Glucokinase and IRS-2 are required for compensatory β cell hyperplasia in response to high-fat diet–induced insulin resistance
J. Clin. Invest. Yasuo Terauchi, et al. 117:246 doi:10.1172/JCI17645 [Go to this article.]

Figure 3
Decreased insulin secretion and glucose oxidation in Gck^+/– islets. (A) Static incubation study of islets from wild-type and Gck^+/– mice after 4 weeks on standard chow or HF diet. Static incubation of 10 islets/tube was performed at 37°C for 1 hour with various glucose concentrations after preincubation with a 2.8-mM glucose concentration for 20 minutes. Results are shown as pg insulin/cell/h (n = 4). (B) Gck and hexokinase (HK) activity of islets. Glucose phosphorylation activity was assessed in pancreatic islets from wild-type and Gck^+/– mice after 20 weeks on standard chow or HF diet. Results are shown as mol/kg DNA/h (n = 16–20). (C) Glucose oxidation by pancreatic islets from wild-type and Gck^+/– mice after 20 weeks on standard chow or HF diet. Results are shown as mol/kg DNA/h (n = 10). *P < 0.05; **P < 0.01.