DRI researchers have identified key molecules involved in insulin release. This finding will help assess beta cell function and may also play a significant role in maintaining long-term function no matter the source of the cells.
Recent findings suggest there might be a link between the development of diabetes and a molecule called nephrin.
Nephrin, derived from the Greek nephros, or kidney, is a substance essential for optimal kidney filtration, which eliminates toxins produced by the body. Although nephrin was once thought to be a kidney-specific molecule with an important role in the pathogenesis factors leading to diabetic kidney disease, scientists recently discovered it in the pancreas, and are characterizing the role it plays in diabetes where its actual role remains unknown.
Preliminary research here at the DRI shows the nephrin molecule is vital for beta cells to secrete insulin in response to blood sugar. Specifically, our research has shown that:
- Persons with early type 2 diabetes and beta cell malfunction do not have sufficient levels of nephrin in their insulin-producing beta cells, suggesting an important role of nephrin in beta cell function. This is seen in both type 1 and type 2 diabetes.
- Human pancreatic beta cells lacking nephrin cannot release insulin in response to glucose.
How might the lack of adequate nephrin contribute to diabetes? In persons with diabetes, insufficient levels of nephrin due to either an autoimmune attack (type 1 diabetes) or to a lower expression (type 2 diabetes) may result in beta cell malfunction and death.
Leading to a Cure: How this Research Supports our Mission
We need to better understand the connection between nephrin and the function of insulin-producing cells in people with diabetes.
By knowing more about how beta cells work, we can develop strategies to better preserve islets and protect cells from the dangerous effects of anti-rejection drugs, inflammatory agents and the immune system.