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. 2014 Oct 31;28(12):2038–2048. doi: 10.1210/me.2014-1207

Figure 2.

Figure 2.

Glucose homeostasis in RIP-HGF TG mice with IRS2 deficiency. TG/KO mice displayed significantly increased body weight (A), significantly decreased nonfasting blood glucose (B), and significantly increased plasma insulin (C) at 12 weeks of age compared with those of KO mice. Results are means ± SEM and were obtained from 5 to 7 mice per genotype. *, P < .05 vs the other 3 groups of mice; #, P < .05 vs WT and TG. D–F, intraperitoneal glucose tolerance test (D), area under the curve (AUC) calculated from these experiments (E), and ITT represented as percentage of the blood glucose value at time 0 minutes (F). Blood glucose values at time 0 minutes in the ITT experiment were as follows: WT mice, 151 ± 4; KO mice, 490 ± 18; TG mice, 134 ± 8; and TG/KO mice, 236 ± 16 mg/dL. Results are means ± SEM for WT (n = 7), TG (n = 6), KO (n = 6), and TG/KO (n = 5) mice at 12 weeks of age. *, P < .05 vs the other 3 groups of mice; #, P < .05 vs WT and TG; ∧, P < .05 vs WT. G, GSIS performed in groups of 20 islets of similar sizes obtained from female WT (n = 4) and IRS2 KO (n = 4) mice, transduced with Adv.GFP or Adv.HGF and incubated for 30 minutes with 5 or 20 mM glucose. Experiments were performed in triplicate. Results are means ± SEM. *, P < .05 vs 5 mM glucose; #, P < .05 vs the same genotype-GFP at 20 mM glucose.

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