Figure 6. Glibenclamide-dependent C-peptide release is restored only in K_ATP-GOF insulin-treated mice.

(A) Insulin secretion from islets isolated from control and K_ATP-GOF untreated and insulin-treated mice (70 days after tamoxifen, ~40 days on insulin therapy). Islets were incubated in low (1mM) and high (23mM) glucose, and in the presence of the sulfonylurea glibenclamide (1μM) or the depolarizing agent KCl (30mM). Significant differences ^#p<0.05 with respect to control under the same condition and *p<0.05 with respect to 1mM glucose within the same group. (B) Plasma C-peptide (individual values) 30 min. after glibenclamide stimulation in control (30 days after Tx: black circles; 40 days after Tx: black squares, and 70 days after Tx: black triangles), K_ATP-GOF untreated 30 days after tamoxifen injection (white, 30 days after Tx, 30d) and K_ATP-GOF treated with insulin for 10 days (10d insulin, total 40 days after Tx, light pink) and 40 days (40d insulin, total 70 days after Tx, dark pink), mice. (C) Delta plasma C-peptide in response to glibenclamide in K_ATP-GOF untreated (white) and K_ATP-GOF insulin-treated (10 and 40 days, light and dark pink, respectively), mice (n=5-9 mice per group, experiments made in triplicates, mean + SEM). Significant differences *p<0.05 with respect to K_ATP-GOF untreated mice.