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自助餐厅饮食会导致肥胖和胰岛素抵抗,与氧化应激有关,但与炎症无关:通过饮食补充甜瓜超氧化物歧化酶可以改善这种情况。

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

机构信息

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.

Nutrition & Métabolisme, UMR 204 NutriPass-Prévention des Malnutritions et des Pathologies Associées, Université Montpellier 1-2, 34095 Montpellier Cedex 05, France.

出版信息

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

DOI:10.1016/j.freeradbiomed.2013.06.022
PMID:23792771
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.

摘要

氧化应激与肥胖有关。然而,膳食抗氧化剂可以预防氧化应激引起的损伤。我们之前已经表明,一种瓜类超氧化物歧化酶(SODB)对氧化应激具有预防作用。然而,SODB 的作用机制尚不清楚。在这里,我们评估了 SODB 治疗性补充 1 个月对肥胖仓鼠肝脏的影响。金黄叙利亚仓鼠接受标准饮食或 cafeteria 饮食(由高脂肪、高糖和高盐的超市产品组成),共 15 周。这种饮食导致胰岛素抵抗和肝脏氧化应激增加。然而,炎症标志物(IL-6、TNF-α 和 NF-κB)并未增强,也未检测到肝脂肪变性,尽管这些标志物通常在肥胖诱导的胰岛素抵抗模型中描述。经过 1 个月的 SODB 补充后, cafeteria 饮食引起的体重增加和胰岛素抵抗得到减轻,肝氧化应激得到纠正。这可能是由于肝脏抗氧化防御蛋白(锰和铜/锌超氧化物歧化酶、过氧化氢酶和谷胱甘肽过氧化物酶)的表达增加所致。尽管肥胖仓鼠没有检测到炎症,但 SODB 补充后炎症标志物减少,可能是通过降低氧化应激。这些发现首次表明,SODB 通过诱导内源性抗氧化防御来发挥其抗氧化特性。需要进一步研究这种诱导的机制。

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