If a drug inhibits pancreatic beta-cell ATP-sensitive potassium (KATP) channels without affecting insulin receptor binding, which consequence follows regarding glucose homeostasis in a patient with insulin resistance?

💡 Explanation

Inhibiting KATP channels in pancreatic beta-cells causes membrane depolarization, leading to increased calcium influx and insulin secretion because these channels normally hyperpolarize the cell. Therefore, insulin secretion increases at baseline, rather than reducing GLUT4 translocation, which depends on insulin receptor signalling.

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