The cause of insulin-dependent, permanent, diabetes in newborn
babies may be a deficiency in the enzyme Pancreatic Endoplasmic
Reticulum Kinase (PERK) during a critical period of development
before birth, according to a new hypothesis put forward by a
team of researchers from Penn State University. In this most
severe type of diabetes, individuals are unable to regulate
glucose normally because they have few insulin-producing beta
cells in their pancreas and the remaining cells do not produce
enough insulin. Using special strains of mice bred to be PERK-
deficient, the researchers demonstrated that the lack of this
enzyme blocked the proliferation of beta cells, hampered the
normal functioning of beta cells, and also kept beta cells from
clustering into islets. "What happens during fetal development
predisposes people either to be able to maintain glucose levels
normally or to have diabetes," says team leader Douglas Cavener,
professor and head of the Department of Biology. The research
results will be publish