Hyperinsulinemia in PRIP-1 gene deleted mice

Naoko Doira, Takashi Kanematsu, Miho Matsuda, Hiroshi Takeuchi, Hito O. Nakano, Yushi Ito, Keiko Nakayama, Kei Ichi Nakayama, Masato Hirata

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

The protein p130, named from its molecular size, was originally identified as an inositol 1, 4,5-trisphosphate binding protein similar to phospholipase C (PLC)-δ1, but lacking any PLC activity. It was recently renamed PLC-related catalytically inactive protein-1 (PRIP-1). In the present study, PRIP-1 gene-targeted mice were analyzed for glycogen metabolism based on the previous finding that PRIP-1 interacts with protein phosphatase-1 (26). Compared to the control mice, mutant mice exhibited lower phosphorylase activity and higher levels of glycogen in the liver, which appeared to be consistent with the inhibition of protein phosphatase-1 by PRIP-1. These observation could also be attributed to the increased levels of plasma insulin. Hyperinsulinemia, observed even in the young mice, was progressive with aging, and was accompanied by the accumulation of fat tissues, increased body weight and decreased sensitivity to insulin in the mutant mice at the age of 12 months. These results suggest that PRIP-1 is a molecule involved in the control of plasma insulin.

Original languageEnglish
Pages (from-to)157-165
Number of pages9
JournalBiomedical Research
Volume22
Issue number3
DOIs
Publication statusPublished - 2001 Jan 1
Externally publishedYes

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

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    Doira, N., Kanematsu, T., Matsuda, M., Takeuchi, H., Nakano, H. O., Ito, Y., Nakayama, K., Nakayama, K. I., & Hirata, M. (2001). Hyperinsulinemia in PRIP-1 gene deleted mice. Biomedical Research, 22(3), 157-165. https://doi.org/10.2220/biomedres.22.157