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首页> 外文期刊>The British Journal of Nutrition >Lipid peroxidation is not a prerequisite for the development of obesity and diabetes in high-fat-fed mice
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Lipid peroxidation is not a prerequisite for the development of obesity and diabetes in high-fat-fed mice

机译：脂质过氧化不是高脂喂养小鼠肥胖和糖尿病发展的先决条件

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摘要

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 l-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.
机译：高脂饮食可能损害葡萄糖代谢的机制尚不完全清楚，但可能与炎症，脂毒性和氧化应激有关。脂质过氧化物已被提议作为细胞内代谢反应的关键介质。本研究的目的是一方面分析用HF饮食喂养的小鼠中肥胖与葡萄糖耐量之间的关联，另一方面分析氧化应激与脂质过氧化之间的关联。目前的结果表明，HF饮食（以脂肪的70％能量）与高碳水化合物食物（对照）相比，增加了体重和脂肪量，并在4周内损害了血糖和胰岛素血症。它还能促进肝脏中NADPH氧化酶的表达-既能氧化也能抑制炎症反应-但会降低肝脏以及附睾，皮下和内脏脂肪组织中硫代巴比妥酸反应性物质的含量。 HF饮食中维生素E含量升高，会在肝脏和脂肪组织中诱导高浓度的l-生育酚，从而有助于防止脂质过氧化。因此，关键器官中的脂质过氧化不一定与糖尿病和肥胖症相关的代谢异常的发展有关。

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