Display Settings:

Format

Send to:

Choose Destination
See comment in PubMed Commons below
Proc Natl Acad Sci U S A. 2003 Mar 18;100(6):3428-32. Epub 2003 Mar 7.

Pituitary tumor transforming gene-null male mice exhibit impaired pancreatic beta cell proliferation and diabetes.

Author information

  • 1Department of Medicine, Cedars-Sinai Research Institute, University of California School of Medicine, Los Angeles, CA 90048, USA.

Abstract

The mammalian securin, pituitary tumor transforming gene (PTTG), regulates sister chromatid separation during mitosis. Mice or cell lines deficient in PTTG expression, however, are surprisingly viable. Here we show that PTTG disruption in mice (PTTG-/-) severely impairs glucose homeostasis leading to diabetes during late adulthood, especially in males associated with nonautoimmune insulinopenia and reversed alphabeta cell ratio. Islet beta cell mass in PTTG-/- mice was already diminished before development of frank diabetes and only increased minimally during growth. BrdUrd incorporation of islet cells in PTTG-null mice was approximately 65% lower (P < 0.005) than in the WT pancreas, whereas apoptosis rates were similar. PTTG-/- beta cells had pleiotropic nuclei, suggesting defects in cell division. The results indicated that securin is indispensable for normal pancreatic beta cell proliferation.

PMID:
12626748
[PubMed - indexed for MEDLINE]
PMCID:
PMC152309
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for HighWire Icon for PubMed Central
    Loading ...
    Write to the Help Desk