Researchers at the University of Stanford have identified a protein in mice that can suppress the production of insulin-producing cells during pregnancy, thus leading to the hallmark signs of gestational diabetes.
If these findings prove applicable to humans, they may help explain the processes behind this common pregnancy complication, and they may suggest new strategies for drug therapies, researchers reported in the Nov. 2 edition of the journal Science.
Previous studies in mice and humans have indicated that so-called beta cells proliferate in the pancreas during pregnancy. This allows the body to produce more insulin in response to the increasing metabolic demands placed on the mother by the growing fetus.
The molecular mechanism controlling this proliferation, which helps prevent the development of gestational diabetes in the mother, has been unclear until now.
Studying mouse models and human cells, Stanford researchers have found that the menin protein inhibits the growth of beta cells during pregnancy. The pregnancy-related hormone prolactin seems keep menin at low levels in pancreatic islets, the regions where beta cells are produced.
These results suggest that menin reduction is a natural way for the body to stimulate beta-cell proliferation and that defects in menin or the signaling pathways that control its activity may contribute to the development of gestational diabetes.
Source:Xinhua
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