Empagliflozin reduces cardiovascular mortality in type 2 diabetes independent of its glycaemic effect. The primary renal mechanism responsible for its glucose-lowering action is:
- A Inhibition of glucokinase in pancreatic beta cells, reducing insulin secretion in a glucose-dependent manner
- B Competitive inhibition of SGLT-2 co-transporters in the proximal convoluted tubule, reducing renal glucose reabsorption ✓
- C Activation of GLP-1 receptors in the kidney, promoting natriuresis and glycosuria
- D Blockade of GLUT-2 transporters in the proximal tubule brush border, preventing glucose reabsorption
Explanation
SGLT-2 inhibitors (gliflozins) block the sodium-glucose co-transporter 2 in the S1 segment of the proximal convoluted tubule, which is responsible for approximately 90% of filtered glucose reabsorption. This causes glucosuria, lowering blood glucose independently of insulin, and also promotes natriuresis. GLUT-2 is the facilitated transporter allowing glucose to enter the cell from the tubular lumen after SGLT-2-mediated uptake — it is not the primary drug target.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
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Written and medically reviewed by the StethoPrep medical team.