The action of metformin on the production of pro-inflammatory cytokines and insulin resistance (NF-kB signal pathway)
The objective of the present study was to estimate the role of the NF-kB signal pathway in the realization of the anti-inflammatory and insulin-synthesizing activities of metformin in the patients presenting with coronary heart disease (CHD) associated with metabolic syndrome (MS). It was shown that the introduction of a one-month course of metformin therapy in the combined treatment of CHD resulted in the decreased production of pro-inflammatory cytokines, such as IL-1-beta, IL-6, IL-8, and TNF-alpha. Simultaneously, the serum C-peptide level decreased. These effects of metformin were mediated through the NF-kB-signal pathway. It is concluded that the inclusion of metformin in the combined treatment of coronary heart disease in the patients with metabolic syndrome prevent activation of NF-kB under the influence of endogeneous pro-inflammatory cytokines.