A novel factor that prevents the loss of beta cells and improves their insulin secretory capabilities has been discovered by Dr. Newgard and his team at Duke University. Their previous research demonstrated that a gene expression factor in human beta cells leads to an increase in beta cell replication, while enhancing beta cell function. However, generally gene expression factors cannot be controlled with traditional drug-type compounds, so an indirect control pathway needed to be found. In this new research they identified the protein called VGF as the factor responsible for controlling the beneficial effects of this beta cell replication gene expression factor. VGF is a protein made and secreted by beta cells and then cut into smaller active fragments. The scientists at Duke found that one particular VGF fragment, called TLQP-21, was responsible for the beneficial effects, preventing death and improving the functioning of human beta cells grown in culture. Also, when given to rats, the group found that TLQP-21 preserves beta cell numbers and delays the onset of diabetes.
Stephens, SB., Schisler, JC., Hohmeier, HE. et al. (2012). A VGF-Derived Peptide Attenuates Development of Type 2 Diabetes via Enhancement of Islet ²-Cell Survival and Function. Cell Metab 16, 33-43.
Investigators and Institutions:
This work was led by Dr. Christopher Newgard at Duke University.
Ramifications for Individuals with Type 1 Diabetes:
This research identified a protein that has the potential to improve the functioning and survival of beta cells in people with T1D. Work can now begin on evaluating the therapeutic potential of this protein in additional studies and on designing related compounds that produce a similar therapeutic benefit by targeting this same pathway.
This work was funded, in part, by a collaborative JDRF grant to Dr. Newgard and a JDRF Postdoctoral Fellowship to Dr. Stephens, the lead author on this paper.