Cardiovascular effects of metformin: focus on adipose tissue metabolism

Abstract

This review is devoted to the analysis of data on the study of the possible effect of metformin on the endocrine function of adipose tissue: the synthesis and secretion of adipocyte hormones – adipokines (leptin, adiponectin, resistin) and the gastrointestinal system (ghrelin). metformin is a biguanide class of hypoglycemic drugs used as a first-line therapy for the correction of carbohydrate metabolism. Currently, there has been a significant increase in interest in the pleiotropic cardioprotective and antiatherogenic properties of metformin. The molecular mechanisms of action of metformin on carbohydrate and lipid metabolism in adipose tissue are shown in the example of isolated adipocytes (in vitro) and in a living organism (in vivo). The key enzyme regulation in metformin action is с-AMPactivated protein kinase (AMPK). Activation of this enzyme blocks fatty acid synthesis, activates lipolysis and fatty acid oxidation; inhibits glucose production in the liver, reducing the expression of AMP-stimulated genes of enzymes of gluconeogenesis, increases insulin sensitivity, which ultimately contributes to the reduction of glucose. However, the dose-dependent effects of metformin are not well understood, there is no data on the long-term effects of the drug on the metabolism of adipose tissue, which requires careful attention to the study of this issue. Overall, metformin seems to be a promising drug to combat hyperglycemia, and dyslipidemia in diabetes mellitus type 2 and obesity, and for the prevention of cardiovascular risks associated with these diseases.

Keywords

• metformin
• adipose tissue
• cardiovascular pleiotropic effects