Skin Cells May Reveal Secret of Type 1 Diabetes
The skin cells of people who have type 1 diabetes may help experts better understand the disease and even identify people at risk of developing the autoimmune condition. What secret do skin cells hide and what could it mean?
Type 1 diabetes is an autoimmune disease that is characterized by the death of the insulin-producing structures in the pancreas called beta cells. So far, experts do not know why this occurs, but there is one theory that says a viral infection may trigger the destruction of these critical cells.
In fact, two studies published online in October 2013 (now in print) reported on the association between type 1 diabetes and enteroviruses. Both studies showed that enterovirus types called group B coxsackieviruses, which includes only six enterovirus members, are associated with a greater risk of developing type 1 diabetes but that other enterovirus types are not.
Previous research has indicated that group B coxsackieviruses are capable of infiltrating the pancreas and damaging beta cells.
Now in a newer study, an investigative team at Boston Medical Center and Boston University School of Medicine (BUSM) has found that skin cells from type 1 diabetes patients respond to stimulation by fat or cytokines (molecules that facilitate cell-to-cell communication in immune responses and have a role in inflammation and infection) by showing elevated levels of calcium. Why is this important?
Levels of cytokines and fatty acids typically rise when the body is under attack by a virus (a viral infection) and individuals reduce or stop their food consumption. When children are ill with a viral infection, for example, they often don’t want to eat.
According to Barbara Corkey, PhD, the new study’s lead investigator and the Zoltan Kohn Professor of Medicine at BUSM, “Our findings that diabetic cells have a different sensitivity as indicated by higher levels of calcium to an environmental event such as a virus, may help to explain why the onset of type 1 diabetes might be triggered by an environmental stimulus as well as a genetic predisposition.”
The authors also found that the skin cells of non-diabetic relatives of individuals with type 1 diabetes also responded to cytokines or fat with a more moderate calcium response. These findings suggest that the combination of a specific environmental trigger and a specific genetic trait in certain individuals may initiate development of type 1 diabetes.
These studies add to the growing evidence that a viral infection can play a role in the development of type 1 diabetes. Hopefully experts will be able to use this information to someday identify who could develop the disease and prevent it and/or find a better way to treat it.
Husni NR et al. Fibroblasts from type 1 diabetics exhibit enhanced Ca2 mobilization after TNF or fat exposure. PLoS ONE 2014; 9(1): V
Laitinen OH et al. Coxsackievirus B1 is associated with induction of B-cell autoimmunity that portends type 1 diabetes. Diabetes 2014 Feb; 63(2): 446-55
Oikarinen S et al. Virus antibody survey in different European populations indicates risk association between doxsackievirus B1 and type 1 diabetes. Diabetes 2014 Feb; 63(2): 655-62