Diabetes induces remodeling in K+ currents in mouse ventricular myocytes. a Representative voltage-gated K+ currents and IK1 traces in normoglycemia and hyperglycemia in streptozotocin (STZ)-induced T1DM, high-fat diet (HFD)-induced T2DM, and db/db mouse myocytes. b–g Decreases of K+ currents in DM vs. corresponding controls: vehicle-injection for STZ, low-fat diet (LFD) for HFD and C57BLKS/J for db/db. Hyperglycemia further reduced Ito and increased IK1 in STZ (and all controls), but not in HFD and db/db. h Representative IK1 traces measured at – 150 mV in STZ-treated WT, O-GlcNAc-resistant CaMKIIδ-S280A knock-in, and vehicle-treated WT control. i The decrease in IK1 density was markedly attenuated in STZ-treated CaMKIIδ-S280A. j The cell capacitance correlated with the decrease in IK1 density in STZ-treated WT, whereas no correlation was found in WT control and STZ-treated CaMKIIδ-S280A. Lines indicate linear regression. Two-way ANOVA; *p < 0.05, **p < 0.01, ***p < 0.001 vs. normoglycemia; †p < 0.05, ††p < 0.01, †††p < 0.001 vs. control