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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
May 16, 2007
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