Common reabsorption system of 1,5-anhydro-d-glucitol, fructose, and mannose in rat renal tubule

SLC5A9/SGLT4, a new Na+-dependent glucose transporter, is an essential transporter for mannose, 1,5-anhydro-D-glucitol, and fructose

“…Its serum level is maintained as low as that of Man (Pitkanen, 1996) by metabolization in the liver, kidney, and intestine (Gitzelmann et al, 1995), and at least to some extent by a renal reabsorption transporter (Yamanouchi et al, 1996). It has been reported that an increased blood Fru level is associated both with diabetes (Kawasaki et al, 2002) and with diabetic retinopathy (Kawasaki et al, 2004).…”

“…The renal common transport system for Man and 1,5AG has been shown to exist in vivo (Pitkanen and Pitkanen, 1992). In addition, it has been suggested that D-fructose (Fru) is a common substrate for the renal Man/1,5AG reabsorption system (Yamanouchi et al, 1996). The inhibition of the renal reabsorption of 1,5AG by urinary Glc is thought to be the major mechanism responsible for the reduction in plasma 1,5AG seen in patients with diabetes (Pitkanen, 1990;Yamanouchi et al, 1992).…”

Identification of phlorizin binding domains in sodium-glucose cotransporter family: SGLT1 as a unique model system

“…Transport Inhibition studies suggest that SGLT4 transports naturally occurring sugars with a rank order of mannose, glucose, fructose, and galactose. D-Mannose, a C-2 epimer of glucose, is essentially required for protein glycosylation [35] whereas fructose is also a common substrate for the renal mannose reabsorption system [36]. Mannose exhibits potent inhibitory activity toward SGLT4 which is almost 50 fold greater than that of galactose (IC 50~0 .15 vs.~8 mM).…”

Glycemic control indicators in patients with neonatal diabetes mellitus

“…After the onset of diabetes mellitus, excretion of glucose will increase; when the increased excretion of glucose exceeds the reabsorption capacity of SGLT2 and SGLT1, reabsorption of glucose via 1,5-AG/mannose/ fructose cotransporter (SGLT4), which is located downstream of SGLT2 and SGLT1, will start. Because glucose is usually not present, 99.9% of 1,5-AG is reabsorbed by SGLT4; however, this reabsorption mechanism is common to glucose; therefore, if inflow of glucose into tubules increases, reabsorption of 1,5-AG will be inhibited [35][36][37] . Therefore, in a hyperglycemic condition, excretion of 1,5-AG into urine will increase and serum 1,5-AG will decrease.…”