1. Br J Nutr. 2009 Aug;102(3):462-9. Epub 2009 Jan 23.

Lipid peroxidation is not a prerequisite for the development of obesity and
diabetes in high-fat-fed mice.

Sohet FM, Neyrinck AM, Dewulf EM, Bindels LB, Portois L, Malaisse WJ, Carpentier 
YA, Cani PD, Delzenne NM.

Unit of Pharmacokinetics, Metabolism, Nutrition and Toxicology, Louvain Drug
Research Institute, Université catholique de Louvain, Avenue E. Mounier 73/69,
Brussels, Belgium.

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.

PMID: 19161640 [PubMed - indexed for MEDLINE]