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高果糖饮食会诱发年轻雌性大鼠内脏脂肪组织发生炎症,并降低其抗氧化防御能力。

Fructose-enriched diet induces inflammation and reduces antioxidative defense in visceral adipose tissue of young female rats.

作者信息

Kovačević Sanja, Nestorov Jelena, Matić Gordana, Elaković Ivana

机构信息

Department of Biochemistry, Institute for Biological Research "Siniša Stanković", University of Belgrade, 142 Despot Stefan Blvd, Belgrade, 11060, Serbia.

出版信息

Eur J Nutr. 2017 Feb;56(1):151-160. doi: 10.1007/s00394-015-1065-0. Epub 2015 Oct 3.

DOI:10.1007/s00394-015-1065-0
PMID:26433940
Abstract

PURPOSE

The consumption of refined, fructose-enriched food continuously increases and has been linked to development of obesity, especially in young population. Low-grade inflammation and increased oxidative stress have been implicated in the pathogenesis of obesity-related disorders including type 2 diabetes. In this study, we examined alterations in inflammation and antioxidative defense system in the visceral adipose tissue (VAT) of fructose-fed young female rats, and related them to changes in adiposity and insulin sensitivity.

METHODS

We examined the effects of 9-week fructose-enriched diet applied immediately after weaning on nuclear factor κB (NF-κB) intracellular distribution, and on the expression of pro-inflammatory cytokines (IL-1β and TNFα) and key antioxidative enzymes in the VAT of female rats. Insulin signaling in the VAT was evaluated at the level of insulin receptor substrate-1 (IRS-1) protein and its inhibitory phosphorylation on Ser.

RESULTS

Fructose-fed rats had increased VAT mass along with increased NF-κB nuclear accumulation and elevated IL-1β, but not TNFα expression. The protein levels of antioxidative defense enzymes, mitochondrial manganese superoxide dismutase 2, and glutathione peroxidase, were reduced, while the protein content of IRS-1 and its inhibitory phosphorylation were not altered by fructose diet.

CONCLUSIONS

The results suggest that fructose overconsumption-related alterations in pro-inflammatory markers and antioxidative capacity in the VAT of young female rats can be implicated in the development of adiposity, but do not affect inhibitory phosphorylation of IRS-1.

摘要

目的

精制的、富含果糖的食物消费量持续增加,且已被证明与肥胖的发生有关,尤其是在年轻人群中。低度炎症和氧化应激增加与包括2型糖尿病在内的肥胖相关疾病的发病机制有关。在本研究中,我们检测了用果糖喂养的年轻雌性大鼠内脏脂肪组织(VAT)中炎症和抗氧化防御系统的变化,并将其与肥胖和胰岛素敏感性的变化相关联。

方法

我们检测了断奶后立即给予9周富含果糖饮食对雌性大鼠VAT中核因子κB(NF-κB)细胞内分布、促炎细胞因子(IL-1β和TNFα)表达以及关键抗氧化酶的影响。在胰岛素受体底物-1(IRS-1)蛋白水平及其丝氨酸残基的抑制性磷酸化水平评估VAT中的胰岛素信号传导。

结果

用果糖喂养的大鼠VAT质量增加,同时NF-κB核内积聚增加,IL-1β表达升高,但TNFα表达未升高。抗氧化防御酶、线粒体锰超氧化物歧化酶2和谷胱甘肽过氧化物酶的蛋白水平降低,而果糖饮食未改变IRS-1的蛋白含量及其抑制性磷酸化。

结论

结果表明,年轻雌性大鼠VAT中与果糖过度摄入相关的促炎标志物和抗氧化能力的改变可能与肥胖的发生有关,但不影响IRS-1的抑制性磷酸化。

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