Figure 2.

Deletion of Pin1 in pancreatic β cells reduced insulin secretion and exacerbated glucose intolerance. A, expressions of Pin1 protein in various tissues of control and βPin1 KO mice. B, Pin1 mRNA levels in isolated islets from control and βPin1 KO mice (n = 5). C and D, immunostaining with anti-insulin, anti-glucagon, or anti-Pin1 antibody in pancreatic sections from control and βPin1 KO mice. E, blood glucose levels in fasted and 1-h re-fed states of 10-week-old male mice fed chow diets (n = 6–9). F, glucose tolerance tests on normal diet-fed mice. Glucose (2 g/kg) was intraperitoneally injected into 8-week-old male mice after they had been fasted overnight (n = 6). G, plasma insulin levels after stimulation with glucose. Mice were fasted overnight and then injected with glucose solution (2 g/kg) (n = 6). H, insulin tolerance tests on 7-week-old male mice fed a normal diet. Insulin solution (0.75 IU/kg) was intraperitoneally injected into the mice after they had been fasted for 4 h (n = 6–8). I, glucose tolerance tests on mice fed the HFHS diet for 14 weeks (n = 6). J, insulin tolerance tests on mice fed the HFHS diet for 15 weeks (n = 6). *, p < 0.05; **, p < 0.01; ***, p < 0.001; n.s., not significant. Representative data from two (A, C, and D) or three independent experiments (B and E–J) are shown. IB, immunoblotting; Error bars, S.E.