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The <jats:italic>Glis3<\/jats:italic>\n<jats:sup>\u2212\/\u2212<\/jats:sup> mice had significant increases in the basal blood sugar level during the first few days after birth. The high levels of blood sugar are attributed to a decrease in the <jats:italic>Insulin<\/jats:italic> mRNA level in the pancreas that is caused by impaired islet development and the subsequent impairment of Insulin\u2010producing cell formation. The pancreatic phenotypes indicate that the <jats:italic>Glis3<\/jats:italic>\u2010deficient mice are a model for <jats:italic>GLIS3<\/jats:italic> mutation and diabetes mellitus in humans.<\/jats:p>","DOI":"10.1016\/j.febslet.2009.05.039","type":"journal-article","created":{"date-parts":[[2009,5,29]],"date-time":"2009-05-29T16:47:13Z","timestamp":1243615633000},"page":"2108-2113","source":"Crossref","is-referenced-by-count":75,"title":["A murine model of neonatal diabetes mellitus in <i>Glis3\u2010<\/i>deficient 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