Wound healing does not always progress normally in people with diabetes, which can lead to chronic ulceration, recurring wounds and amputations. Mast cells are granular haematopoietic stem cell-derived leukocytes known to participate in the inflammation, proliferation and maturation phases of cutaneous wound healing. The few studies that examine the influence of diabetes on mast cells are contradictory, and the effect of diabetes on mast cells in the absence of wounds is unknown. We hypothesised that diabetes influences cutaneous mast cell maturation, survival and function, eventually contributing to delayed wound healing in some people with diabetes. We examined the effect of streptozotocin-induced diabetes (4x65mg/kg STZ, i.p.) on mast cell density in murine skin (n = 6/group) and observed that mast cells were preserved after a long duration (15 weeks) of diabetes compared to age matched controls. To investigate the mechanism of this finding, we examined the effect of hyperglycaemia on the differentiation, survival and function of bone marrow-derived mast cells (BMMC) in vitro. High glucose culture conditions (25 mmol/L) had no effect on maturation or survival of mast cells determined by flow cytometry. However, functional analysis by β‑hexosaminidase assay indicates that high glucose conditions reduce the sensitivity of BMMC to stimulation with Compound 48/80 compared to osmolarity control (13.16 vs 26.33, p < 0.05). The preservation of mast cells observed in our murine model does not seem to be a direct effect of hyperglycaemia on mast cell maturation. However, our results suggest that hyperglycaemia alters mast cell sensitivity to stimulation, which could contribute to their preservation in skin and eventually to delayed wound healing. Our future studies will continue to investigate the mechanisms of altered mast cell density in diabetic skin and how cutaneous mast cell density and function can be modulated to improve wound healing in people with diabetes.