HNF1alpha controls renal glucose reabsorption in mouse and man.

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.
Authors	M Pontoglio, D Prié, C Cheret, A Doyen, C Leroy, P Froguel, G Velho, M Yaniv, G Friedlander
Journal	EMBO reports (EMBO Rep) Vol. 1 Issue 4 Pg. 359-65 (Oct 2000) ISSN: 1469-221X [Print] England
PMID	11269503 (Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't)
Chemical References	Blood Glucose DNA Primers DNA-Binding Proteins HNF1A protein, human HNF1B protein, human Hepatocyte Nuclear Factor 1-alpha Hnf1a protein, mouse Hnf1b protein, mouse Monosaccharide Transport Proteins Nuclear Proteins SLC5A2 protein, human Slc5a2 protein, mouse Sodium-Glucose Transporter 2 Transcription Factors Hepatocyte Nuclear Factor 1 Hepatocyte Nuclear Factor 1-beta Luciferases Glucose
Topics	Absorption Adult Animals Biological Transport Blood Glucose (metabolism) Blotting, Northern DNA Primers (chemistry) DNA-Binding Proteins Diabetes Mellitus, Type 1 (genetics, metabolism) Female Genomic Library Glucose (metabolism) Hepatocyte Nuclear Factor 1 Hepatocyte Nuclear Factor 1-alpha Hepatocyte Nuclear Factor 1-beta Humans Kidney Tubules, Proximal (metabolism) Luciferases (metabolism) Male Mice Mice, Knockout Middle Aged Monosaccharide Transport Proteins (genetics, metabolism) Mutation Nuclear Proteins Promoter Regions, Genetic Reverse Transcriptase Polymerase Chain Reaction Sodium-Glucose Transporter 2 Transcription Factors (genetics, physiology) Transfection

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