XXXX and glucagon secretory responses to @entity369 , glucagon, and @entity2544 during perifusion of @entity1 fetal @entity14380 .

@entity1 @entity268 @entity2544 @entity14380 @entity2690 @entity369 @entity413
The secretory responsiveness of @entity1 fetal pancreatic endocrine cells was studied by perifusion of cultured @entity14380 ( @entity14380 ). @entity14380 were obtained from 7 fetuses at 13-15 weeks gestation and 21 fetuses at 17-22 weeks gestation. The @entity14380 were challenged with @entity413 (20 mmol/L), @entity369 (10 mmol/L), glucagon (1.4 mumol/L), and @entity2544 (10 mmol/L) combined with zero, low (2 mmol/L), or high (20 mmol/L) @entity413 . At 13-15 weeks, @entity413 and @entity369 enhanced @entity2690 release in some experiments, whereas glucagon and @entity2544 were always potent stimuli (mean response, 4-fold regardless of the @entity413 concentration). At 17-22 weeks, both @entity413 alone (20 mmol/L) and @entity369 (10 mmol/L, with 2 mmol/L @entity413 ) induced a small (1.4- to 1.5-fold) increase in @entity2690 release. When @entity369 was combined with 20 mmol/L @entity413 , the response was potentiated to become a 2.3-fold increase. In contrast, glucagon was equally effective in 2 and 20 mmol/L @entity413 (2.9- and 2.6-fold responses, respectively) and produced a half-maximal response even in the absence of @entity413 . In this age range the most potent stimulus for @entity2690 release was clearly @entity2544 . The effect of @entity2544 was also remarkably independent of the @entity413 concentration of the perifusate (5.6-, 8.1-, and 8.6-fold responses at 0, 2, and 20 mmol/L @entity413 , respectively). Glucagon release from the @entity14380 of the 17- to 22-week-old fetuses was low (mean basal glucagon release, 2.9; @entity2690 , 24.8 fmol/100 @entity14380 /min). Glucagon release was not affected by 20 mmol/L @entity413 , but was stimulated by @entity369 and @entity2544 . These findings suggest that in the fetal pancreas, in contrast to the adult organ, @entity2690 release results from elevation of intracellular @entity268 concentrations (by glucagon or @entity2544 ) relatively independent of the exogenous @entity413 concentration. Therefore, glucagon may have an important role in regulating @entity2690 release during the early development of @entity1 fetal B-cells.
