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Am J Physiol Endocrinol Metab 274: E265-E270, 1998;
0193-1849/98 $5.00
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Vol. 274, Issue 2, E265-E270, February 1998

A disrupted cholecystokinin A receptor gene induces diabetes in obese rats synergistically with ODB1 gene

Soichi Takiguchi1, Yutaka Takata1,3, Nobuhiko Takahashi4, Kazuhiro Kataoka1, Tsukasa Hirashima5, Kazuya Kawano5, Kyoko Miyasaka3, Akihiro Funakoshi2, and Akira Kono1

Divisions of 1 Chemotherapy and 2 Gastroenterology, National Kyushu Cancer Center, Fukuoka 815; 3 Department of Clinical Physiology, Tokyo Metropolitan Institute of Gerontology, Tokyo 173; 4 Third Department of Internal Medicine, Asahikawa Medical College, Asahikawa Hokkaido 078; and 5 Tokushima Research Institute, Otsuka Pharmaceutical, Tokushima 771-01, Japan

Otsuka Long-Evans Tokushima fatty (OLETF) rats develop hyperglycemia, hyperinsulinemia, and mild obesity, which are characteristic of human non-insulin-dependent diabetes mellitus. We have shown that two recessive genes, ODB1 mapped on the X chromosome and ODB2 mapped on chromosome 14, are involved in the induction of the diabetes in OLETF rats. Recently we found that OLETF rats are the naturally occurring cholecystokinin type A receptor (CCKAR) gene knockout rats. In this study, we focused on the genotype of CCKAR gene and the ODB1 gene in regulation of glucose homeostasis in the F2 cross of the OLETF rats. Relatively high plasma glucose levels were observed in the F2 offspring with the homozygously disrupted CCKAR gene. A synergistic effect for increasing plasma glucose levels in F2 rats between disrupted CCKAR gene and the ODB1 gene was shown. The CCKAR gene was found to map very close to ODB2 by a linkage analysis using microsatellite markers. These results suggest that CCKAR gene maintains normoglycemia in rats.

Otsuka Long-Evans Tokushima fatty rats; non-insulin-dependent diabetes mellitus model; ODB2 gene


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