title: Lipid peroxidation is not a prerequisite for the development of obesity and diabetes in high-fat-fed mice.
abstract: The mechanism, by which a high-fat (HF) diet could impair glucose metabolism, is not completely understood but could be related to inflammation, lipotoxicity and oxidative stress. Lipid peroxides have been proposed as key mediators of intracellular metabolic response. The purpose of the present study was to analyse, in mice fed with a HF diet, the possible association between obesity and glucose tolerance on the one hand, and between oxidative stress and lipid peroxidation on the other hand. The present results show that a HF diet (70 % energy as fat), v. a high-carbohydrate chow diet (control), increases body weight and fat mass development, and impairs glycaemia and insulinaemia within 4 weeks. It also promotes the expression of NADPH oxidase in the liver--signing both oxidative and inflammatory stress--but decreases thiobarbituric acid-reactive substances content in the liver as well as in epididymal, subcutaneous and visceral adipose tissues. HF diet, with elevated vitamin E content, induces high concentration of alpha-tocopherol in liver and adipose tissues, which contributes to the protection against lipid peroxidation. Thus, lipid peroxidation in key organs is not necessarily related to the development of metabolic disorders associated with diabetes and obesity.
authors.affiliation: Unit of Pharmacokinetics, Metabolism, Nutrition and Toxicology, Louvain Drug Research Institute, Université catholique de Louvain, Avenue E. Mounier 73/69, Brussels, Belgium.
authors.forename: Florence M
authors.initials: FM
authors.lastname: Sohet
authors.forename: Audrey M
authors.initials: AM
authors.lastname: Neyrinck
authors.forename: Evelyne M
authors.initials: EM
authors.lastname: Dewulf
authors.forename: Laure B
authors.initials: LB
authors.lastname: Bindels
authors.forename: Laurence
authors.initials: L
authors.lastname: Portois
authors.forename: Willy J
authors.initials: WJ
authors.lastname: Malaisse
authors.forename: Yvon A
authors.initials: YA
authors.lastname: Carpentier
authors.forename: Patrice D
authors.initials: PD
authors.lastname: Cani
authors.forename: Nathalie M
authors.initials: NM
authors.lastname: Delzenne
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism; D000818:Animals; D000975:Antioxidants / Q000032:analysis; D015415:Biomarkers / Q000032:analysis; D003920:Diabetes Mellitus / Q000276:immunology / Q000378:metabolism*; D004041:Dietary Fats / Q000009:adverse effects*; D019587:Dietary Supplements; D005227:Fatty Acids / Q000032:analysis; D007249:Inflammation; D007333:Insulin Resistance; D015227:Lipid Peroxidation / Q000502:physiology*; D008055:Lipids / Q000032:analysis; D008099:Liver / Q000737:chemistry / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D019255:NADPH Oxidases / Q000032:analysis / Q000235:genetics; D009765:Obesity / Q000378:metabolism*; D018384:Oxidative Stress; D012333:RNA, Messenger / Q000032:analysis; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000379:methods; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis; D014810:Vitamin E / Q000008:administration & dosage; D014815:Vitamins / Q000008:administration & dosage; D024502:alpha-Tocopherol / Q000032:analysis
chemical_list: D000975:Antioxidants; D015415:Biomarkers; D004041:Dietary Fats; D005227:Fatty Acids; D008055:Lipids; D012333:RNA, Messenger; D017392:Thiobarbituric Acid Reactive Substances; D014815:Vitamins; D014810:Vitamin E; D019255:NADPH Oxidases; D024502:alpha-Tocopherol