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氧化应激、胰岛素抵抗、血脂异常与2型糖尿病

Oxidative stress, insulin resistance, dyslipidemia and type 2 diabetes mellitus.

作者信息

Tangvarasittichai Surapon

机构信息

Surapon Tangvarasittichai, Chronic Disease Research Unit, Department of Medical Technology, Faculty of Allied Health Sciences, Naresuan University, Phitsanulok 65000, Thailand.

出版信息

World J Diabetes. 2015 Apr 15;6(3):456-80. doi: 10.4239/wjd.v6.i3.456.

Abstract

Oxidative stress is increased in metabolic syndrome and type 2 diabetes mellitus (T2DM) and this appears to underlie the development of cardiovascular disease, T2DM and diabetic complications. Increased oxidative stress appears to be a deleterious factor leading to insulin resistance, dyslipidemia, β-cell dysfunction, impaired glucose tolerance and ultimately leading to T2DM. Chronic oxidative stress, hyperglycemia and dyslipidemia are particularly dangerous for β-cells from lowest levels of antioxidant, have high oxidative energy requirements, decrease the gene expression of key β-cell genes and induce cell death. If β-cell functioning is impaired, it results in an under production of insulin, impairs glucose stimulated insulin secretion, fasting hyperglycemia and eventually the development of T2DM.

摘要

氧化应激在代谢综合征和2型糖尿病(T2DM)中增加,这似乎是心血管疾病、T2DM和糖尿病并发症发生发展的基础。氧化应激增加似乎是导致胰岛素抵抗、血脂异常、β细胞功能障碍、糖耐量受损并最终导致T2DM的有害因素。慢性氧化应激、高血糖和血脂异常对β细胞尤其危险,因为β细胞抗氧化剂水平最低、氧化能量需求高、关键β细胞基因的基因表达降低并诱导细胞死亡。如果β细胞功能受损,就会导致胰岛素分泌不足,损害葡萄糖刺激的胰岛素分泌,导致空腹血糖升高,并最终发展为T2DM。

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