An energetic tale of AMPK-independent effects of metformin

Metformin has become a mainstay in the modest therapeutic armamentarium for the treatment of the insulin resistance of type 2 diabetes mellitus. Although metformin functions primarily by reducing hepatic glucose output, the molecular mechanism mediating this effect had remained elusive until recentl...

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Vydáno v:	The Journal of clinical investigation Ročník 120; číslo 7; s. 2267 - 2270
Hlavní autoři:	Miller, Russell A., Birnbaum, Morris J.
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	United States American Society for Clinical Investigation 01.07.2010
Témata:	AMP-Activated Protein Kinases Biomedical research Carbohydrate Metabolism Care and treatment Cyclic adenylic acid Diabetes Mellitus, Type 2 - drug therapy Diabetes Mellitus, Type 2 - metabolism Gene expression Gene Expression - drug effects Genetic aspects Health aspects Hepatocytes - drug effects Hepatocytes - metabolism Humans Hypoglycemic Agents - metabolism Hypoglycemic Agents - pharmacology Hypoglycemic Agents - therapeutic use Insulin Resistance Liver - drug effects Liver - metabolism Metformin Metformin - metabolism Metformin - pharmacology Metformin - therapeutic use Physiological aspects Protein kinases Protein Kinases - metabolism Protein Kinases - pharmacology Signal Transduction - drug effects Type 2 diabetes United States
ISSN:	0021-9738, 1558-8238, 1558-8238
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Abstract	Metformin has become a mainstay in the modest therapeutic armamentarium for the treatment of the insulin resistance of type 2 diabetes mellitus. Although metformin functions primarily by reducing hepatic glucose output, the molecular mechanism mediating this effect had remained elusive until recently. Metformin impairs ATP production, activating the conserved sensor of nutritional stress AMP-activated protein kinase (AMPK), thus providing a plausible and generally accepted model for suppression of gluconeogenic gene expression and glucose output. In this issue of the JCI, Foretz et al. refute this hypothesis by showing that AMPK is dispensable for the effects of metformin on hepatic glucose output in primary hepatocytes; rather, their data suggest that the antidiabetic effects of metformin in the liver are mediated directly by reducing energy charge.
AbstractList	Metformin has become a mainstay in the modest therapeutic armamentarium for the treatment of the insulin resistance of type 2 diabetes mellitus. Although metformin functions primarily by reducing hepatic glucose output, the molecular mechanism mediating this effect had remained elusive until recently. Metformin impairs ATP production, activating the conserved sensor of nutritional stress AMP-activated protein kinase (AMPK), thus providing a plausible and generally accepted model for suppression of gluconeogenic gene expression and glucose output. In this issue of the JCI, Foretz et al. refute this hypothesis by showing that AMPK is dispensable for the effects of metformin on hepatic glucose output in primary hepatocytes; rather, their data suggest that the antidiabetic effects of metformin in the liver are mediated directly by reducing energy charge. Metformin has become a mainstay in the modest therapeutic armamentarium for the treatment of the insulin resistance of type 2 diabetes mellitus. Although metformin functions primarily by reducing hepatic glucose output, the molecular mechanism mediating this effect had remained elusive until recently. Metformin impairs ATP production, activating the conserved sensor of nutritional stress AMP-activated protein kinase (AMPK), thus providing a plausible and generally accepted model for suppression of gluconeogenic gene expression and glucose output. In this issue of the JCI, Foretz et al. refute this hypothesis by showing that AMPK is dispensable for the effects of metformin on hepatic glucose output in primary hepatocytes; rather, their data suggest that the antidiabetic effects of metformin in the liver are mediated directly by reducing energy charge.Metformin has become a mainstay in the modest therapeutic armamentarium for the treatment of the insulin resistance of type 2 diabetes mellitus. Although metformin functions primarily by reducing hepatic glucose output, the molecular mechanism mediating this effect had remained elusive until recently. Metformin impairs ATP production, activating the conserved sensor of nutritional stress AMP-activated protein kinase (AMPK), thus providing a plausible and generally accepted model for suppression of gluconeogenic gene expression and glucose output. In this issue of the JCI, Foretz et al. refute this hypothesis by showing that AMPK is dispensable for the effects of metformin on hepatic glucose output in primary hepatocytes; rather, their data suggest that the antidiabetic effects of metformin in the liver are mediated directly by reducing energy charge.
Audience	Academic
Author	Birnbaum, Morris J. Miller, Russell A.
AuthorAffiliation	The Institute for Diabetes, Obesity, and Metabolism, University of Pennsylvania, Philadelphia, Pennsylvania, USA
AuthorAffiliation_xml	– name: The Institute for Diabetes, Obesity, and Metabolism, University of Pennsylvania, Philadelphia, Pennsylvania, USA
Author_xml	– sequence: 1 givenname: Russell A. surname: Miller fullname: Miller, Russell A. – sequence: 2 givenname: Morris J. surname: Birnbaum fullname: Birnbaum, Morris J.
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/20577046$$D View this record in MEDLINE/PubMed
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Snippet	Metformin has become a mainstay in the modest therapeutic armamentarium for the treatment of the insulin resistance of type 2 diabetes mellitus. Although...
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SubjectTerms	AMP-Activated Protein Kinases Biomedical research Carbohydrate Metabolism Care and treatment Cyclic adenylic acid Diabetes Mellitus, Type 2 - drug therapy Diabetes Mellitus, Type 2 - metabolism Gene expression Gene Expression - drug effects Genetic aspects Health aspects Hepatocytes - drug effects Hepatocytes - metabolism Humans Hypoglycemic Agents - metabolism Hypoglycemic Agents - pharmacology Hypoglycemic Agents - therapeutic use Insulin Resistance Liver - drug effects Liver - metabolism Metformin Metformin - metabolism Metformin - pharmacology Metformin - therapeutic use Physiological aspects Protein kinases Protein Kinases - metabolism Protein Kinases - pharmacology Signal Transduction - drug effects Type 2 diabetes
Title	An energetic tale of AMPK-independent effects of metformin
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