A 58-year-old man with heart failure on carvedilol develops worsening hyperglycemia. The mechanism by which carvedilol impairs glucose homeostasis differs from that of selective beta-1 blockers because carvedilol additionally blocks:
- A Alpha-2 adrenoceptors on pancreatic beta cells, inhibiting insulin release
- B Beta-3 adrenoceptors in adipose tissue, preventing lipolysis-linked glucose oxidation
- C Beta-2 adrenoceptors on skeletal muscle, reducing glucose uptake stimulation ✓
- D Alpha-1 adrenoceptors in the liver, promoting glycogen synthesis over gluconeogenesis
Correct answer: C. Beta-2 adrenoceptors on skeletal muscle, reducing glucose uptake stimulation
Explanation
Carvedilol is a non-selective beta-1/beta-2 and alpha-1 blocker. Beta-2 adrenoceptors on skeletal muscle normally stimulate glucose uptake and glycogen synthesis; blockade of beta-2 receptors therefore impairs insulin-stimulated glucose disposal, worsening glycemic control compared to selective beta-1 blockers. Beta-2 blockade also masks tachycardia and tremor as warning signs of hypoglycemia. Selective beta-1 blockers (metoprolol, bisoprolol) spare beta-2 receptors and are therefore preferred in diabetic heart-failure patients when possible.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
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