Metformin: Difference between revisions
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Metformin works primarily by reducing hepatic [[Gluconeogenesis|gluconeogensis]], ultimately lowering blood/sugar levels and preventing [[Hyperglycemia|hyperglycemia]]<ref>Kirpichnikov D, McFarlane SI, Sowers JR. Metformin: an update. Ann Intern Med. 2002;137(1):25–33. PMID 12093242</ref>.<br> | Metformin works primarily by reducing hepatic [[Gluconeogenesis|gluconeogensis]], ultimately lowering blood/sugar levels and preventing [[Hyperglycemia|hyperglycemia]]<ref>Kirpichnikov D, McFarlane SI, Sowers JR. Metformin: an update. Ann Intern Med. 2002;137(1):25–33. PMID 12093242</ref>.<br> | ||
Metformin has also shown to inhibit the growth of pancreatic cancer by disrupting crosstalk between [[G-protein Coupled Receptor|G protein-coupled receptors]] and insulin receptor signalling systems in the [[Pancreas|pancreas]]<ref>Krisztina Kisfalvi, Guido Eibl, James Sinnett-Smith, and Enrique Rozengurt. Cancer Res August 15, 2009 69; 6539</ref>. | Metformin has also shown to inhibit the growth of pancreatic cancer by disrupting crosstalk between [[G-protein Coupled Receptor|G protein-coupled receptors]] and insulin receptor signalling systems in the [[Pancreas|pancreas]]<ref>Krisztina Kisfalvi, Guido Eibl, James Sinnett-Smith, and Enrique Rozengurt. Cancer Res August 15, 2009 69; 6539</ref>. | ||
=== References === | |||
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Revision as of 07:06, 24 October 2013
Metformin is a drug used primarily to treat type II diabetes.
Metformin works primarily by reducing hepatic gluconeogensis, ultimately lowering blood/sugar levels and preventing hyperglycemia[1].
Metformin has also shown to inhibit the growth of pancreatic cancer by disrupting crosstalk between G protein-coupled receptors and insulin receptor signalling systems in the pancreas[2].
References