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

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
Affiliation:
Journal:
FEBS letters

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.

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