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A murine model of neonatal diabetes mellitus in Glis3‐ deficient mice
Author(s) -
Watanabe Naoki,
Hiramatsu Kentaro,
Miyamoto Rieko,
Yasuda Kaoru,
Suzuki Norihiko,
Oshima Naoko,
Kiyonari Hiroshi,
Shiba Dai,
Nishio Saori,
Mochizuki Toshio,
Yokoyama Takahiko,
Maruyama Shoichi,
Matsuo Seiichi,
Wakamatsu Yuko,
Hashimoto Hisashi
Publication year - 2009
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2009.05.039
Subject(s) - diabetes mellitus , endocrinology , islet , medicine , phenotype , pancreas , basal (medicine) , biology , mutation , gene , genetics
Glis3 is a member of the Gli‐similar subfamily. GLIS3 mutations in humans lead to neonatal diabetes, hypothyroidism, and cystic kidney disease. We generated Glis3 ‐deficient mice by gene‐targeting. The Glis3 −/− 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 Insulin mRNA level in the pancreas that is caused by impaired islet development and the subsequent impairment of Insulin‐producing cell formation. The pancreatic phenotypes indicate that the Glis3 ‐deficient mice are a model for GLIS3 mutation and diabetes mellitus in humans.