Mutations in UCP2 in congenital hyperinsulinism reveal a role for regulation of insulin secretion.
Although the most common mechanism underlying congenital hyperinsulinism is dysfunction of the pancreatic ATP-sensitive potassium channel, the pathogenesis and genetic origins of this disease remains largely unexplained in more than half of all patients. UCP2 knockout mice exhibit an hyperinsulinemi...
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Autores principales: | , , , , , , , , |
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Formato: | article |
Lenguaje: | EN |
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Public Library of Science (PLoS)
2008
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Acceso en línea: | https://doaj.org/article/1d46ac5c1e6e4f8aa527d7b2e5f7cdd6 |
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