Mikael Rydén and Paul Petrus, Unit for Endocrinology and Diabetes, have, in collaboration with researchers from the University of British Columbia, conducted a study on type 2 diabetes, published in EBiomedicine.

In joint analyses in human adipose tissue and mice, they found that the levels of an extracellular receptor protein, called CD248, were higher in the fat cells of people with obesity and type 2 diabetes. Experiments in fat cell-specific knockout mice showed that reduced CD248 expression improved fat tissue function and glucose tolerance.

“The levels of CD248 in human fat are strongly associated with clinical measures of type 2 diabetes risk. This, together with experiments in which we reduced the CD248 gene in both human and mouse fat cells, suggested that CD248 inhibition could be relevant in future treatments of type 2 diabetes,” says professor Rydén.