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Cell Metab. 2014 Aug 5;20(2):197-9. doi: 10.1016/j.cmet.2014.07.013.

Control of gluconeogenesis by metformin: does redox trump energy charge?

Author information

1
Institute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA; Department of Physiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Electronic address: baur@mail.med.upenn.edu.
2
Institute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Electronic address: birnbaum@mail.med.upenn.edu.

Abstract

Metformin is the most widely prescribed drug to lower glucose in type II diabetics, yet its mechanism of action remains controversial. A new study reveals that metformin inhibits mitochondrial glycerol-3-phosphate dehydrogenase, triggering reduction of the cytosolic NADH/NAD(+) pool and impaired utilization of redox-dependent substrates for gluconeogenesis (Madiraju et al., 2014).

PMID:
25100057
PMCID:
PMC4154964
DOI:
10.1016/j.cmet.2014.07.013
[Indexed for MEDLINE]
Free PMC Article

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