Phosphoinositide hydrolysis and insulin release in fetal rat islets.
The association between phosphoinositide hydrolysis and insulin release in fetal islets was investigated. Islets from 21.5-day-old fetal rats were cultured for 7 days in inositol-free RPMI 1640 containing 11.1 mM glucose and labeled with 20 microCi/ml [3H]inositol for the final 2 days. The labeled islets were then perifused under various conditions for 60 min. Glucose (16.7 mM) caused a modest increase in [3H] efflux from labeled islets, but there was a subsequent fall-off in [3H] efflux. Fetal islets showed the first phase of insulin release without the continued rising second phase. When islets were perifused with 5 mM LiCl, the glucose-induced efflux of [3H] was greatly reduced, whereas glucose-induced insulin release was not affected. A pronounced effect of LiCl was an increase in inositol monophosphate, indicating increased phospholipase C activity. Although marked release of [3H] from labeled islets occurred in the presence of 5 mM inositol, the decreases in radioactive inositol lipid and insulin release induced by glucose were not changed. These data suggest that the fall-off in the second phase of insulin release from fetal islets may be partly due to blunted phosphoinositide hydrolysis.
Tanigawa
K
K
Department of Medicine, Northwestern University Medical School, Chicago, Illinois.
Lewis
N J
NJ
D000818:Animals; D046508:Culture Techniques; D005333:Fetus / Q000502:physiology; D006868:Hydrolysis; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000378:metabolism*; D010716:Phosphatidylinositols / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley
D007328:Insulin; D010716:Phosphatidylinositols