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Pituitary Tumor Transforming Gene-Null Male Mice Exhibit Impaired Pancreatic Beta Cell Proliferation and Diabetes
Zhiyong Wang, Enrico Moro, Kalman Kovacs, Run Yu and Shlomo Melmed
Proceedings of the National Academy of Sciences of the United States of America
Vol. 100, No. 6 (Mar. 18, 2003), pp. 3428-3432
Published by: National Academy of Sciences
Stable URL: http://www.jstor.org/stable/3139376
Page Count: 5
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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 alpha/beta cell ratio. Islet beta cell mass in PTTG-/- mice was already diminished before development of frank diabetes and only increased minimally during growth. Br-dUrd incorporation of islet cells in PTTG-null mice was ≈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.
Proceedings of the National Academy of Sciences of the United States of America © 2003 National Academy of Sciences