Document Detail


Biguanides suppress hepatic glucagon signalling by decreasing production of cyclic AMP.
MedLine Citation:
PMID:  23292513     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Glucose production by the liver is essential for providing a substrate for the brain during fasting. The inability of insulin to suppress hepatic glucose output is a major aetiological factor in the hyperglycaemia of type-2 diabetes mellitus and other diseases of insulin resistance. For fifty years, one of the few classes of therapeutics effective in reducing glucose production has been the biguanides, which include phenformin and metformin, the latter the most frequently prescribed drug for type-2 diabetes. Nonetheless, the mechanism of action of biguanides remains imperfectly understood. The suggestion a decade ago that metformin reduces glucose synthesis through activation of the enzyme AMP-activated protein kinase (AMPK) has recently been challenged by genetic loss-of-function experiments. Here we provide a novel mechanism by which metformin antagonizes the action of glucagon, thus reducing fasting glucose levels. In mouse hepatocytes, metformin leads to the accumulation of AMP and related nucleotides, which inhibit adenylate cyclase, reduce levels of cyclic AMP and protein kinase A (PKA) activity, abrogate phosphorylation of critical protein targets of PKA, and block glucagon-dependent glucose output from hepatocytes. These data support a mechanism of action for metformin involving antagonism of glucagon, and suggest an approach for the development of antidiabetic drugs.
Authors:
Russell A Miller; Qingwei Chu; Jianxin Xie; Marc Foretz; Benoit Viollet; Morris J Birnbaum
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2013-01-06
Journal Detail:
Title:  Nature     Volume:  494     ISSN:  1476-4687     ISO Abbreviation:  Nature     Publication Date:  2013 Feb 
Date Detail:
Created Date:  2013-02-14     Completed Date:  2013-03-12     Revised Date:  2013-04-16    
Medline Journal Info:
Nlm Unique ID:  0410462     Medline TA:  Nature     Country:  England    
Other Details:
Languages:  eng     Pagination:  256-60     Citation Subset:  IM    
Affiliation:
Institute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.
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MeSH Terms
Descriptor/Qualifier:
AMP-Activated Protein Kinases / metabolism
Adenylate Cyclase / metabolism
Animals
Biguanides / pharmacology*
Cells, Cultured
Cyclic AMP / biosynthesis,  metabolism*
Cyclic AMP-Dependent Protein Kinases / metabolism
Diabetes Mellitus, Type 2 / drug therapy
Enzyme Activation / drug effects
Glucagon / antagonists & inhibitors*,  metabolism*
Glucose / metabolism
Hepatocytes / drug effects*,  metabolism*
Hypoglycemic Agents
Liver / cytology,  drug effects,  metabolism
Metformin / pharmacology,  therapeutic use
Mice
Phenformin / pharmacology
Phosphorylation
Signal Transduction / drug effects*
Grant Support
ID/Acronym/Agency:
P01 DK049210/DK/NIDDK NIH HHS; P01 DK49210/DK/NIDDK NIH HHS; P30 DK19525/DK/NIDDK NIH HHS; R01 DK056886/DK/NIDDK NIH HHS; R01 DK56886/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Biguanides; 0/Hypoglycemic Agents; 114-86-3/Phenformin; 50-99-7/Glucose; 60-92-4/Cyclic AMP; 657-24-9/Metformin; 9007-92-5/Glucagon; EC 2.7.11.1/AMP-Activated Protein Kinases; EC 2.7.11.11/Cyclic AMP-Dependent Protein Kinases; EC 4.6.1.1/Adenylate Cyclase
Comments/Corrections
Comment In:
Nat Rev Endocrinol. 2013 Mar;9(3):132   [PMID:  23358356 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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