Diabetes mellitus (DM), an important public health problem worldwide, can cause imbalances in the homeostasis of trace elements such as zinc (Zn). It is possible that an adequate nutritional status related to nutrients is essential for the normal functioning of antioxidant defense systems, and any change in the concentration of these substances could increase the chances of DM complications. To present a review on the effect of zinc supplementation on glycemic control and oxidative stress in experimental diabetes. This is a systematic review of articles that investigated the effects of zinc supplementation on glycemic control and oxidative stress in diabetic rats. The PICOS strategy was used for the development of the research question, and the Syrcle tool for the quality assessment of the studies included in the review. Articles available in the PubMed, Scopus, and Web of Science databases were included without restriction on year of publication. The Syrcle tool was used to assess the risk of bias of the included studies. Fifteen studies were included in the review, seven of which evaluated glycemic control and oxidative stress after zinc supplementation, five only oxidative stress and three only glycemic control after zinc treatment. In all the studies included, diabetes was induced by the administration of streptozotocin (STZ) at doses ranging from 40 to 100mg/kg. Zinc supplementation was made in the diet or drinking water or by gavage or intraperitoneal injection. The most used doses were 100mg/kg of body weight by gavage and 0.32 and 0.64g/kg in diet. The supplementation period ranged from 14 days to 8 weeks. Six studies revealed that zinc supplementation decreased fasting blood glucose as well as insulin resistance; nine studies included in this review reported decreased MDA concentration; in five studies, there was an increase in the activity of antioxidant enzymes (GPx, SOD, GSH and catalase); and one of the studies reported a reduction in glycated hemoglobin. Zinc supplementation improved hyperglycemia and revealed a protective potential against oxidative stress associated with experimental diabetes.