Metformin increases AMP-activated protein kinase activity in skeletal muscle of subjects with type 2 diabetes.
By N. Musi, M. Hirshman, J. Nygren, M. Svanfeldt, P. Båvenholm, O. Rooyackers, Gaochao Zhou, J. Williamson, O. Ljunqvist, S. Efendić and 3 more. Diabetes, 2002
858 citations recorded by the source corpus.
Subfields: Molecular Biology, Physiology, Surgery
View Paper: https://www.semanticscholar.org/paper/012b3140305deeede07960e97afa19cb9b5bb951
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In Molecular Biology
- Michael Pollak
- Ralph DeFronzo
- Gerald I. Shulman
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- M. Karin
In Physiology
In Surgery
Citations in the corpus
- Upregulated NLRP3 Inflammasome Activation in Patients With Type 2 Diabetes (2012, background): “Earlier studies showed that treatment with metformin for 10 weeks significantly increased AMPK activity and Thr172 phosphorylation in skeletal muscle (38).”
- From the Triumvirate to the Ominous Octet: A New Paradigm for the Treatment of Type 2 Diabetes Mellitus (2009, background): “Since the TZDs work through the classic insulin signaling pathway (150,254), whereas metformin works through the AMP kinase pathway (255,256), combination therapy with a TZD plus metformin gives a completely additive effect to reduce the A1C (257–265), and hypoglycemia is not encountered because the”
- Metformin inhibits mammalian target of rapamycin-dependent translation initiation in breast cancer cells. (2007, background): “Because metformin is a drug used for the treatment of type 2 diabetes, the majority of studies focusing on the effects of metformin have been carried out in tissues involved in insulin signaling and metabolism, such as muscle, adipose tissue, and liver (20, 39, 40).”
- Cellular and Molecular Mechanisms of Metformin Action (2020, background): “Additionally, AMPK activity and phosphorylation was increased in muscle biopsies from patients with T2D following metformin treatment (72).”