FIG. 3.
In vitro isolated islet experiments demonstrate that G6pc2 deletion results in a leftward shift in the dose-response curve for GSIS. A and D: Schematics to explain the effect of G6pc2 deletion on the dose-response curve for GSIS. The model in A proposes that at submaximal glucose concentrations, insulin secretion from G6pc2 KO mouse islets will be enhanced relative to WT islets due to a leftward shift in the dose-response curve for GSIS. The model in D proposes that at high glucose concentrations, flux through glucokinase is much greater than flux through G6pc2 such that deletion of G6pc2 does not affect the Vmax of GSIS. B, C, and E: GSIS from and insulin content in isolated ∼13-week-old male WT and G6pc2 KO mouse islets were assayed in vitro as described in Research Design and Methods following stimulation with 5 (B), 11 (C), or 16.7 mmol/L (E) glucose. The results in B, C, and E show the mean insulin concentrations ± SEM determined using six (at 5 mmol/L) or three (at 11 and 16.7 mmol/L) independent islet preparations. The experiments shown in B, C, and E were done at separate times and because the actual level of insulin secretion can vary significantly between different islet preparations the level of secretion between the graphs is not directly comparable. *P < 0.05 vs. WT. IEQ, islet equivalents.