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Deficiency of the secondary active sodium/glucose transporters result in glucose/galactose malabsorption or congenital renal glycosuriäGLUT1 deficiency produces a seizure disorder with low glucose concentration in cerebrospinal fluid and GLUT2 deficiency is the basis of the Fanconi–Bickel syndrome, which resembles type I glycogen storage disease.ījorbaek C, Echwald SM, Hubricht P, et al (1994) Genetic variants in promoters and codingregions of the muscle glycogen synthase and the insulin-responsive GLUT4 genes in NIDDM. Primary defects in glucose transport all appear to be extremely rare and not all possible deficiencies have been identified. The pattern of expression of the GLUT transporters in different tissues is related to the different roles of glucose metabolism in different tissues. In all other cells, glucose transport is mediated by one or more of the members of the closely related GLUT family of glucose transporters. In the intestine and renal proximal tubule, glucose is transported against a concentration gradient by a secondary active transport mechanism in which glucose is cotransported with sodium ions. There are two mechanisms for glucose transport across cell membranes.
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