Control of gluconeogenesis by metformin: does redox trump energy charge?
editorial · Level V
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- Record sourced from PubMed, PMID 25100057.
- Also identified by DOI 10.1016/j.cmet.2014.07.013 and PMC identifier 4154964.
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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).
Medical subject headings
- Gluconeogenesis
- Glycerolphosphate Dehydrogenase
- Metformin
- Mitochondria