A 38-year-old woman with type 1 diabetes for 15 years has well-controlled glucose on basal-bolus insulin but significant postprandial hyperglycemia and weight gain of 5 kg over a year. Pramlintide is considered as adjunctive therapy. Pramlintide exerts its glucose-lowering effect by which mechanism?
- A Activating GLP-1 receptors to enhance glucose-dependent insulin secretion
- B Inhibiting sodium-glucose cotransporter 2 in the proximal renal tubule
- C Replacing endogenous amylin to slow gastric emptying and suppress glucagon secretion ✓
- D Activating PPAR-gamma to improve peripheral insulin sensitivity
Correct answer: C. Replacing endogenous amylin to slow gastric emptying and suppress glucagon secretion
Explanation
Pramlintide is a synthetic amylin analog. Endogenous amylin is co-secreted with insulin by beta cells. Pramlintide slows gastric emptying, suppresses postprandial glucagon secretion, and promotes satiety. It does not activate GLP-1 receptors (A), inhibit SGLT2 (B), or activate PPAR-gamma (D).
Reference: Goodman and Gilman's The Pharmacological Basis of Therapeutics, 14th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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