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EMBO Rep ; 1(4): 359-65, 2000 Oct.
Article in English | MEDLINE | ID: mdl-11269503

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.


Subject(s)
DNA-Binding Proteins , Diabetes Mellitus, Type 1/metabolism , Glucose/metabolism , Kidney Tubules, Proximal/metabolism , Monosaccharide Transport Proteins/genetics , Nuclear Proteins , Transcription Factors/genetics , Transcription Factors/physiology , Absorption , Adult , Animals , Biological Transport , Blood Glucose/metabolism , Blotting, Northern , DNA Primers/chemistry , Diabetes Mellitus, Type 1/genetics , Female , Genomic Library , Hepatocyte Nuclear Factor 1 , Hepatocyte Nuclear Factor 1-alpha , Hepatocyte Nuclear Factor 1-beta , Humans , Luciferases/metabolism , Male , Mice , Mice, Knockout , Middle Aged , Monosaccharide Transport Proteins/metabolism , Mutation , Promoter Regions, Genetic , Reverse Transcriptase Polymerase Chain Reaction , Sodium-Glucose Transporter 2 , Transfection
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