Scientists at Stanford University School of Medicine may be on the right path of discovering the pathology behind the development of diabetes during pregnancy, commonly known as Gestational Diabetes Mellitus (GDM).
"The basis of gestational diabetes has been a black box," said Seung Kim, MD, PhD, associate professor of developmental biology and senior author on the study.
Researchers studied menin, a protein responsible for prevention of cancer in various organs, including the pancreas. Menin’s role is to block cell growth, thus potentially preventing cancer. During pregnancy pancreas adapts to the increased metabolic demands by producing less menin, which in turn allows for increased growth of the islet cells that produce insulin. After pregnancy, levels of menin rise back to pre-pregnancy levels and islet cells shrink.
It was observed that mice, genetically were engineered to produce increased levels of menin, developed gestational diabetes during pregnancy. "This suggests that there is an internal code for controlling pancreatic islet growth, a code we intend to crack," Kim said. That code appears to be regulated partly by the level of menin.
To further test the idea, non-pregnant mice received increased levels of prolactin, to simulate pregnant state. As hypothesized, menin levels decreased and islet cells began proliferating, as is the case during pregnancy.
Researchers noted that it is very probable that prolactin is only one of many factors which regulate menin production. Detailed knowledge of the entire mechanism of menin regulation may potentially help treat individuals with Type I Diabetes Mellitus and Gestational Diabetes.
journal Science, Nov 2, 2007