ARMA identification

Alengrin, G.; Bucy, R. S.; Moura, M. F.; Pagès, Jaume; Ribeiro, M. Isabel

doi:10.1007/bf00941173

Cited by 6 publications

(1 citation statement)

References 3 publications

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“…The pyruvate-kinase flux is dependent on the ATP concentration. Wollen and Bailey (1988a) and Alengrin et al (1987) did not find a change in the ATP concentration, although a change was observed in this study. This discrepancy could be related to the experimental procedure, i.e.…”

Section: Dihydroxyacetonecontrasting

confidence: 69%

Metformin decreases gluconeogenesis by enhancing the pyruvate kinase flux in isolated rat hepatocytes

Argaud

Roth

Wiernsperger

et al. 1993

European Journal of Biochemistry

144

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Metformin (dimethylbiguanide) has been used for more than 30 years as an antihyperglycemic agent in the treatment of diabetes mellitus, but its effect on gluconeogenesis is still controversial. In isolated hepatocytes from fasted rats, a significant inhibition of glucose production from lactate/ pyruvate (10: 1, mol/mol), fructose, alanine or glutamine, following metformin addition, is observed. Moreover, in hepatocytes perifused with dihydroxyacetone as the gluconeogenic substrate and treated with 0.5 mM metformin, an inhibition of the glucose flux and a simultaneous stimulation of the lactate/pyruvate flux were observed. This enhancement of lactate/pyruvate formation appears to be due to an effect on the pyruvate-kinase enzyme. A direct effect of metformin on pyruvate kinase cannot explain this result, since pyruvate-kinase activity was not affected by metformin at this concentration. In contrast, the addition of metformin caused a significant decrease in the cellular ATP concentration, a known allosteric inhibitor of this enzyme. This could explain the stimulation of pyruvate-kinase activity following metformin addition and thus the inhibition of gluconeogenesis.

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Section: Dihydroxyacetonecontrasting

confidence: 69%