Type 2 diabetes mellitus (DM-2) is a chronic disease characterized by disturbances in insulin action. Recent evidence suggests that environmental factors, such as nutrition, can play a profound role in modulating both the initiation and progression of the disease. One of the possible nutritional factors that may influence diabetic pathogenesis is zinc. Zinc is crucial to pancreatic insulin storage and animals deficient in zinc exhibit a higher degree of insulin resistance, impaired glucose tolerance, and reduced insulin secretion. The objective of this thesis was to investigate the effects of dietary zinc deficiency and zinc supplementation on diabetic parameters in db/db mice, a genetic model for DM-2. Weanling db/db mice and their lean littermate controls (db/m) were fed zinc deficient (dbZD or lnZD), zinc adequate control (dbC or lnC), or zinc supplemented (dbZS or lnZS) diets (3, 30, 300 ppm zinc, respectively) for 6 weeks. At 10 weeks of age, mice were assessed for zinc status (serum, femur, pancreas, kidney), serum (glucose, insulin) and urinary (glucose, protein, zinc) indices of diabetes, as well as skeletal muscle (gastrocnemius) insulin receptor concentrations and tyrosine kinase activity. (Abstract shortened by UMI.)