Not everything is known about Type 1 diabetes even as it is pretty well known that it is a genetically driven autoimmune disease of pancreatic beta-cells. Yet its origin remains unknown.
In a recent study, researchers from the Boston Medical Center (BMC) and Boston University School of Medicine (BUSM) found that skin cells from patients with type 1 diabetes display abnormal activity. This abnormal activity is triggered by immune response mechanisms to environmental stimuli like a viral infection. The findings are published online in PLoS One.
The researchers found that these skin cells when exposed to cytokines or fat have elevated levels of calcium. It is known that cytokines or cells signalling molecules essential to the body's immune response in humans increase with the onset of infection. This is quite similar to increased fatty acids when people stop eating or are sick. This is a common occurrence in children when they are infected with virus.
"This is significant as it is known that a viral illness usually precedes the development of type 1 diabetes in children but no one knows why it should be related," says Barbara Corkey, PhD, Zoltan Kohn Professor of Medicine at BUSM and vice chair for Research in the Obesity Research Center at BMC. "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 data collected by scientists showed that skin cells of those relatives of someone with type 1 diabetes who do not have type 1 diabetes themselves show an intermediate calcium response to circulating signaling molecules. These data indicate that a genetic trait in combination with unique environmental stimulus may likely initiate diabetes.
"Determination of this trait before development of diabetes could help to identify susceptible individuals prior to disease onset," Corkey said.
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