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. Author manuscript; available in PMC: 2010 Apr 1.
Published in final edited form as: Diabetes Res Clin Pract. 2009 Jan 31;84(1):19–26. doi: 10.1016/j.diabres.2008.12.014

FIG. 2.

FIG. 2

FIG. 2

A. Insulin secretion to glucose and arginine in the in situ-perfused pancreas. During the first part of each experiment, the perfusate glucose concentration was increased progressively from 2 to 26 mM. The mean insulin output by pancreata of 10-wk HNF-1α (+/−)/RIP-Tag mice (H1A (+/−)-Tag) (closed squares, n = 5) was significantly less than that from age-matched HNF-1α (+/+)/RIP-Tag mice (H1A (+/+)-Tag) (open squares, n = 5) in response to glucose (P<0.005). (insert) Thereafter, in the continued presence of 26 mM glucose, 20 mM arginine was added to the perfusate (solid black bar). [Inset] The mean insulin output in response to arginine was also significantly less from 10-wk HNF-1α (+/−)/RIP-Tag mice (H1A (+/−)-Tag) compared to age-matched HNF-1α (+/+)/RIP-Tag mice (H1A (+/+)-Tag) (P<0.005). B. Measurements of intracellular calcium mobilization in perifused islets. Changes in intracellular calcium in response to a progressive increase in perfusate glucose from 2 to 26 mM are shown. Thin line: HNF-1α (+/−)/RIP-Tag mice (H1A (+/−)-Tag, n = 4); thick line: HNF-1α (+/+)/RIP-Tag mice (H1A (+/+)-Tag, n = 3). C: Summary of area under the intracellular calcium response curve. Results from HNF-1α (+/+)/RIP-Tag islets (white bars) and HNF-1α (+/−)/RIP-Tag islets (black bars) are depicted. Data are means ± SEM. P<0.05 compared to HNF-1α (+/+)/RIP-Tag islets.