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A drug initially designed to treat the autoimmune disease of juvenile rheumatoid arthritis has been found helpful in treating type 2 diabetes. The drug is an “interleukin-1-receptor antagonist” that goes by the name of anakinra (Kineret).
Interleukins are a type of cytokine, special messenger proteins that communicate between cells. The message sent by interleukin-1 (IL-1) triggers action by disease-fighting cells that, in diabetes and rheumatoid arthritis, are misguided and cause inflammation. Anakinra is “antagonistic” to the IL-1 receptor; that is, it keeps IL-1 from binding to its receptor on the cell at the receiving end of the message. If IL-1 can’t bind, the message doesn’t get through. Anakinra binds to the same receptor on the cell as IL-1 ordinarily would. By hogging the spot and keeping IL-1 from sending its signal to that cell, it stops IL-1 from triggering inflammation.
High glucose concentrations increase the production of a certain interleukin, IL-1 beta. IL-1 beta causes impaired insulin secretion, decreased beta cell growth, and beta cell death. Furthermore, natural IL-1 receptor antagonist is reduced in the islets of people with type 2 diabetes. The upshot is that you’ve got too much IL-beta and too little IL-1 receptor antagonist, resulting in inflammation and beta cell destruction.
In the Swiss study, a thirteen-week treatment of daily injections of anakinra increased insulin production and led to a 0.33% drop in A1c’s in 34 people with type 2 diabetes. The A1c’s of the control group increased 0.13%. The researchers theorize that the drop was due to enhanced beta cell secretory function. Oddly enough, the drug was more effective in thinner people.
The New England Journal of Medicine