Metformin and Inflammation: Its Potential Beyond Glucose-lowering Effect
Metformin and Inflammation: Its Potential Beyond Glucose-lowering Effect
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DOI：
10.2174/1871530315666150316124019
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发表时间：
2015-01-01
影响因子：
1.9
通讯作者：
Saisho, Yoshifumi
中科院分区：
文献类型：
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作者：
Saisho, Yoshifumi
二甲双胍是一种口服降糖药，最广泛用于2型糖尿病的一线治疗。二甲双胍通过抑制肝脏葡萄糖的产生和增加肌肉对葡萄糖的摄取来改善高血糖。在随机对照试验中，二甲双胍也被证明可以减少心血管事件；然而，潜在的机制仍有待确定。最近的临床前和临床研究表明，二甲双胍不仅通过改善高血糖、胰岛素抵抗和致动脉粥样硬化性血脂等代谢参数来改善慢性炎症，而且还具有直接的抗炎作用。研究表明，二甲双胍通过AMPK依赖和非依赖途径抑制核因子-kappaB，从而抑制炎症反应。本文综述了二甲双胍抗炎作用的基础和临床证据，并讨论了其临床意义。
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 kappa B (NF kappa B) 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.