Control of Gluconeogenesis by Metformin: Does Redox Trump Energy Charge?

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 utili...

Full description

Saved in:
Bibliographic Details
Published inCell metabolism Vol. 20; no. 2; pp. 197 - 199
Main Authors Baur, Joseph A., Birnbaum, Morris J.
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 05.08.2014
Subjects
Animals
Gluconeogenesis - drug effects
Glycerolphosphate Dehydrogenase - antagonists & inhibitors
Humans
Male
Metformin - pharmacology
Mitochondria - enzymology
Online AccessGet full text
ISSN1550-4131
1932-7420
1932-7420
DOI10.1016/j.cmet.2014.07.013

Cover

More Information
Summary: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). 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).
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
ObjectType-Commentary-3
content type line 23
ISSN:1550-4131
1932-7420
1932-7420
DOI:10.1016/j.cmet.2014.07.013