首页> 外文期刊>American Journal of Physiology >A disrupted cholecystokinin A receptor gene induces diabetes in obese rats synergistically with ODB1 gene.
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A disrupted cholecystokinin A receptor gene induces diabetes in obese rats synergistically with ODB1 gene.

机译:破裂的胆囊收缩素A受体基因与ODB1基因协同诱导肥胖大鼠的糖尿病。

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摘要

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.
机译:Otsuka Long-Evans Tokushima肥胖(OLETF)大鼠出现高血糖,高胰岛素血症和轻度肥胖,这是人类非胰岛素依赖型糖尿病的特征。我们已经表明,两个隐性基因,映射在X染色体上的ODB1和映射在14号染色体上的ODB2,都参与了OLETF大鼠的糖尿病诱导。最近,我们发现OLETF大鼠是天然存在的A型胆囊收缩素受体(CCKAR)基因敲除大鼠。在这项研究中,我们集中于CCKAR基因和ODB1基因的基因型在OLETF大鼠F2交叉中葡萄糖稳态的调节中。在具有纯合破坏的CCKAR基因的F2后代中观察到相对较高的血浆葡萄糖水平。显示了在破坏的CCKAR基因和ODB1基因之间增加F2大鼠血浆葡萄糖水平的协同作用。通过使用微卫星标记的连锁分析,发现CCKAR基因非常接近ODB2。这些结果表明CCKAR基因维持大鼠正常血糖。

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