Inactivation of UCP1 and the glycerol phosphate cycle synergistically increases energy expenditure to resist diet-induced obesity.

摘要: Our current paradigm for obesity assumes that reduced thermogenic capacity increases susceptibility to obesity, whereas enhanced protects against obesity. Here we report elimination of two major pathways encoded by the mitochondrial uncoupling protein (Ucp1) and glycerol-3-phosphate dehydrogenase (Gdm) result in mice with increased resistance diet-induced when housed at 28 °C, provided prior adaptation occurred 20 °C. Obesity resistant Gdm-/-·Ucp1-/- maintained °C have energy expenditure, part through conversion white brown adipocytes inguinal fat. Increased oxygen consumption fat cell suspensions up-regulation genes function metabolism indicated activity, despite absence UCP1, liver skeletal muscle showed no changes gene expression. Additionally, comparisons expenditure UCP1-deficient wild type fed an obesogenic diet indicates UCP1-based fat-based thermogenesis plays role so-called thermogenesis. Accordingly, a new emerges which inactivation force induction alternative increase metabolic inefficiency.