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用热氧化单不饱和脂肪配制的高果糖饮食加重大鼠结肠上皮组织的代谢失调。

A High-Fructose Diet Formulated with Thermally Oxidized Monounsaturated Fat Aggravates Metabolic Dysregulation in Colon Epithelial Tissues of Rats.

作者信息

Narayanankutty Arunaksharan, Kuzhivelil Balu T, Raghavamenon Achuthan C

机构信息

Department of Biochemistry, Amala Cancer Research Centre (Recognized Centre of University of Calicut), Thrissur, Kerala, India.

Department of Zoology, Applied Biochemistry and Biotechnology Laboratory, Christ College, University of Calicut, Irinjalakuda, Kerala, India.

出版信息

J Am Nutr Assoc. 2022 Jan;41(1):38-49. doi: 10.1080/07315724.2020.1846145. Epub 2020 Dec 1.

DOI:10.1080/07315724.2020.1846145
PMID:33259276
Abstract

BACKGROUND

Various epidemiological and clinical studies have indicated a positive association of colon cancer with high sugar and thermally oxidized fats consumption. The present study evaluated the effects of fresh and thermally oxidized coconut (CO) and mustard oils (MO) along with a high-sugar diet in the rat colon mucosa.

METHODS

The animals were fed with a modified diet containing high-fructose and different edible oils as fatty acids sources over a period of 30 weeks. Further, the development of insulin resistance and hyperglycemia were estimated biochemically. The changes in the redox status were estimated in terms of reduced glutathione (GSH), antioxidant enzymes and thiobarbituric acid reactive substances (TBARS). Changes in the expression of genes associated with inflammation and cell proliferation were evaluated by qPCR.

RESULTS

The animals fed with high-fructose developed hyperglycemia and insulin resistance over 30 weeks. These animals had diminished GSH level, SOD activity and a concomitant increase in the TBARS level in the colon epithelial tissues. In addition, the expression of pro-inflammatory cytokines (IL-6 and TNF-α) was elevated while P53 and PPARγ were down-regulated. This heightened body metabolic dysregulation and associated oxidative damage and inflammation in the colon were exacerbated by thermally oxidized edible oils incorporated in the diet, with a more prominent effect was observed with TMO.

CONCLUSION

Feeding high-fructose diet with TMO increases the oxidative and inflammatory damages in the colon epithelium of Wistar rats. Therefore, the study cautions the prolonged consumption of thermally oxidized monounsaturated fat-rich edible oils, especially by individuals with type 2 diabetes.

摘要

背景

多项流行病学和临床研究表明,结肠癌与高糖及热氧化脂肪的摄入呈正相关。本研究评估了新鲜椰子油(CO)和热氧化椰子油以及芥子油(MO)与高糖饮食对大鼠结肠黏膜的影响。

方法

在30周的时间里,给动物喂食含有高果糖和不同食用油作为脂肪酸来源的改良饮食。此外,通过生化方法评估胰岛素抵抗和高血糖的发展情况。根据还原型谷胱甘肽(GSH)、抗氧化酶和硫代巴比妥酸反应性物质(TBARS)来评估氧化还原状态的变化。通过qPCR评估与炎症和细胞增殖相关基因的表达变化。

结果

喂食高果糖的动物在30周内出现了高血糖和胰岛素抵抗。这些动物结肠上皮组织中的GSH水平降低,超氧化物歧化酶(SOD)活性降低,同时TBARS水平升高。此外,促炎细胞因子(IL-6和TNF-α)的表达升高,而P53和过氧化物酶体增殖物激活受体γ(PPARγ)下调。饮食中添加的热氧化食用油加剧了这种身体代谢失调以及结肠中相关的氧化损伤和炎症,其中热氧化芥子油(TMO)的影响更为显著。

结论

喂食高果糖饮食并添加TMO会增加Wistar大鼠结肠上皮的氧化和炎症损伤。因此,该研究提醒人们要谨慎长期食用富含热氧化单不饱和脂肪的食用油,尤其是2型糖尿病患者。

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