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.
Keywords: AMPK, anti-inflammatory effect, biguanide, NFκB, type 2 diabetes.
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