medwireNews: Research shows increased levels of proinsulin in the beta cells of autoantibody-positive people who have not yet developed type 1 diabetes, offering clues to the pathogenic process.
As reported in Diabetes, the area of pancreatic tissue that stained positive for proinsulin was increased by 54–60%, relative to the insulin-positive area, in autoantibody-positive donors from the nPOD study but not in nondiabetic controls. And the ratio of the two areas was 32–40% higher in autoantibody-positive donors versus controls.
Matthias von Herrath (La Jolla Institute for Allergy and Immunology, California, USA) and co-researchers suggest that the accumulation of proinsulin seen in their study “might ultimately lead to beta cell exhaustion and death, with the subsequent release of beta cell antigens which initiate the autoimmune process.”
The elevated proinsulin-to-insulin ratio persisted in tail pancreatic tissue from four of six living, newly diagnosed type 1 diabetes patients from the Diabetes Virus Detection study, despite an overall reduction in beta cell mass. The team says this suggests that insulin therapy “might not fully alleviate the dysfunctional beta cells” and implies a need for earlier intervention if diabetes is to be averted.
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