menke Thomas, Cani Patrice D, Delzenne Nathalie M
Louvain Drug Research Institute, Nutrition and Metabolism Research Group, Université Catholique de Louvain, Brussels, Belgium.
Biochem Pharmacol. 2009 Dec 1;78(11):1391-400. doi: 10.1016/j.bcp.2009.07.008. Epub 2009 Jul 23.
Diabetes and obesity are metabolic disorders induced by an excessive dietary intake of fat, usually related to inflammation and oxidative stress.
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.
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).
HFF mice exhibit increased energy consumption, fat mass development, fasting glycaemia and insulinemia and impaired glucose tolerance. HFF treatment promoted the expression of genes involved in reactive oxygen species production (NADPH oxidase), inflammation (CRP, STAMP2) and metabolism (CPT1alpha) 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.
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.
糖尿病和肥胖是因过量摄入脂肪性饮食引起的代谢紊乱，通常与炎症和氧化应激有关。
本研究旨在探究抗氧化剂辅酶Q10（CoQ10）对与饮食诱导的肥胖和葡萄糖不耐受相关的肝脏代谢及炎症紊乱的影响。
将C57bl6/j小鼠分为两组，一组喂食对照饮食（CT）8周，另一组喂食高脂肪饮食并在饮用水中添加21%的果糖（HFF）8周。在HFF组小鼠中进行CoQ10补充（HFFQ）。
HFF组小鼠表现出能量消耗增加、脂肪量增加、空腹血糖和胰岛素水平升高以及葡萄糖耐量受损。HFF处理促进了肝脏中参与活性氧生成（NADPH氧化酶）、炎症（CRP、STAMP2）和代谢（CPT1α）的基因表达。与HFF组小鼠相比，CoQ10补充降低了肝脏炎症和代谢应激标志物的整体mRNA表达，而肥胖和组织脂质过氧化物水平未发生变化。与CT组相比，HFF饮食反常地降低了肝脏、肌肉和脂肪组织中的TBARS（反映脂质过氧化物）水平，这一效应与饮食中的维生素E含量有关。
总之，HFF模型通过一种独立于组织过氧化物水平的机制促进葡萄糖不耐受和肥胖。CoQ10倾向于降低肝脏应激基因表达，而与脂质过氧化的任何调节无关，脂质过氧化通常被认为是其最相关的效应。
