Kinetics of Blood Glucose in Mice Carrying Hemizygous Pax6

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  • NITTA Yumiko
    Department of Anatomy and Neuroscience, Faculty of Medicine, Kinki University
  • SHIGEYOSHI Yasufumi
    Department of Anatomy and Neuroscience, Faculty of Medicine, Kinki University
  • NAKAGATA Naomi
    Center for Animal Resources and Development, Kumamoto University
  • KANEKO Takehito
    Center for Animal Resources and Development, Kumamoto University
  • NITTA Kohsaku
    Misasakai Social Welfare Clinic
  • HARADA Toshihide
    Department of Medical Management, Faculty of Health Services Management, Hiroshima International University
  • ISHIZAKI Fumiko
    Department of Communication Disability, Faculty of Health Science, Hiroshima Prefectural University
  • TOWNSEND Jana
    Department of Language, Culture and Information, Suzugamine Women's College

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説明

The genotype-phenotype relationship was examined experimentally for the Pax6Sey-4H mutant, which carries deletion of its chromosome 2 middle region hemizygously. The genotyping has indicated that this deleted segment is between 102.6 and 109.2 Mb from the centromere. The glucose-6-phosphatase gene followed by the glucagon and carboxyl ester lipase genes were mapped adjacent to the deleted region. Phenotyping indicates that the Pax6Sey-4H mutant is more susceptible to diabetes. The glucose tolerance test showed that the mutants were less capable of reducing their level of blood glucose to the standard level than the normal sibs. The insulin-loading test revealed their inability to elevate their blood glucose levels up to normal levels. The time it took for the onset of diabetes induced by streptozotocin was shorter in the mutants than in normal sibs. Both the haploinsufficiency of the genes in the hemizygous segment of chromosome 2 and the quantitative imbalance of the whole genome could contribute the development of this phenotype in the mutant.<br>

収録刊行物

  • Experimental Animals

    Experimental Animals 58 (2), 105-112, 2009

    公益社団法人 日本実験動物学会

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