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A murine model of neonatal diabetes mellitus in Glis3-deficient mice |
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| Authors: | Naoki Watanabe Kentaro Hiramatsu Rieko Miyamoto Kaoru Yasuda Naoko Oshima Dai Shiba Toshio Mochizuki Shoichi Maruyama Yuko Wakamatsu Hisashi Hashimoto |
| Institution: | a Bioscience and Biotechnology Center, Nagoya University, Furo-cho, Chikusa-ku, Nagoya 464-8601, Japan b Graduate School of Science, Nagoya University, Furo-cho, Chikusa-ku, Nagoya 464-8601, Japan c Graduate School of Medicine, Nagoya University, Nagoya 466-8550, Japan d Laboratory for Animal Resources and Genetic Engineering, Center for Developmental Biology (CDB), RIKEN, Kobe 650-0047, Japan e Department of Anatomy and Developmental Biology, Kyoto Prefecture University of Medicine, Kyoto 602-0841, Japan f Second Department of Medicine, Hokkaido University Graduate School of Medicine, Sapporo 060-8638, Japan |
| 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. |
| Keywords: | P postnatal days |
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