16 March 2012

New Study on the Development of Gestational Diabetes

Pregnancy hormones can block insulin from performing its function. When this happens, sugar or glucose levels may increase in a pregnant woman's blood and high blood sugar occurs. This condition is called Gestational Diabetes. The woman does not have to be previously diagnosed with diabetes to exhibit high blood glucose levels.

Babies born to mothers with gestational diabetes are typically at increased risk of problems such as being large for gestational age (which may lead to delivery complications), low blood sugar, and jaundice. Gestational diabetes is a treatable condition and women who have adequate control of glucose levels can effectively decrease these risks.

Treatment of pregnant women with gestational diabetes focuses on keeping blood sugar at normal levels through diet and exercise and to make sure that the growing baby is healthy. In most cases, there will be no need for diabetes medicine or insulin.

Researchers at the University of Pittsburgh School of Medicine have identified a cell-signaling pathway that plays a key role in increasing insulin secretion during pregnancy and, when blocked, leads to the development of gestational diabetes. Their findings are available online today in Diabetes, one of the journals of the American Diabetes Association.

During pregnancy, pancreatic beta cells should expand and produce more insulin to adapt to the needs of the growing baby, explained senior investigator Adolfo Garcia-Ocana, Ph.D., associate professor of medicine, Division of Endocrinology and Metabolism, Pitt School of Medicine. Newborns can suffer complications if the mother's blood glucose is abnormally high during pregnancy.

Video: What is Gestational Diabetes

"Not much was known about the maternal mechanisms that lead to increased beta cell number and function during pregnancy," Dr. Garcia-Ocana said. "But research has shown that high blood glucose in pregnancy can have long-term health consequences for the child, as well as a greater risk of hypertension, type 2 diabetes, and high cholesterol for the mother."

His team began studying a protein called hepatocyte growth factor (HGF), which was discovered by George K. Michalopoulos, M.D., Ph.D., professor and chair, Department of Pathology, Pitt School of Medicine, in 1990. Blood levels of HGF are markedly increased in pregnancy. The protein interacts with a cell surface receptor called c-MET.

The researchers engineered mice that lacked the c-MET receptor in pancreatic cells and found that their beta cells functioned correctly, keeping blood glucose within normal parameters in adult mice. But when the mice got pregnant, they took on the features of gestational diabetes.

"Mice that didn't have the c-MET receptor in their pancreas had lower plasma insulin levels, higher blood glucose and impaired ability to regulate glucose levels," Dr. Garcia-Ocana said. "Without the receptor, they couldn't respond to HGF." Also, unlike normal healthy pregnant females, these mice didn't produce more beta cells, had more beta cell death and so had reduced beta cell mass.

"These findings provide the first direct evidence that HGF/C-MET signaling pathway has an important role in maternal beta cell adaptation during pregnancy," Dr. Garcia-Ocana noted. "Perhaps women who have a variation in the HGF gene or in the c-MET receptor are predisposed to developing gestational diabetes because they cannot adequately compensate for the increased insulin demands of pregnancy."

In future work, he and his team will explore HGF signaling in pregnant women, which could one day provide a new means of diagnosing, treating or preventing gestational diabetes.


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