Childhood gastro link to type 1 diabetes
New research by scientists at the Hudson Institute of Medical Research suggests that the immune response to a common childhood viral infection that causes gastroenteritis, could trigger type 1 diabetes in children with a specific genetic predisposition.
Dr Sadler said there is an urgent need to better understand the cause of childhood diabetes to enable the development of more effective treatments and to try to prevent this disease.
“Understanding how type 1 diabetes starts will enable clinicians to better identify children who may be at risk and intervene earlier in the progress of the disease,” Dr Sadler said.
An overzealous antiviral response
The study shows how a child’s immune response to rotavirus, a common cause of gastroenteritis, puts in motion a chain of events that may culminate in type 1 diabetes.
“We showed in mice that a protein called MDA5, which regulates our immune response, overcompensates in its response to this infection, rotavirus, inducing cell death and damaging inflammation in the pancreas,” Dr Sadler said.
Inflammation – ‘a double-edged sword’
“While MDA5 initially helps the body to fight off the virus, this immune response also increases the risk of autoimmunity that destroys insulin producing cells in the pancreas,” said Dr Sadler.
The findings of the study build on work by researchers at the Cambridge Institute of Medical Research at Cambridge University in the UK, which identified a genetic link between MDA5 and risk for type 1 diabetes.
This new study identifies how variance in the gene that encodes MDA5 alters the body’s immune response to rotavirus and, by identifying that this activity is particular to the pancreas, links MDA5 to the development of type 1 diabetes.
“Identifying how the autoimmunity in type I diabetes begins and is then sustained may help us to pinpoint opportunities to prevent the destruction of beta-cells in the pancreas. This could help to sustain and even recover insulin production to prevent childhood diabetes.”
Hudson Institute Communications
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