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Sci. STKE, 6 November 2007
Vol. 2007, Issue 411, p. tw406
[DOI: 10.1126/stke.4112007tw406]

EDITORS' CHOICE

Physiology Molecular Culprit in Gestational Diabetes

Paula A. Kiberstis

Science, AAAS, Washington, DC 20005, USA

During pregnancy, maternal pancreatic islet beta-cells expand to accommodate the increasing physiological demands placed on the mother by the growing fetus. The molecular mechanisms controlling this physiological response, which helps prevent the development of "gestational diabetes" in the mother, have been unclear. Studying mouse models, Karnik et al. now show that menin, a protein previously identified as an endocrine tumor suppressor and transcriptional regulator, inhibits the growth of islet beta-cells during pregnancy. Transgenic expression of menin in maternal beta-cells prevented islet expansion and caused the mice to develop several hallmark features of gestational diabetes. Menin appears to be maintained at low levels in islets through the actions of the pregnancy-associated hormone prolactin.

S. K. Karnik, H. Chen, G. W. McLean, J. J. Heit, X. Gu, A. Y. Zhang, M. Fontaine, M. H. Yen, S. K. Kim, Menin controls growth of pancreatic beta-cells in pregnant mice and promotes gestational diabetes mellitus. Science 318, 806-809 (2007). [Abstract] [Full Text]

Citation: P. A. Kiberstis, Molecular Culprit in Gestational Diabetes. Sci. STKE 2007, tw406 (2007).


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