Development of consomic mouse model for metabolic syndrome

在NZO/HILtJ小鼠中发现代谢综合征的发生，而在C3H/HeJ小鼠中没有发现。我们确定了与肥胖、糖代谢异常和高血压相关的数量性状基因座。为了建立了解代谢综合征分子机制的动物模型，我们成功地培育了三个体细胞系小鼠：NZO/HILtd J-Chr 7^&lt；C3H/Hej，&gt；NZO/HILtd J-Chr 12^&lt；C3H/Hej&gt；和Nzo/HILtd J-Chr 17^&lt；家系小鼠与NZO/HILtJ小鼠在肥胖、糖代谢和血压方面无显著差异。这些结果表明，与代谢综合征相关的单个主效基因不位于NZO/HILtJ小鼠的7、12和17号染色体上。此外，我们从ICR小鼠群体中发现了Fgf5缺陷的自然突变小鼠，支持NZO/HILtJ小鼠的选育。Fgf5基因突变的小鼠可能是高血压和代谢综合征基础研究的有用动物模型，因为人类高血压与Fgf5基因多态性有很强的相关性。

The development of metabolic syndrome is found in NZO/HILtJ mice, but not in C3H/HeJ mice. We identified quantitative trait loci associated with obesity, abnormal glucose metabolism and hypertension. To develop the animal model for understanding the molecular mechanism of metabolic syndrome, we successfully produced three consomic mouse strains, NZO/HILtJ-Chr 7^<C3H/HeJ,>, NZO/HILtJ-Chr 12^<C3H/HeJ> and NZO/HILtJ-Chr 17^<C3H/HeJ>. There were no significant differences in obesity, glucose metabolism and blood pressure between the consomic mice and NZO/HILtJ mice. These results demonstrate that a single major gene associated with metabolic syndrome was not located on the chromosome 7, 12 and 17 of NZO/HILtJ mice. Furthermore, we found Fgf5-deficient natural mutant mice from ICR mouse colony supporting the breeding of NZO/HILtJ mice. The Fgf5-decifient mice might be useful animal model for the basic research of hypertension and metabolic syndrome, because there is strong significant association between hypertension and Fgf5 polymorphism in human.