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Nov. 1, 2007 -- A protein in the pancreas may offer new clues on the cause of gestational diabetes as well as type 2 diabetes.
A new study of mice shows that during pregnancy the pancreas has less of the protein called menin. This protein acts like a brake on the growth of insulin-producing cells in the pancreas. With less menin, the body's insulin production is allowed to increase to meet the demands of the developing pregnancy.
But with gestational diabetes this brake is released and not enough insulin is produced.
Researchers say the finding could lead to new treatments for gestational diabetes as well as other forms of the disease.
"The basis of gestational diabetes has been a black box," says researcher Seung Kim, MD, PhD, associate professor of developmental biology at Stanford University of Medicine, in a news release.
According to the American Diabetes Association, about 4% of pregnant women develop gestational diabetes, which is when a previously non-diabetic woman's body isn't able to make enough insulin needed during pregnancy.
Researchers focused on the insulin-producing parts of the pancreas, called the islets.
In laboratory tests with mice, researchers found that when mice produced too much of the protein menin, the islets couldn’t grow properly and the mice developed gestational diabetes.
"This suggests that there is an internal code for controlling pancreatic islet 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 the amount of menin in the pancreas via a hormone called prolactin. This hormone is elevated during pregnancy. When they gave non-pregnant mice this hormone, the menin 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 2 diabetes.