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Free Radic Biol Med. 2013 Dec;65:254-261. doi: 10.1016/j.freeradbiomed.2013.06.022. Epub 2013 Jun 20.

Cafeteria diet induces obesity and insulin resistance associated with oxidative stress but not with inflammation: improvement by dietary supplementation with a melon superoxide dismutase.

Author information

1
Nutrition & Métabolisme, UMR 204 NutriPass-Prévention des Malnutritions et des Pathologies Associées, Université Montpellier 1-2, 34095 Montpellier Cedex 05, France; Bionov Sarl, Avignon, France.
2
Nutrition & Métabolisme, UMR 204 NutriPass-Prévention des Malnutritions et des Pathologies Associées, Université Montpellier 1-2, 34095 Montpellier Cedex 05, France.
3
Département de Biochimie, Centre Hospitalier Universitaire Montpellier, Université Montpellier 1, Montpellier, France.
4
INRA, UMR 866, Unité Différenciation Cellulaire et Croissance, Montpellier, France.
5
Bionov Sarl, Avignon, France.
6
Nutrition & Métabolisme, UMR 204 NutriPass-Prévention des Malnutritions et des Pathologies Associées, Université Montpellier 1-2, 34095 Montpellier Cedex 05, France; Département de Biochimie, Centre Hospitalier Universitaire Montpellier, Université Montpellier 1, Montpellier, France.
7
Nutrition & Métabolisme, UMR 204 NutriPass-Prévention des Malnutritions et des Pathologies Associées, Université Montpellier 1-2, 34095 Montpellier Cedex 05, France. Electronic address: jm.rouanet@univ-montp2.fr.

Abstract

Oxidative stress is involved in obesity. However, dietary antioxidants could prevent oxidative stress-induced damage. We have previously shown the preventive effects of a melon superoxide dismutase (SODB) on oxidative stress. However, the mechanism of action of SODB is still unknown. Here, we evaluated the effects of a 1-month curative supplementation with SODB on the liver of obese hamsters. Golden Syrian hamsters received either a standard diet or a cafeteria diet composed of high-fat, high-sugar, and high-salt supermarket products, for 15 weeks. This diet resulted in insulin resistance and in increased oxidative stress in the liver. However, inflammatory markers (IL-6, TNF-α, and NF-κB) were not enhanced and no liver steatosis was detected, although these are usually described in obesity-induced insulin resistance models. After the 1-month supplementation with SODB, body weight and insulin resistance induced by the cafeteria diet were reduced and hepatic oxidative stress was corrected. This could be due to the increased expression of the liver antioxidant defense proteins (manganese and copper/zinc superoxide dismutase, catalase, and glutathione peroxidase). Even though no inflammation was detected in the obese hamsters, inflammatory markers were decreased after SODB supplementation, probably through the reduction of oxidative stress. These findings suggest for the first time that SODB could exert its antioxidant properties by inducing the endogenous antioxidant defense. The mechanisms underlying this induction need to be further investigated.

KEYWORDS:

Antioxidant defense; Free radicals; Inflammatory markers; Insulin sensitivity; Obesity; Oxidative status

[Indexed for MEDLINE]

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