A murine model of neonatal diabetes mellitus in Glis3-deficient mice

• Published in: FEBS letters Vol. 583; no. 12; pp. 2108 - 2113
• Main Authors: 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
• Format: Journal Article
• Language: English
• Published: England Elsevier B.V 18.06.2009
• Subjects: Animals; Animals, Newborn; Base Sequence; Blood Glucose - metabolism; Carboxypeptidases A - metabolism; Diabetes; Diabetes Mellitus, Type 1 - genetics; Diabetes Mellitus, Type 1 - metabolism; Diabetes Mellitus, Type 1 - pathology; Disease Models, Animal; DNA Primers - genetics; Humans; Infant, Newborn; Insulin - genetics; Islets of Langerhans - metabolism; Islets of Langerhans - pathology; Mice; Mice, Knockout; Mutation; Pancreas - metabolism; Pancreas - pathology; PKD; postnatal days; Repressor Proteins - genetics; RNA, Messenger - genetics; RNA, Messenger - metabolism; Trans-Activators - deficiency; Trans-Activators - genetics; Transcription Factors - deficiency; Transcription Factors - genetics; P; PKD; Diabetes
• ISSN: 0014-5793; 1873-3468
• DOI: 10.1016/j.febslet.2009.05.039

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.