| First Author | Pontoglio M | Year | 2000 |
| Journal | EMBO Rep | Volume | 1 |
| Issue | 4 | Pages | 359-65 |
| PubMed ID | 11269503 | Mgi Jnum | J:106621 |
| Mgi Id | MGI:3619106 | Doi | 10.1093/embo-reports/kvd071 |
| Citation | Pontoglio M, et al. (2000) HNF1alpha controls renal glucose reabsorption in mouse and man. EMBO Rep 1(4):359-65 |
| abstractText | Recently it has been shown that dominant mutations in the human hepatocyte nuclear factor 1alpha (HNF1alpha) gene, encoding for a homeoprotein that is expressed in liver, kidney, pancreas and intestine, result in maturity onset diabetes of the young type 3 (MODY3). HNF1alpha-null mice are diabetic, but at the same time suffer from a renal Fanconi syndrome characterized by urinary glucose loss. Here we show that MODY3 patients are also characterized by a reduced tubular reabsorption of glucose. The renal murine defect is due to reduced expression of the low affinity/high capacity glucose cotransporter (SGLT2). Our results show that HNF1alpha directly controls SGLT2 gene expression. Together these data indicate that HNF1alpha plays a key role in glucose homeostasis in mammals. |
