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- Title
Insulin Secretagogues, But Not Glucose, Stimulate an Increase in [Ca<sup>2+</sup>]<sub>i</sub> in the Fetal Human and Porcine β-Cell.
- Authors
WEINHAUS, ANTHONY J.; TABIIN, MUHAMMAD T.; PORONNIK, PHILIP; PALMA, CATALINA A.; COOK, DAVID I.; TUCH, BERNARD E.
- Abstract
Fetal pancreatic -cells release insulin poorly in response to glucose; however, the cellular mechanism for this is unknown. By using fura-2 to measure changes in the cytoplasmic free Ca2+ concentration in -cells, we examined human/porcine fetal islet-like cell clusters (ICCs) and human adult islets for the presence of functional K+ATP and voltage-activated Ca2+ ion channels. The effects of glucose, glyceraldehyde, leucine, KCl, and the channel effectors glipizide and BAY K8644 were studied. In fetal human/porcine ICCs and adult islets, KCl, glipizide, and BAY K8644 increased [Ca2+]i. Both glucose and glyceraldehyde increased [Ca2+]i in islets but had no effect on ICCs. Leucine increased [Ca2+]i in islets and porcine but not human ICCs. We hypothesize that the beneficial effect of leucine in fetal porcine, but not human ICCs, is attributable to time-dependent maturation of the -cells, because porcine ICCs examined were at 87% of the gestational period, and human ICCs were at 42%. Our data demonstrate that both K+ ATP and voltage-activated Ca2+ channels, required for glucose-stimulated increase in [Ca2+]i, are functional early in gestation. This suggests that the cause of the immaturity of fetal human/porcine -cells is at a more proximal step of glucose-induced metabolism than the channels on the cell surface.
- Publication
Journal of Clinical Endocrinology & Metabolism, 2003, Vol 88, Issue 6, p2753
- ISSN
0021-972X
- Publication type
Article
- DOI
10.1210/jc.2002-021542