UTHealth research: Misfolded form of pancreatic protein could induce type 2 diabetes symptoms
HOUSTON – (Aug. 1, 2017) – The symptoms of type 2 diabetes can be induced by a misfolded form of a pancreatic protein and possibly be transmitted by a mechanism similar to prion diseases such as Creutzfeldt-Jakob disease or bovine spongiform encephalopathy (mad cow disease), according to researchers from McGovern Medical School at The University of Texas Health Science Center at Houston (UTHealth).
The findings were reported today in a paper published in The Journal of Experimental Medicine.
The Centers for Disease Control and Prevention estimates that 29 million Americans suffer from type 2 diabetes, a condition in which the body is unable to regulate blood glucose levels using the hormone insulin. Although the disease has been linked to a variety of genetic and environmental risk factors, what causes type 2 diabetes is still not completely understood.
More than 90 percent of type 2 diabetes patients show abnormal protein deposits in their pancreatic islets that are aggregates of a misfolded form of a protein called islet amyloid polypeptide (IAPP). The precise role of these IAPP aggregates in type 2 diabetes is unclear, but they may damage and kill the pancreatic beta cells that secrete insulin in response to elevated blood glucose levels. In this respect, type 2 diabetes could be similar to other diseases caused by misfolded protein aggregates, such as Alzheimer’s disease, Parkinson’s disease and prion disorders.
“Until now, this concept has not been considered,” said Claudio Soto, Ph.D., senior author, professor in the Department of Neurology and the directo Continue reading