title: Mitochondrial dysfunction and oxidative damage in the brain of diet-induced obese rats but not in diet-resistant rats.
abstract: OBJECTIVE
  It 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.
  
  
  METHODS
  Sprague-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.
  
  
  RESULTS
  HF 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.
  
  
  CONCLUSIONS
  The current results demonstrated that mitochondrial dysfunction and oxidative damage in the brains of DIO rats, induced by HF diets, might be measurable.
authors: School of Public Health, Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing 100069, China.
authors: Weiwei
authors: W
authors: Ma
authors: School of Public Health, Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing 100069, China.
authors: Linhong
authors: L
authors: Yuan
authors: School of Public Health, Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing 100069, China.
authors: Huanling
authors: H
authors: Yu
authors: School of Public Health, Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing 100069, China.
authors: Yuandi
authors: Y
authors: Xi
authors: School of Public Health, Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing 100069, China. Electronic address: xiaor22@ccmu.edu.cn.
authors: Rong
authors: R
authors: Xiao
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000032:analysis; D001921:Brain / Q000503:physiopathology*; D002374:Catalase / Q000378:metabolism; D059305:Diet, High-Fat / Q000009:adverse effects*; D004797:Enzyme-Linked Immunosorbent Assay; D054439:Ghrelin / Q000378:metabolism; D015227:Lipid Peroxidation / Q000502:physiology; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D028361:Mitochondrial Diseases / Q000209:etiology* / Q000473:pathology*; D009478:Neuropeptide Y / Q000378:metabolism; D009765:Obesity / Q000150:complications* / Q000209:etiology; D018384:Oxidative Stress / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D000975:Antioxidants; D054439:Ghrelin; D009478:Neuropeptide Y; D008315:Malondialdehyde; D002374:Catalase
keywords: Diet-induced obese rat; Diet-resistant rats; High-fat diet; Mitochondrial dysfunction; Oxidative damage