Sulfonylurea drugs stimulate insulin secretion from pancreatic beta cells even when ambient glucose is low, producing hypoglycemia as their chief adverse effect. Their molecular site of action is:
- A Inhibition of glucokinase, slowing glucose phosphorylation
- B Activation of GLP-1 receptors, raising intracellular cAMP
- C Binding to the SUR1 regulatory subunit of the KATP channel, closing the channel independently of ATP ✓
- D Blockade of potassium efflux through voltage-gated Kv channels
Correct answer: C. Binding to the SUR1 regulatory subunit of the KATP channel, closing the channel independently of ATP
Explanation
Sulfonylureas bind the SUR1 regulatory subunit of the beta-cell ATP-sensitive potassium channel and close it directly, bypassing the need for ATP generated by glucose metabolism. Channel closure depolarizes the membrane, opens voltage-gated calcium channels, and triggers insulin exocytosis regardless of glucose level, hence the risk of hypoglycemia. They neither inhibit glucokinase nor engage incretin receptors, and voltage-gated Kv channels are not the target.
Reference: Katzung Basic and Clinical Pharmacology, 16th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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