Zinc plays a key role in the synthesis and action on insulin both physiologically and in the pathologic state of diabetes. Hyperglycemia from either type I or type II diabetes causes physiologically important losses of zinc from the body. These losses may worsen the underlying diabetes, but are probably not responsible as the causal agent. The complications of diabetes may be mediated, at least in part, through oxidative stress, and zinc plays a key role in the cellular antioxidative defense. If there is insufficient zinc, oxidative stress may damage the cell irreversibly, producing or exacerbating some of the classic complications of diabetes. Studies consistently note that diabetic subjects are characterized by increased plasma copper compared with control subjects. It is of interest to note higher concentrations in diabetics with macro and microangiopathy or with altered lipid metabolism. There is growing but conflicting evidence of an association between selenium status and diabetes mellitus. In the urine, a positive association has been shown between HbA1c and urinary excretion of selenium, indicating that urinary selenium is inversely related to the degree of diabetes control. There is evidence that selenium could affect carbohydrate metabolism. Oral selenate improves glucose homeostasis and partly reverses abnormal expression of liver glycolytic (GK, LPK) and gluconeogenic enzymes (PEPCK) in diabetic rats. If there is a genuine biological role for these trace elements, why have clinicians shown only muted interest in their potential use as adjunct to therapy in diabetic patients? The answer must lie in the requirement for a genuine, demonstrable, biochemical effect that is either imitated or augmented by these trace elements. Until this can be clearly shown, their utilisation as an aid to improved glucose control will remain on the sidelines of clinical practice.