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. 2008 Sep 5;118(10):3378–3389. doi: 10.1172/JCI34587

Figure 2. Chop-null mutation prevents hyperglycemia and glucose intolerance by maintaining insulin content and secretion in a HF diet–fed, STZ-treated nongenetic model of T2D.

Figure 2

Chop+/+ and Chop–/– mice were fed a 60% HF diet (HFD) for 5.5 weeks prior to administration of a dosage of 150 mg/kg STZ as described in Methods, and measurements were performed for up to 16 days after STZ with continued HF feeding. (A) Body weight. (B) Fed blood glucose levels. (C and D) Glucose tolerance measurements. Glucose tolerance was tested after HF diet alone for 5.5 weeks (C) and 4 days after STZ treatment and continued HF diet (D). (E and F) Fasting and refed blood glucose and serum insulin levels. Glucose and insulin measurements were taken 13 days after STZ treatment from mice that were fasted overnight and refed for 3.5 hour. (G–I) Serum was collected for measurement and mice were sacrificed for determination of pancreatic insulin content and histology 16 days after STZ administration. (G) Fed serum insulin levels, (H) pancreatic insulin content, and (I) islet morphology stained with H&E. Scale bars: 500 μm (top), 100 μm (bottom). (J) Insulin tolerance measurements. Insulin tolerance was tested 15 days after STZ treatment. *P < 0.05, **P < 0.01, ***P < 0.001.