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• W2087485736 abstract "The pdx1 gene is essential for pancreatic organogenesis in humans and mice; pdx1 mutations have been identified in human diabetic patients. Specific inactivation of pdx1 in adult β cells revealed that this gene is required for maintenance of mature β cell function. In the following study, a Cre-lox strategy was used to remove pdx1 function specifically from embryonic β cells beginning at late-gestation, prior to islet formation. Animals in which pdx1 is lost in insulin-producing cells during embryogenesis had elevated blood glucose levels at birth and were overtly diabetic by weaning. Neonatal and adult mutant islets showed a dramatic reduction in the number of insulin+ cells and an increase in both glucagon+ and somatostatin+ cells. Lineage tracing revealed that excess glucagon+ and somatostatin+ cells did not arise by interconversion of endocrine cell types. Examination of mutant islets revealed a decrease in proliferation of insulin-producing cells just before birth and a concomitant increase in proliferation of glucagon-producing cells. We propose that pdx1 is required for proliferation and function of the β cells generated at late gestation, and that one function of normal β cells is to inhibit the proliferation of other islet cell types, resulting in the appropriate numbers of the different endocrine cell types." @default.
• W2087485736 created "2016-06-24" @default.
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• W2087485736 date "2008-02-01" @default.
• W2087485736 modified "2023-10-17" @default.
• W2087485736 title "pdx-1 function is specifically required in embryonic β cells to generate appropriate numbers of endocrine cell types and maintain glucose homeostasis" @default.
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• W2087485736 doi "https://doi.org/10.1016/j.ydbio.2007.10.038" @default.
• W2087485736 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2269701" @default.
• W2087485736 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/18155690" @default.
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