Visiting Professor Kozo Matsumoto

Area and Subject Taught Genetics in Experimental Medicine
Research Theme(s) Type 2 diabetes with obesity
Academic Degrees DVM (Hokkaido Univ.), Ph.D. (Hokkaido Univ.)
Keywords for Research Field type 2 diabetes, obesity, genetics, QTL analysis, animal model, OLETF rat, congenic rats
Office Phone Number 81-75-705-1718

Research Overview

Diabetes mellitus is considered one of the main threats to human health in both developed and developing world. Common diseases such as type 2 diabetes mellitus result from complex interplay among multiple genes, signaling pathways and environmental factors. Numerous diabetes animal models have been developed using gene knockout techniques, which have revealed the critical molecular events involved in glucose metabolism and the development of complications. However, it is believed that in common diseases complete deficiency of a given gene activity is unlikely the causative mutation, but rather the effect of each allele induces small changes of gene activity. There are genetic analyses in human on genes extrapolated from the functional studies in vitro or in rodents in order to confirm the significance in the development of human diseases. Yet causative polymorphisms were still largely elusive. An alternative to the gene knockout model is the use of spontaneous animal models. The OLETF rat is such a model of obesity-based type 2 diabetes. Subsequently produced congenic strains showed that most of the loci examined were shown to contribute to the increased glucose levels in 30 week-old males. Interestingly, the phenotypic features observed in single congenic strain, low fat weight and low leptin levels for Nidd1/of and high fat weight for Nidd2/of, were masked in the double congenic, yet hyperglycemia were further aggravated than either single congenic strain. In order to investigate an affect of obesity to these loci, we have also generated a congenic strain introgressed obesity gene (lpr deficiency). We could produce a double congenic line with a hyperglycemic gene (Nidd1 or Nidd2) under obesity condition by crossing both strains, so that it would be possible to define a gene specifically affecting hyperglycemia under obesity condition.

Notable Publications and Works in the Last Three Years

  1. Sasase, T., et al. J. Diabetes Res. Vol. 2013, Article ID 281928
  2. Da-Yong Yu et al. Apoptosis 17, 636-645,2012
  3. Blevins, J., et al. American J Physiol.-Regulatory, Integrative and Comparative Physiology USA 303, R1231-R1240, 2012
  4. Yamada, T., et al. Exp. Diabetes Res. Vol. 2012.1-6, Article ID 582546 doi: 10.1155/2012/582546
  5. Kose, H., et al. Exp. Daibetes Res. Vol. 2012.1-5, Article ID 858121 doi: 10.1155/2012/858121
  6. Fukumura, T., et al. Exp. Animals, 60, 125-132, 2011