Mitochondrial dysfunction and oxidative damage in the brain of diet-induced obese rats but not in diet-resistant rats

Abstract

AimsIt has been suggested that obesity triggered by consuming a high-fat diet (HF) can account for oxidative damage and mitochondrial dysfunction. Thus, we aim to explore the oxidative stress and mitochondrial dysfunction detected in the brain of diet-induced obese (DIO) rats. Main methodsSprague–Dawley (SD) rats were fed either a HF diet or a normal-fat (NF) diet for 10weeks to obtain the control (CON), DIO and diet-resistant (DR) rats. d-Galactose was injected subcutaneously for 10weeks to establish oxidative stress model (MOD) rats. Then, the levels of total antioxidant capacity (T-AOC), lipid peroxidation (LPO), malondialdehyde (MDA), both in plasma and brain tissue, and catalase (CAT) in plasma were measured using enzymic assay kits and the levels of ghrelin, neuropeptide Y (NPY) and leptin in both plasma and brain tissue were measured by using enzyme-linked immunosorbent assay (ELISA) kits. Mitochondrial reactive oxygen species (ROS) formation in brain tissues was detected with 2, 7-dichlorofluorescein diacetate (DCFH2-DA) dyeing. The mitochondrial membrane potential (MMP) was measured with tetrachloro-tetraethyl benzimidazol carbocyanine iodide (JC-1) by a flow cytometer. Key findingsHF diet leads to an obese or DR state characterized by increased or decreased adiposity. The HF diet increased brain LPO, which was accompanied by lower ghrelin levels in DIO rats compared with DR rats. In addition, the increased mitochondrial ROS and lower MMP were detected in DIO rat comparing with DR rats. SignificanceThe current results demonstrated that mitochondrial dysfunction and oxidative damage in the brains of DIO rats, induced by HF diets, might be measurable.