二甲双胍
安普克
医学
胰岛素抵抗
血脂异常
2型糖尿病
炎症
内科学
糖尿病
药理学
葡萄糖摄取
内分泌学
胰岛素
蛋白激酶A
激酶
生物
细胞生物学
出处
期刊:Endocrine, metabolic & immune disorders
[Bentham Science]
日期:2015-08-27
卷期号:15 (3): 196-205
被引量:335
标识
DOI:10.2174/1871530315666150316124019
摘要
Metformin is an oral hypoglycemic agent which is most widely used as first-line therapy for type 2 diabetes. Metformin improves hyperglycemia by suppressing hepatic glucose production and increasing glucose uptake in muscle. Metformin also has been shown to reduce cardiovascular events in randomized controlled trials; however, the underlying mechanism remains to be established. Recent preclinical and clinical studies have suggested that metformin not only improves chronic inflammation through the improvement of metabolic parameters such as hyperglycemia, insulin resistance and atherogenic dyslipidemia, but also has a direct anti-inflammatory action. Studies have suggested that metformin suppresses inflammatory response by inhibition of nuclear factor κB (NFκB) via AMP-activated protein kinase (AMPK)-dependent and independent pathways. This review summarizes the basic and clinical evidence of the anti-inflammatory action of metformin and discusses its clinical implication.
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