Diabetes is one of the fastest growing diseases in the world. Every seven seconds a person dies because of diabetes. Researchers have uncovered the role of a key hormone that might allow the development of new treatments for the disease.
Researchers at NTNU and Oxford have found a hormone that may offer an effective treatment for type 2 diabetes. The incidence of diabetes, especially type 2 diabetes, has skyrocketed over the last few decades, according to a report from the World Health Organization. The report says that there were 108 million adults with diabetes in 1980, but by 2014, that number had grown to 422 million.
Hormone reduces appetite
“Many people who are morbidly obese also have type 2 diabetes,” says Magnus Kringstad Olsen, a PhD candidate at the Department of Cancer Research and Molecular Medicine at NTNU.
Bariartic surgery is the most effective form of weight loss for the morbidly obese. Patients who undergo the surgery also show great improvements in their diabetes after surgery. Many scientists have wondered why.
Researchers have long believed that the remisssion in type 2 diabetes after bariatic surgery is due to the increased production of GLP-1, an appetite-reducing hormone, says Olsen.
Could be used as a treatment
Researchers at NTNU and Oxford have discovered that another hormone called PYY has many of the characteristics that cause this effect.
The finding offers the possibility that drugs could be used to stimulate the production of the hormone to treat type 2 diabetes.
Professor Duan Chen was head of the NTNU group that undertook the study in cooperation with the Oxford Centre for Diabetes, Endocrinology and Metabolism at the University of Oxford.
Reference: Reshma D. Ramracheya, Laura J. McCulloch, Anne Clark, David Wiggins, Helene Johannessen, Magnus Kringstad Olsen, Xing Cai, Chun-Mei Zhao, Duan Chen, Patrik Rorsman. PYY-Dependent Restoration of Impaired Insulin and Glucagon Secretion in Type 2 Diabetes following Roux-En-Y Gastric Bypass Surgery. Cell Reports. 3 May 2016. DOI:10.1016/j.celrep.2016.03.091