Perda e/ou ganho de massa corporal afeta estresse oxidativo e esteatose hepática em camundongos

Abstract

Nonalcoholic fatty liver disease (NAFLD) is emerging as the most common chronic liver condition in the Western world, due to its association with obesity. The objective of this study was to investigate the impact of changes in body mass on oxidative stress markers in livers of mice fed a high-fat (HF) diet and their association with liver function tests and structure, adiposity, glucose and lipid profile. Three-month-old male C57BL/6 mice were divided into four groups (n = 10, each): standard chow (SC, 10% of total energy from fat) during 16 weeks, high-fat diet (HF, 50% of total energy from fat) during 16 weeks, one group who changed the SC to the HF diet (SC-HF), and another group who changed the HF to the SC diet (HF-SC). In SC-HF and HF-SC groups, each diet period lasted for 8 weeks. The HF diet during 8 (SC-HF) and 16 weeks (HF) repressed mRNA levels and protein expression of anti-oxidants enzymes (superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase) in the liver. These groups also showed liver steatosis, affected liver function markers, and increased intra-abdominal and subcutaneous adiposity, and induced glucose intolerance and hypercholesterolemia compared to SC group, which could be reversed by body mass loss due to dietary intervention (HF-SC). Our findings demonstrate that diet-induced body mass loss is an important strategy to reduce intra-hepatic lipid accumulation and to improve its adverse metabolic effects, and part of this benefit may be conferred by a reduced hepatic oxidative stress.