Research yields new insights into the cause o...( enn State Team is that PERK deficiency ...)

enn State Team is that PERK deficiency blocks both the proliferation of beta cells after birth and the differentiation of those cells into fully functioning units. They found that thirty to forty percent of the beta cells of PERK-deficient mice are physically unusual. The most obvious abnormality is that proinsulin is found the endoplasmic reticulum, instead of being found in or around the nucleus. Apparently, proinsulin is produced as usual, but the normal modification process is blocked, leaving large quantities of proinsulin trapped inside the enlarged and distended organelle.

Another important finding was that beta cells in these mice do not develop into organized clusters or islets within the pancreas. Normally, the protein GLUT2 transports glucose across plasma membranes among the islets, triggering the secretion of insulin in the beta cells. But without the islet architecture, communication among the beta cells breaks down and the cells fail to respond to glucose by secreting insulin. Thus, PERK-deficiency both hampers cell-to-cell signaling of glucose levels and greatly diminishes insulin production at the cellular level.

The Penn State team's understanding of the role of PERK was advanced by additional experiments to pinpoint the time during development when PERK is required. Cavener's team found that PERK must be expressed during a critical period between 13.5 fetal days and 4 days after birth if the beta cells of the pancreas are to regulate glucose normally for the rest of the animal's life. PERK may play an essential role in sensing fetal environment and modulating the development of beta cells in response to it.

"The genetic program of the fetus and the in-utero environment work together to set up the apparatus that regulates glucose in postnatal life," Cavener explains.

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Contact: Barbara K. Kennedy
science@psu.edu
814-863-4682
Penn State
5-Dec-2006

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