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. 2016 Jan 6;65(4):981–995. doi: 10.2337/db15-0529

Figure 2.

Figure 2

Glucose-induced proliferation in mouse islets does not require the insulin receptor (IR). A–L: IR blockers S961 (A–F; 100 nmol/L added 120 min before glucose or insulin [100 nmol/L] stimulation) or HNMPA (G–L; 10 μmol/L added 60 min before glucose stimulation) prevented activation of insulin signaling 2 min after glucose treatment (whole islets, n = 4; A and B and G and H) but did not prevent the glucose-induced increase in PCNA abundance after 72 h of glucose treatment (whole islets, n = 3–4; C and D and I and J) or the glucose-induced increase in the percent of β-cells incorporating BrdU (dispersed islets, n = 4–8; E and F and K and L). Adenovirus expressing an shRNA targeting the mouse IR (MOI 50) in dispersed islets reduced IR expression 72 h after glucose exposure (n = 5; M and N) but did not prevent the glucose-induced increase in PCNA abundance (n = 5; O and P) or β-cell BrdU incorporation (n = 4; Q and R). Arrows point to BrdU-positive β-cell nuclei. Data are mean ± SEM. *P < 0.05, **P < 0.01 vs. 15 mmol/L glucose control condition (marked by dotted line); #P < 0.05 vs. 5 mmol/L control. gluc, glucose; ns, not significant; p, phosphorylated; tot, total; veh, vehicle.