Table 1. Histopathology evaluations link time exposure and dose concentration dependent increases in exocrine pancreatic injury to exenatide treatments.

Categories of individualinjury	Mean Category and Cumulative Histopathology Score of Injury in Exenatide Treated Mice(0–3 range for each category)
	3 weeks, EXE				6 weeks, EXE				12 weeks, EXE
	0 µg(n = 12)	3 µg(n = 10)	10 µg(n = 10)	30 µg(n = 10)	0 µg(n = 10)	3 µg(n = 11)	10 µg(n = 12)	30 µg(n = 12)	0 µg(n = 12)	3 µg(n = 11)	10 µg(n = 11)	30 µg(n = 12)
Acinar cell hypertrophy	0.7	0.6	1.3	1.1	0.7	1.2	1.3	1.6	0.6	1.9	2.0	2.6
Acinar cell autophagy	0.8	0.9	1.2	1.1	0.9	1.4	1.4	2.0	0.6	1.6	1.6	2.5
Acinar cell apoptosis	1.1	1.0	1.1	1.1	1.0	1.6	1.5	2.1	1.1	2.0	2.1	2.5
Acinar cell necrosis	0.0	0.1	0.1	0.4	0.0	0.1	0.3	0.8	0.0	0.5	0.6	1.8
Vascularinjury	0.0	0.3	0.0	0.0	0.1	0.1	0.2	0.1	0.0	0.1	0.4	1.6
Interstitial inflammatory edema	0.9	0.9	1.2	1.0	0.6	0.2	1.0	0.8	0.8	0.3	2.5	2.8
Fat necrosis	0.0	0.1	0.0	0.0	0.0	0.1	0.2	0.0	0.0	0.3	0.3	2.5
Duct changes	0.3	0.4	0.6	0.6	0.7	1.0	1.3	1.5	0.5	1.8	2.0	2.8
Acinar cell atrophy	0.2	0.8	0.5	0.6	0.2	1.2	1.9	2.7	0.5	2.5	2.8	2.9
Group Mean Scores of combined all Injuries	4.0	5.3	6.0	5.9	4.2	6.9*	8.8*	11.0*	4.0	12.8*	14.5*	18.6*

µg = microgram per kg dose of exenatide for treatment group; weeks = the weeks of daily subcutaneous exenatide injections; *indicates significant difference (p<0.05) from control.