Abstract
Methyl pyruvate, when tested at a 10 mM concentration, caused a rapid and sustained
increase of insulin release evoked by either 7.0 or 16.7 mM D-glucose in the isolated
perfused rat pancreas. Under these conditions, methyl pyruvate caused a modest and
biphasic stimulation of glucagon release. In anaesthetized fed rats, methyl pyruvate
(1.0 to 2.5 µmol/g body wt) given intravenously provoked a short-lived and dose-related
increase in plasma insulin concentration, but failed to affect plasma glucagon concentration.
D-glucose and methyl pyruvate, when injected together, acted additively upon insulin
release. The in vivo secretory response to methyl pyruvate was comparable in fed, overnight fasted and
2-d starved rats, and only slightly decreased in fed animals that were injected with
streptozotocin during the neonatal period. These results suggest that methyl pyruvate
could be used as an insulinotropic agent to bypass site-specific defects of D-glucose
metabolism in the B-cell, such as those found in starvation or non-insulin-dependent
diabetes mellitus.
Key words
Methyl Pyruvate - Insulin Secretion - Perfused Pancreas
