Add time:07/13/2019         Source:sciencedirect.com

Pirogliride, a new orally active hypoglycemic agent, was shown to be an effective inhibitor of renal and hepatic gluconeogenesis in isolated rat kidney cortex slices, hepatocytes and perfused liver. The inhibition was concentration dependent (0.1–1.0 mM), with 1.0 mM pirogliride producing virtually total inhibition. The previously reported inhibitors of gluconeogenesis, cyclopropanecarboxylic acid and phenformin, were slightly less potent than pirogliride, while 3-mercaptopicolinic acid was at least ten times more potent. Unlike phenformin, pirogliride did not stimulate ketogenesis and did inhibit gluconeogenesis regardless of its apparent effects on the redox state. While the mechanism responsible for the inhibition of gluconeogenesis requires further study, several pieces of evidence point to a decrease of the ATP/ADP ratio, possibly secondary to an effect on the respiratory chain. Inhibition of gluconeogenesis, however, does not appear to be the primary mechanism responsible for the hypoglycemic action of pirogliride. While pretreatment of fasted rats with either 3-mercaptopicolinic acid or pirogliride produced hypoglycemia, only 3-mercaptopicolinic acid lowered the gluconeogenic capacity of kidney cortex slices incubated in vitro and inhibited the appearance of [14C]glucose in the blood following intraperitoneal injection of [3-14C]pyruvate.

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