Reporting their findings in the journal Cell Death and Disease, the researchers reveal how blocking the gene – called TNFR5 – halted the destruction process, a discovery that could lead to new treatments for type 2 diabetes.
The majority of these cases are type 2 diabetes, where the beta cells in the pancreas either do not produce enough insulin or the body is unable the use the insulin that is produced. Insulin is the hormone that helps regulate blood sugar levels.
While regular blood glucose testing and medications can help people with type 2 diabetes manage their blood sugar levels, there is a need for more effective therapies.
Lead researcher Dr. Mark Turner, of the School of Science and Technology at Nottingham Trent University in the U.K., and colleagues believe their gene discovery may have the potential to meet this need.
TNFR5 gene destroys beta cells in response to high levels of sugar, fat
The team says it is well established that long-term exposure to a high-fat and high-sugar diet can exacerbate destruction of beta cells among people with type 2 diabetes, but the mechanisms behind this process have been unclear.
For their study, Dr. Turner and colleagues set out to determine whether there is a genetic explanation.
Using high-density microarray analysis, the researchers evaluated more than 31,000 genes associated with the pancreas, with the aim of pinpointing which ones were most sensitive to glucose and fatty acids – the products of diets high in fat and sugar.
The researchers found that the gene TNFR5 had the highest sensitivity to glucose and fatty acids, and overexpression of this gene in response to high levels of fat and sugar led to beta cell destruction.
The authors say these findings suggest that people with type 2 diabetes – particularly those with poor blood glucose management or who have not been diagnosed – are more likely to overexpress the TNFR5 gene, and, therefore, beta cell damage is exacerbated.
But there is some good news; in laboratory tests, the team found that blocking TNFR5 in beta cells exposed to glucose and fatty acids halted their destruction.
This suggests that inhibiting TNFR5 activity could be a promising treatment strategy for type 2 diabetes.