Figure 122

Physiology and pathophysiology of glucose titration curves. Under normal physiologic conditions, filtered glucose is almost entirely reabsorbed in the proximal tubule by way of two distinct sodium-coupled glucose transport systems. In the S1 and S2 segments, bulk reabsorption of glucose load occurs by way of a kidney-specific high-capacity transporter, the sodium-glucose transporter-2 (SGLT2) [1]. The residual glucose is removed from the filtrate in the S3 segment by way of the high-affinity sodium-glucose transporter-1 (SGLT1) [2]. This transporter also is present in the small intestine.

As are all membrane transport systems, glucose transporters are saturable. The top panel shows that increasing the glucose concentration in the tubular fluid accelerates the transport rate of the glucose transporters until a maximal rate is achieved. The term threshold applies to the point that glucose first appears in the urine. The maximal overall rate of glucose transport by the proximal tubule SGLT1 and SGLT2 is termed the Tmax. Glucose is detected in urine either when the filtered load is increased (as in diabetes mellitus) or, as shown in the bottom panel, when a defect occurs in tubular reabsorption (as in renal glucosuria). Kinetic studies have demonstrated two types of glucosuria caused by either reduced maximal transport velocity (type A) or reduced affinity of the transporter for glucose (type B) [3]. Mutations in the gene encoding SGLT1 cause glucose-galactose malabsorption syndrome, a severe autosomal recessive intestinal disorder associated with mild renal glucosuria (type B). Defects in SGLT2 result in a comparatively more severe renal glucosuria (type A). However, this disorder is clinically benign. Among members of the basolateral glucose transporter (GLUT) family, only GLUT1 and GLUT2 are relevant to renal physiology [4]. Clinical disorders associated with mutations in the genes encoding these transporters have yet to be described. (From Morris and Ives [5]; with permission.)

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