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 1
Development of diabetes in Gck^+/– mice fed HF diet. (A and B) Body weight (A) and total weight of white adipose tissue (epididymal and retroperitoneal fat pads) (B) in wild-type and Gck^+/– mice after 20 weeks on a standard chow or HF diet (n = 17–20). (C) Cell size in epididymal white adipose tissue (n = 600–900). (D) Serum FFA levels (n = 8–10). (E) Insulin tolerance in wild-type and Gck^+/– mice after 4 weeks (left) and 20 weeks (right) on a standard chow or HF diet. Mice were given free access to food and then intraperitoneally injected with 0.75 mU of human insulin per gram body weight. n = 8 (standard chow–fed wild-type), 9 (HF diet–fed wild-type), 12 (standard chow–fed Gck^+/–), 14 (HF diet–fed Gck^+/–). (F and G) Glucose tolerance in wild-type and Gck^+/– mice after 4 and 20 weeks on standard chow or HF diet. (F) Plasma glucose levels. (G) Serum insulin levels. n = 12 (standard chow–fed wild-type), 13 (HF diet–fed wild-type, standard chow– and HF diet–fed Gck^+/–). (H) Insulin secretory index, defined as the ratio of insulin to glucose at 30 minutes after a glucose load. Values represent mean ± SEM. *P < 0.05; **P < 0.01.