News & Research

By: Tory Asfahani

A paper published in the journal Science this month reports that a protein known as menin appears to play a role in the development of diabetes in pregnant women.

American Diabetes Association Medical Scholars Award recipient Jeremy Heit, along with his sponsor Seung Kim, PhD, and other researchers at Stanford University, studied the beta cells of pregnant mice. They found that in healthy mice, beta cell mass doubled in size during pregnancy, helping the mice produce enough insulin for their growing bodies. Beta cell mass then returned to pre-pregnancy size after the mice gave birth.

The researchers knew that a protein called menin had a role in controlling beta cell mass. Menin is important because it prevents “over-growth” of pancreatic cells and thus prevents pancreatic cancer. Normally, however, the amount of menin decreases during pregnancy so that the beta cells can expand and produce enough insulin for the pregnant mother. To see if menin played a role in gestational diabetes, the Stanford group genetically engineered mice to produce too much menin. Indeed, they found that the excess amounts of menin prevented beta cell mass from increasing and caused the mice to develop gestational diabetes.

Other research has shown that the hormone prolactin, which is produced in high amounts during pregnancy, helps the beta cells expand during pregnancy. Drs. Kim, Heit and their colleagues then administered prolactin to mice, which lowered menin levels and increased beta cell mass. Therefore, not only did the researchers determine a potential cause of gestational diabetes—too much menin—they proposed a potential therapy for reversing the disease—prolactin.