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

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.

Pubmed ID: 19481545

Authors

  • Watanabe N
  • Hiramatsu K
  • Miyamoto R
  • Yasuda K
  • Suzuki N
  • Oshima N
  • Kiyonari H
  • Shiba D
  • Nishio S
  • Mochizuki T
  • Yokoyama T
  • Maruyama S
  • Matsuo S
  • Wakamatsu Y
  • Hashimoto H

Journal

FEBS letters

Publication Data

June 18, 2009

Associated Grants

None

Mesh Terms

  • Animals
  • Animals, Newborn
  • Base Sequence
  • Blood Glucose
  • Carboxypeptidases A
  • DNA Primers
  • Diabetes Mellitus, Type 1
  • Disease Models, Animal
  • Humans
  • Infant, Newborn
  • Insulin
  • Islets of Langerhans
  • Mice
  • Mice, Knockout
  • Mutation
  • Pancreas
  • RNA, Messenger
  • Repressor Proteins
  • Trans-Activators
  • Transcription Factors