Metformin suppresses glucose-6-phosphatase expression by a complex I inhibition and AMPK activation-independent mechanism

S Ota, K Horigome, T Ishii, M Nakai, K Hayashi… - Biochemical and …, 2009 - Elsevier
S Ota, K Horigome, T Ishii, M Nakai, K Hayashi, T Kawamura, A Kishino, M Taiji, T Kimura
Biochemical and biophysical research communications, 2009Elsevier
Metformin is widely used as a hypoglycemic agent for the treatment of type 2 diabetes. Both
metformin and rotenone, an inhibitor of respiratory chain complex I, suppressed glucose-6-
phosphatase (G6pc), a rate limiting enzyme of liver glucose production, mRNA expression in
a rat hepatoma cell line accompanied by a reduction of intracellular ATP concentration and
an activation of AMP-activated protein kinase (AMPK). When yeast NADH-quinone
oxidoreductase 1 (NDI1) gene was introduced into the cells, neither inhibition of ATP …
Metformin is widely used as a hypoglycemic agent for the treatment of type 2 diabetes. Both metformin and rotenone, an inhibitor of respiratory chain complex I, suppressed glucose-6-phosphatase (G6pc), a rate limiting enzyme of liver glucose production, mRNA expression in a rat hepatoma cell line accompanied by a reduction of intracellular ATP concentration and an activation of AMP-activated protein kinase (AMPK). When yeast NADH-quinone oxidoreductase 1 (NDI1) gene was introduced into the cells, neither inhibition of ATP synthesis nor activation of AMPK was induced by these agents. Interestingly, in contrast to rotenone treatment, G6pc mRNA down-regulation was observed in the NDI1 expressing cells after metformin treatment. Since NDI1 can functionally complement the complex I under the presence of metformin or rotenone, our results indicate that metformin induces down-regulation of G6pc expression through an inhibition of complex I and an activation of AMPK-independent mechanism.
Elsevier