Metformin is not just an antihyperglycaemic drug but also has protective effects on the vascular endothelium Review uri icon

Overview

MeSH Major

  • Cardiovascular Diseases
  • MicroRNAs

abstract

  • Metformin, a synthetic dimethyl biguanide, has been in clinical use for over 55 years and today is considered the first-choice drug for the treatment of type 2 diabetes used by an estimated 125 million people worldwide. Metformin is orally effective, not metabolized, excreted unchanged by the kidney, relatively free of side effects and well tolerated by the majority of patients. Of importance is that the United Kingdom Prospective Diabetes Study 20 year study of type 2 diabetics, completed in 1998, compared patients treated with insulin, sulfonylureas and metformin and concluded that metformin provided vascular protective actions. Cardiovascular disease is the primary basis for the high morbidity and mortality that is associated with diabetes and that metformin proved to be protective resulted in a dramatic increase in its use. The vascular protective actions of metformin are thought to be secondary to the anti-hyperglycaemic effects of metformin that are mediated via activation of AMP kinase and subsequent inhibition of hepatic gluconeogenesis, fatty acid oxidation as well as an insulin sensitizing action in striated muscle and adipose tissue. As reflected by a number of clinical studies patients treated with metformin also have improvement in endothelial function as measured by the use of plethysmography and measurement of flow-mediated vasodilatation. These data as well as data from animal studies are supportive that metformin has a direct protective action on the vascular endothelium. In this review article we discuss the pharmacology of metformin and critique the literature as to its cellular sites and mechanism(s) of action. This article is protected by copyright. All rights reserved.

publication date

  • January 2016

Research

keywords

  • Review

Identity

Language

  • eng

Digital Object Identifier (DOI)

  • 10.1111/apha.12644

PubMed ID

  • 26680745

Additional Document Info