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Increased glucose production through abnormally elevated hepatic gluconeogenesis is central to the onset of hyperglycaemia in type 2 diabetes patients. Metformin corrects hyperglycaemia through inhibition of gluconeogenesis, but its mechanism of action is yet to be fully described.

Caton et al. investigated whether metformin inhits gluconeogenic gene expression by modulating changes in hepatic SIRT1 and GCN5 in db/db mice or in cultured HepG2 cells. Their stubby shows that increases in GCN5 and SIRT1 potentially represent a mechanism by which metformin inhibits gluconeogenesis. In addition, they provide data to identify induction of hepatic GCN5 as a potential therapeutic strategy for treatment of type 2 diabetes. Caton et al., Journal of Endocrinology.

Read full article at DOI:10.1677/JOE-09-0345

Suppression of gluconeogenesis by Metformin

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