The prostaglandins system and insulin release. Studies with the isolated perfused rat pancreas.
Using the isolated perfused rat pancreas PGE2 (1 MUM and 10 muM) had no effect on basal or glucose (10 and 20 mM)-induced insulin release (IR). PGF2 alpha stimulated basal IR at 1 muM and inhibited IR at 10 muM. The glucose-induced IR was unaffected by this PG. Furosemide (5 and 10 mM) led to a monophastic IR at low glucose (glu) and to a potentiation of IR at high glu. Only high indomethacin (Indo) (50 microgram/ml) inhibited glu-induced IR. The stimulatory effect of furosemide on IR could not be inhibited by indomethacin. However mepacrine (0.1 mM) abolished the furosemide effect. Also glu-induced IR was inhibited by mepacrine. Acetylsalicylic acid (30 mg/100 ml) had no significant influence on glu-induced IR. These findings provide evidence that phospholipase activation rather than increased PG synthesis might primarily be involved in the secretory process of insulin.
D000818:Animals; D001241:Aspirin / Q000494:pharmacology; D005665:Furosemide / Q000494:pharmacology; D005947:Glucose / Q000494:pharmacology; D007213:Indomethacin / Q000494:pharmacology; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000378:metabolism*; D008297:Male; D011453:Prostaglandins / Q000502:physiology*; D011458:Prostaglandins E / Q000494:pharmacology*; D011460:Prostaglandins F / Q000494:pharmacology*; D011796:Quinacrine / Q000494:pharmacology; D051381:Rats
D007328:Insulin; D011453:Prostaglandins; D011458:Prostaglandins E; D011460:Prostaglandins F; D005665:Furosemide; D011796:Quinacrine; D005947:Glucose; D001241:Aspirin; D007213:Indomethacin