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High blood glucose prompts pancreatic β cells to produce and release interleukin 1β, which inhibits the function of β cells and promotes their apoptosis. Its natural competitor for binding to the type I receptor, interleukin 1 receptor antagonist, protects β cells from functional decline and apoptosisapoptosis.
Anakinra, a recombinant human interleukin-1 receptor antagonist, seems to improve glycaemia and pancreatic β cell function, and it reduces the markers of systemic inflammation in people with type 2 diabetes. A trial randomised 34 patients to receive 100 mg of anakinra subcutaneously once daily and 36 patients to receive placebo.
After 13 weeks, patients who received the intervention had lower concentrations of glycated haemoglobin, higher serum concentrations of C peptide, a lower ratio of proinsulin to insulin, and lower concentrations of interleukin 6 and C reactive protein. Patients measured their fasting glucose concentrations at home once a week, and these values were consistently lower in the intervention group.
Researchers didn't find any evidence of anakinra changing sensitivity to insulin, but they suggest that it might improve with higher doses. They call for larger trials with longer follow-up and dose finding to test the effectiveness of interleukin 1 antagonists at preventing β cell destruction and promoting their regeneration in type 2 diabetes.