Journal
DIABETES OBESITY & METABOLISM
Volume 18, Issue 10, Pages 955-961Publisher
WILEY
DOI: 10.1111/dom.12697
Keywords
antidiabetic drug; DPP-IV inhibitor; drug mechanism; GLP-1; incretin therapy; metformin
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Funding
- NNF Center for Basic Metabolic Research [Holst Group] Funding Source: researchfish
- Novo Nordisk Fonden [NNF16OC0020224, NNF12OC1015904, NNF15OC0016230] Funding Source: researchfish
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Metformin is an oral antihyperglycaemic drug used in the first-line treatment of type 2 diabetes. Metformin's classic and most well-known blood glucose-lowering mechanisms include reduction of hepatic gluconeogenesis and increased peripheral insulin sensitivity. Interestingly, intravenously administered metformin is ineffective and recently, metformin was shown to increase plasma concentrations of the glucose-lowering gut incretin hormone glucagon-like peptide-1 (GLP-1), which may contribute to metformin's glucose-lowering effect in patients with type 2 diabetes. The mechanisms behind metformin-induced increments in GLP-1 levels remain unknown, but it has been hypothesized that metformin stimulates GLP-1 secretion directly and/or indirectly and that metformin prolongs the half-life of GLP-1. Also, it has been suggested that metformin may potentiate the glucose-lowering effects of GLP-1 by increasing target tissue sensitivity to GLP-1. The present article critically reviews the possible mechanisms by which metformin may affect GLP-1 levels and sensitivity and discusses whether such alterations may constitute important and clinically relevant glucose-lowering actions of metformin.
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