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

Joseph A Baur; Morris J Birnbaum

doi:10.1016/j.cmet.2014.07.013

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

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

Authors

Joseph A Baur¹, Morris J Birnbaum²

Affiliations

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).

Publication types

Comment

MeSH terms

Animals
Gluconeogenesis / drug effects*
Glycerolphosphate Dehydrogenase / antagonists & inhibitors*
Humans
Male
Metformin / pharmacology*
Mitochondria / enzymology*

Substances

Metformin
Glycerolphosphate Dehydrogenase

Grants and funding

P01 DK049210/DK/NIDDK NIH HHS/United States