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Diabetes is closely associated with K + disturbances during disease progression and treatment. However, it remains unclear whether K + imbalance occurs in diabetes with normal kidney function. In this study, we examined the effects of dietary K + intake on systemic K + balance and renal K + handling in streptozotocin (STZ)-induced diabetic mice. The control and STZ mice were fed low or high K + diet for 7 days to investigate the role of dietary K + intake in renal K + excretion and K + homeostasis and to explore the underlying mechanism by evaluating K + secretion-related transport proteins in distal nephrons. K + -deficient diet caused excessive urinary K + loss, decreased daily K + balance, and led to severe hypokalemia in STZ mice compared with control mice. In contrast, STZ mice showed an increased daily K + balance and elevated plasma K + level under K + -loading conditions. Dysregulation of the NaCl cotransporter (NCC), epithelial Na + channel (ENaC), and renal outer medullary K + channel (ROMK) was observed in diabetic mice fed either low or high K + diet. Moreover, amiloride treatment reduced urinary K + excretion and corrected hypokalemia in K + -restricted STZ mice. On the other hand, inhibition of SGLT2 by dapagliflozin promoted urinary K + excretion and normalized plasma K + levels in K + -supplemented STZ mice, at least partly by increasing ENaC activity. We conclude that STZ mice exhibited abnormal K + balance and impaired renal K + handling under either low or high K + diet, which could be primarily attributed to the dysfunction of ENaC-dependent renal K + excretion pathway, despite the possible role of NCC. NEW & NOTEWORTHY Neither low dietary K + intake nor high dietary K + intake effectively modulates renal K + excretion and K + homeostasis in STZ mice, which is closely related to the abnormality of ENaC expression and activity. SGLT2 inhibitor increases urinary K + excretion and reduces plasma K + level in STZ mice under high dietary K + intake, an effect that may be partly due to the upregulation of ENaC activity.