Rosuvastatina melhora a intolerância à glicose, doença gordurosa não alcoólica do fígado e distribuição do tecido adiposo em camundongos C57BL/6 alimentados com uma dieta rica em lipídios

Abstract

Colocar a parte do ingles Our aim was to evaluate if rosuvastatin (HMG-CoA reductase inhibitor) modulates carbohydrate and lipid metabolism, non-alcoholic fatty liver disease (NAFLD), and body mass gain in a model of diet-induced obesity. Male C57Bl/6 mice (3-months-old) were fed with a high-fat diet (HF, 60% lipids) or a standard chow (SC, 10% lipids) for 15 weeks. After, they were treated with rosuvastatin at 10 mg/Kg/day (HF-R10 group), 20 mg/Kg/day (HF-R20), or 40 mg/Kg/day (HF-R40) for five weeks. The HF diet led to glucose intolerance, insulin resistance, weight gain, increased visceral adiposity with adipocyte hypertrophy, and hepatic steatosis (micro and macrovesicular). Rosuvastatin treatment decreased adiposity and adipocyte size in HF-R10 and HF-R20 groups. In addition, rosuvastatin changed the pattern of fat distribution in HF-R40 group, since more fat was stored subcutaneously compared with visceral depots. This redistribution improved fast glucose and glucose intolerance. Rosuvastatin also restored liver morphology and ultrastructure dose-dependently. In conclusion, rosuvastatin exerted pleiotropic effects by improving glucose intolerance, insulin sensitivity and NAFLD in a dose-dependent manner, and it also changed fat distribution from visceral to the subcutaneous fat depot in a mouse model of diet-induced obesity.