Animal Models Offer Newborn Opportunity to Permanently Rescue Insulin-making Cells and Possibly Even Protect Against Future Onset
A common condition that leads to low birthweight babies may predispose the infants to obesity and diabetes later in life by denying cells in the pancreas access to the chemical signals they need to mature, according to researchers at the University of Pennsylvania School of Medicine. Moreover, the condition, which they have successfully modeled in rodents, may be reversed soon after birth by the administration of hormones that stimulate the maturation of the pancreatic beta cells, which produce insulin. Their findings suggest a way of preventing diabetes in people at-risk for the disease by boosting the creation of beta cells soon after birth.
According to Rebecca A. Simmons, MD, assistant professor in Penns Department of Pediatrics, "the condition, called intrauterine growth retardation (IUGR), is generally caused by the inability of a developing fetus to receive adequate nutrition and can effect as many as one in 10 newborns." Diminished fetal growth is due to a number of different processes such as high blood pressure and intrauterine infections. Epidemiological studies have also shown that there is a strong link between IUGR and the development of obesity and diabetes in adulthood. The Penn researchers believe the link may be due to the decreased formation of blood vessels in the pancreas.
Greg Lester | EurekAlert!
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