These findings are supported by observations that glucose reabsorption is reduced by approximately 60% in SGLT2-null mice, compared with normal mice [12], and that subjects with familial renal glycosuria, who have mutations in the gene coding for SGLT2, excrete significant amounts of glucose (up to ≥10 g/1.73 m2/day) in the absence of hyperglycaemia and with no evidence of generalized proximal tubule dysfunction [13]. Here, SLC5A2 is linked to Hyperglycemia.