A new study of mice shows that during pregnancy the pancreas has less of theprotein called menin. This protein acts like a brake on the growth ofinsulin-producing cells in the pancreas. With less menin, the body’s insulinproduction is allowed to increase to meet the demands of the developingpregnancy.
But with gestational diabetes this brake is released and not enough insulinis produced.
Researchers say the finding could lead to new treatments for gestationaldiabetes as well as other forms of the disease.
“The basis of gestational diabetes has been a black box,” saysresearcher Seung Kim, MD, PhD, associate professor of developmental biology atStanford University of Medicine, in a news release.
According to the American Diabetes Association, about 4% of pregnant womendevelop gestational diabetes, which is when a previously non-diabetic woman’sbody isn’t able to make enough insulin needed during pregnancy.
Protein Tied to Gestational Diabetes
Researchers focused on the insulin-producing parts of the pancreas, calledthe islets.
In laboratory tests with mice, researchers found that when mice produced toomuch of the protein menin, the islets couldn’t grow properly and the micedeveloped gestational diabetes.
“This suggests that there is an internal code for controlling pancreaticislet growth,” says Kim.
Kim says that code appears to be regulated partly by the level of menin.
Researchers also found that the body has a natural way of regulating theamount of menin in the pancreas via a hormone called prolactin. This hormone iselevated during pregnancy. When they gave non-pregnant mice this hormone, themenin levels dropped and the islet cells grew as during pregnancy.
Kim found that obese mice also have less menin circulating in their system,which suggests that the protein may play a role in obesity-related type 2diabetes.