title: A murine model of neonatal diabetes mellitus in Glis3-deficient mice.
abstract: 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.
authors.affiliation: Bioscience and Biotechnology Center, Nagoya University, Chikusa-ku, Nagoya, Japan.
authors.forename: Naoki
authors.initials: N
authors.lastname: Watanabe
authors.forename: Kentaro
authors.initials: K
authors.lastname: Hiramatsu
authors.forename: Rieko
authors.initials: R
authors.lastname: Miyamoto
authors.forename: Kaoru
authors.initials: K
authors.lastname: Yasuda
authors.forename: Norihiko
authors.initials: N
authors.lastname: Suzuki
authors.forename: Naoko
authors.initials: N
authors.lastname: Oshima
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Kiyonari
authors.forename: Dai
authors.initials: D
authors.lastname: Shiba
authors.forename: Saori
authors.initials: S
authors.lastname: Nishio
authors.forename: Toshio
authors.initials: T
authors.lastname: Mochizuki
authors.forename: Takahiko
authors.initials: T
authors.lastname: Yokoyama
authors.forename: Shoichi
authors.initials: S
authors.lastname: Maruyama
authors.forename: Seiichi
authors.initials: S
authors.lastname: Matsuo
authors.forename: Yuko
authors.initials: Y
authors.lastname: Wakamatsu
authors.forename: Hisashi
authors.initials: H
authors.lastname: Hashimoto
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D001483:Base Sequence; D001786:Blood Glucose / Q000378:metabolism; D043422:Carboxypeptidases A / Q000378:metabolism; D017931:DNA Primers / Q000235:genetics; D004268:DNA-Binding Proteins; D003922:Diabetes Mellitus, Type 1 / Q000235:genetics* / Q000378:metabolism* / Q000473:pathology; D004195:Disease Models, Animal; D006801:Humans; D007231:Infant, Newborn; D007328:Insulin / Q000235:genetics; D007515:Islets of Langerhans / Q000378:metabolism / Q000473:pathology; D051379:Mice; D018345:Mice, Knockout; D009154:Mutation; D010179:Pancreas / Q000378:metabolism / Q000473:pathology; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D012097:Repressor Proteins / Q000235:genetics; D015534:Trans-Activators / Q000172:deficiency* / Q000235:genetics; D014157:Transcription Factors / Q000172:deficiency / Q000235:genetics
chemical_list: D001786:Blood Glucose; D017931:DNA Primers; D004268:DNA-Binding Proteins; C512851:GLIS3 protein, human; C478000:Glis3 protein, mouse; D007328:Insulin; D012333:RNA, Messenger; D012097:Repressor Proteins; D015534:Trans-Activators; D014157:Transcription Factors; D043422:Carboxypeptidases A