Rat beta-cells in the Islet of Langerhans, a region of the pancreas. The cells are stained green, with blue nuclei. Glucagon, a peptide hormone that raises blood glucose levels (the opposite effect of insulin) is stained red.
Building better beta-cells
In the brain, synapse formation is driven by contact between neuronal axons and dendrites. The more sites of contact between axons and dendrites, the greater the number of synapses that form.
In a recent paper in the Journal of Biological Chemistry, Steven Chessler, MD, PhD, associate professor of medicine at the University of California, San Diego School of Medicine, and colleagues, report that a similar phenomenon occurs among pancreatic beta-cells, the cells responsible for creating, storing and releasing insulin.
Insulin, of course, is a critical hormone that regulates fat and carbohydrate metabolism in the body. It prompts cells in the liver, muscle and fat tissues to take up glucose from the blood and store it as glycogen, a fuel. In type 2 diabetes, cells become resistant to insulin signals and the beta cells malfunction, producing too little insulin. This results in a host of dysfunctions and potentially life-threatening health problems.
The researchers found that neuroligin-2 protein and another binding protein protrude from the surface of insulin-producing beta-cells. The only other place neuroligin-2 is found is in specialized synapses in the brain. Binding between neuroligin-2 and the other protein is brought about by contact between beta cells, the scientists said, driving beta-cell maturation in the same way that neuronal contact boosts synapse formation. Fully developed beta cells function better and secrete more insulin.
“The significance of this to diabetes is that we have found a mechanism whereby engagement of proteins protruding from the pancreatic beta cell surface influences beta-cell maturation and function and insulin secretion,” said Chessler, who is also a member of the UC San Diego Pediatric Diabetes Research Center.
“These proteins could serve as targets for therapies to improve beta-cell function and insulin secretion and thus treat type 2 diabetes. Also, since this mechanism triggers beta-cell maturation, it may also be important for making new beta cells (from stem cells, for example) in culture.”
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