Coenzyme Q as an Antiadipogenic Factor

Abstract

Coenzyme Q (CoQ) is not only the single antioxidant synthesized in humans but also an obligatory element of mitochondrial functions. We have previously reported CoQ deficiency in white adipose tissue of ob/ob mice. We sought to determine (i) whether this deficit exists in all species and its relevance in human obesity and (ii) to what extent CoQ could be involved in adipocyte differentiation. Here we identified in rodents as well as in humans a specific very strong nonlinear negative correlation between CoQ content in subcutaneous adipose tissue and obesity indexes. This striking correlation reveals a threshold value similar in both species. This relative deficit in CoQ content in adipose tissue rapidly took place during the time course of high-fat-diet-induced obesity in mice. Adipocyte differentiation was assessed in vitro using the preadipocyte 3T3-F442A cell line. When CoQ synthesis was inhibited by a pharmacological approach using chlorobenzoic acid, this strongly triggered adipose differentiation. In contrast, adipogenesis was strongly inhibited when a long-term increase in CoQ content was obtained by overexpressing human 4-hydroxy benzoate acid polyprenyltransferase gene. Altogether, these data suggest that a strict level of CoQ remains essential for adipocyte differentiation, and its impairment is associated with obesity.

Omental adipocyte hypertrophy relates to coenzyme Q10 redox state and lipid peroxidation in obese women

“…Overexpression of COQ2 in 3T3-F442A preadipocytes decreased the CoQ redox state and promoted ROS synthesis by the mitochondria ( 13 ). Interestingly, the adipogenic potential of these cells was almost completely blunted, suggesting an important role of CoQ content and redox state during adipogenesis and adipose tissue expansion.…”

“…Depletion of CoQ10 content was found in subcutaneous adipose tissue of obese subjects and mice ( 13 ). Overexpression of COQ2 in 3T3-F442A preadipocytes decreased the CoQ redox state and promoted ROS synthesis by the mitochondria ( 13 ).…”

“…were selected from a previous publication ( 13 ). Differences between women with low and high concentrations of CoQ10 were analyzed by Student's t -test or Mann-Whitney test.…”

“…In a previous study, the concentration of 13.26 nmol of CoQ10 per gram of subcutaneous adipose tissue was identifi ed as a phenotypic threshold value below which 95% of volunteers are obese ( 13 ). To quantify the metabolic effect of low and high CoQ10 content, we used a cutoff value of 14.0 and 15.0 nmol/g of subcutaneous and omental adipose tissues.…”

Effects of coenzyme Q10 supplementation on the anthropometric variables, lipid profiles and liver enzymes in patients with non-alcoholic fatty liver disease

“…The primary function of CoQ10 in cells is in generating energy; being at the core of cellular energy processes CoQ10 has potential for reduce weight by improving (Alam and Rahman, 2014) ; Inhibition of CoQ10 synthesis strongly triggered adipocyte differentiation while increment of CoQ10 acts in inverse direction (Bour et al, 2011). CoQ10 treatment increases fat oxidation and energy consumption in adipose tissue.…”