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EMBO Rep. 2000 Oct;1(4):359-65.

HNF1alpha controls renal glucose reabsorption in mouse and man.

Author information

1
Unité des Virus Oncogènes, URA 1644 CNRS, Département des Biotechnologies, Institut Pasteur, Paris, France. marcop@pasteur.fr

Abstract

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.

PMID:
11269503
PMCID:
PMC1083745
DOI:
10.1093/embo-reports/kvd071
[Indexed for MEDLINE]
Free PMC Article

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