News Release

Protein may provide the key to arresting development of diabetes

Book Announcement

University of Gothenburg

Emmelie Cansby, University of Gothenburg

image: This is Emmelie Cansby, Doctoral Student, Sahlgrenska Academy, University of Gothenburg. view more 

Credit: University of Gothenburg

The STK25 protein contributes to cell growth. Researchers at Sahlgrenska Academy have discovered that the protein also affects metabolism, demonstrating that elevated levels accelerate the progress of diabetes in mice.

Researchers at Sahlgrenska Academy, University of Gothenburg have discovered a protein that may open the door to a new method of treating type 2 diabetes and other diseases caused by metabolic disorders.

Current methods not effective

Emmelie Cansby's doctoral thesis has shown that the reduction of STK25 protein in cell cultures improves metabolism. The studies also found that mice that have elevated STK25 levels and are fed a high-fat diet are more likely to develop symptoms of diabetes.

"Current methods for treating diabetes are not effective enough," Emmelie Cansby says. "Furthermore, they have various adverse effects, including hypoglycemia, weight gain, edema and gastrointestinal problems. New, supplementary drugs for type 2 diabetes are badly needed."

Potential treatment

Her thesis concludes that the STK25 protein offers the potential for an entirely new way of treating diabetes.

"Future treatment of diabetes and other metabolic disorders will hopefully include drugs that inhibit the action of STK25," she says.

###

Emmelie Cansby will present her thesis, Regulation of metabolism and inflammation by two protein kinases – AMPK and STK25, on September 5.

Link to thesis: http://hdl.handle.net/2077/35938

Contact:

Emmelie Cansby
Doctoral Student
Sahlgrenska Academy
University of Gothenburg
emmelie.cansby@gu.se

Supervisor Margit Mahlapuu
Associate Professor
+46 706 310109
margit.mahlapuu@gu.se


Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.