Patrick Rowe, PhD, a researcher at the UF Diabetes Institute, is using groundbreaking technology to better understand the early stages of type 1 diabetes. Via a laser microdissection system, he is investigating whether islet autoantibodies, early markers of risk for type 1 diabetes, are associated with stressed/overworked insulin-producing beta cells of the pancreas. This system, priced at $224,000, is one of only a few in the state of Florida.
In an attempt to better understand the process leading to insulitis (inflammation of the beta cells) and beta cell destruction, he is researching the question “Why does the immune system initially come to, and eventually destroy, the beta cells and not another cell type?”. Funded by a JDRF grant that utilizes nPOD tissues, Rowe studies pancreatic tissues from two different donor groups: those without diabetes and those without diabetes but positive for one or more islet autoantibodies. The latter group represents an early stage of disease when the function of beta cells can be assessed prior to the appearance of insulitis, which Rowe believes is a late stage event, and the beta cell dysfunction/destruction that accompanies it. Loss of beta cells is the hallmark of type 1 diabetes, wherein insulin production is lost resulting in elevated blood glucose levels.
Using a technique called laser capture microdissection, Rowe dissects islets, the 1-2% of the pancreas that contains beta cells, from thin sections of pancreas tissue using a laser rather than a scalpel, and measures which genes are turned on and which are turned off. He then compares the gene expression of islets from individuals without diabetes to those without diabetes but positive for islet autoantibodies. He anticipates that islets from autoantibody-positive individuals will show increased expression of genes related to beta cell function, stress responses, and inflammatory pathways, indicating that beta cells are stressed/overworked prior to the appearance of insulitis and disease onset.
His research is based on the theory that the environmental triggers in people at genetic risk for type 1 diabetes are factors that place greater demand on the beta cells to secrete insulin, possibly due to an inherited defect in beta cell function. Under certain conditions when an individual is exposed to these ‘stressors’, inflammation may be initiated that leads to the eventual destruction of beta cells.