Type II Diabetes Mellitus (T2DM) has quickly become one of the leading causes of morbidity in developed nations, believed to be mostly a result of modern lifestyles. The prevalence of T2DM has caused a demand for new treatments to help combat the disease in patients. AC3174 is a compound in a new class of drugs known as incretin mimetics. Compounds in this class mimic natural hormones in the body that produce antidiabetic effects. AC3174 shares some sequence homology with the endogenous endocrine hormone glucagon-like peptide-1 (GLP-1). These compounds are known to stimulate the pancreas to secrete insulin in response to food intake and therefore serve to maintain glucose homeostasis. GLP-1 can enhance β cell mass and function by activating β cell proliferation, stimulating islet cell neogenesis, and suppressing β cell apoptosis. The purpose of this study was to quantify the response of the male CD-1 mouse pancreas to a glucose challenge following exposure to a pancreatic toxicant following 12 weeks of daily AC3174 administration. The expectation was that treatment with AC3174 would increase the mass and function of the pancreas, and potentially provide a protective effect against the oxidative damage resulting from the alloxan insult. In contrast to the expectation, following treatment with the pancreatic toxicant alloxan blood sugar measurements revealed animals treated subcutaneously with AC3174 were less able to control their blood sugar levels than those treated with alloxan alone. Necropsy data also showed an apparent increase in damage to the pancreatic tissue of alloxan and AC3174 treated animals versus those treated with alloxan alone. The cause of this unexpected result may be related to the AC3174 treated β cells having a greater susceptibility to the damage caused by the toxicant due to the effects of withdrawal of AC3174 prior to the toxicant administration.