Dmitri Kirpichnikov, MD; Samy I. McFarlane, MD; James R. Sowers, MD
Acknowledgments: The authors thank Jun Ren, PhD; Amy Davidoff, PhD; and Jacob Peuler, PhD, for their seminal contribution to work on the cardiovascular effects of metformin.
Grant Support: By the National Institutes of Health (RO1-HL-63904-01), the Veterans Affairs Merit Review, and the American Diabetic Association.
Requests for Single Reprints: James R. Sowers, MD, State University of New York Health Science Center at Brooklyn, 450 Clarkson Avenue, Box 1205, Brooklyn, NY 11203; e-mail, firstname.lastname@example.org.
Current Author Addresses: Drs. Kirpichnikov, McFarlane, and Sowers: State University of New York Health Science Center at Brooklyn, 450 Clarkson Avenue, Box 1205, Brooklyn, New York 11203.
Metformin is an insulin-sensitizing agent with potent antihyperglycemic properties. Its efficacy in reducing hyperglycemia in type 2 diabetes mellitus is similar to that of sulfonylureas, thiazolidinediones, and insulin. Metformin-based combination therapy is often superior to therapy with a single hypoglycemic agent. The antihyperglycemic properties of metformin are mainly attributed to suppressed hepatic glucose production, especially hepatic gluconeogenesis, and increased peripheral tissue insulin sensitivity. Although the precise mechanism of hypoglycemic action of metformin remains unclear, it probably interrupts mitochondrial oxidative processes in the liver and corrects abnormalities of intracellular calcium metabolism in insulin-sensitive tissues (liver, skeletal muscle, and adipocytes) and cardiovascular tissue.
Kirpichnikov D, McFarlane SI, Sowers JR. Metformin: An Update. Ann Intern Med. 2002;137:25–33. doi: 10.7326/0003-4819-137-1-200207020-00009
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Published: Ann Intern Med. 2002;137(1):25-33.
Cardiology, Coronary Risk Factors, Diabetes, Endocrine and Metabolism, Updates.
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