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- W2069271978 abstract "Mutations in the gene encoding hepatocyte nuclear factor-4α (HNF-4α) result in maturity-onset diabetes of the young (MODY). To determine the contribution of HNF-4α to the maintenance of glucose homeostasis by the β cell in vivo, we derived a conditional knockout of HNF-4α using the Cre-loxP system. Surprisingly, deletion of HNF-4α in β cells resulted in hyperinsulinemia in fasted and fed mice but paradoxically also in impaired glucose tolerance. Islet perifusion and calcium-imaging studies showed abnormal responses of the mutant β cells to stimulation by glucose and sulfonylureas. These phenotypes can be explained in part by a 60% reduction in expression of the potassium channel subunit Kir6.2. We demonstrate using cotransfection assays that the Kir6.2 gene is a transcriptional target of HNF-4α. Our data provide genetic evidence that HNF-4α is required in the pancreatic β cell for regulation of the pathway of insulin secretion dependent on the ATP-dependent potassium channel." @default.
- W2069271978 created "2016-06-24" @default.
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- W2069271978 date "2005-03-03" @default.
- W2069271978 modified "2023-10-05" @default.
- W2069271978 title "The MODY1 gene HNF-4α regulates selected genes involved in insulin secretion" @default.
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- W2069271978 doi "https://doi.org/10.1172/jci22365" @default.
- W2069271978 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1059446" @default.
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