Glukosereabsorption

Glukosereabsorption, or glucose reabsorption, is the kidney's process of reclaiming filtered glucose from the tubular fluid and returning it to the bloodstream. Under normal conditions, nearly all filtered glucose is reabsorbed in the proximal tubule of the nephron, preventing urinary loss.

The reabsorption is mediated primarily by two sodium-glucose cotransporters. SGLT2, located in the early proximal tubule (S1 and S2 segments), reabsorbs the majority of filtered glucose. SGLT1, found in the late proximal tubule (S3 segment), handles the remaining glucose with high affinity but lower capacity. Glucose then exits the tubular epithelial cells on the basolateral side through facilitative transporters, mainly GLUT2, and enters the peritubular capillaries. The process relies on the sodium gradient maintained by Na+/K+-ATPase activity in the basolateral membrane, making glucose reabsorption a secondary active transport phenomenon.

Renal glucose reabsorption exhibits a threshold: when plasma glucose levels exceed about 180 mg/dL (roughly 10 mmol/L), the transporters become saturated and glucose appears in the urine (glucosuria). This threshold can shift in certain physiological and pathological states.

Clinical relevance includes genetic and pharmacological modulation of the transporters. Mutations in SLC5A2, encoding SGLT2, cause familial renal glycosuria with typically mild symptoms. Pharmacologic SGLT2 inhibitors reduce proximal tubule glucose reabsorption, increasing urinary glucose excretion and lowering plasma glucose, a strategy used in type 2 diabetes management. Glukosereabsorption remains a fundamental example of how organ systems regulate energy substrates through coordinated transporter activity.