Time Magazine: Inflammation Part 4 of 8

A New View of Diabetes 

Before Dr. Frederick Banting and his colleagues at the University of Toronto isolated insulin in the 1920s, doctors tried to treat diabetes with high doses of salicylates, a group of aspirin-like compounds. (They were desperate and also tried morphine and heroin.) Sure enough, the salicylate approach reduced sugar levels, but at a high price: side effects included a constant ringing in the ears, headaches and dizziness. Today's treatments for diabetes are much safer and generally work by replacing insulin, boosting its production or helping the

 body make more efficient use of the hormone. But researchers over the past few years have been re-examining the salicylate approach for new clues about how diabetes develops.

What they have discovered is a complex interplay between inflammation, insulin and fat — either in the diet or in large folds under the skin. (Indeed, fat cells behave a lot like immune cells, spewing out inflammatory cytokines, particularly as you gain weight.) Where inflammation fits into this scenario — as either a cause or an effect — remains unclear. But the case for a central role is getting stronger. Dr. Steve Shoelson, a senior investigator at the Joslin Diabetes Center in Boston, has bred a strain of mice whose fat cells are supercharged inflammation factories. The mice become less efficient at using insulin and go on to develop diabetes. "We can reproduce the whole syndrome just by inciting inflammation," Shoelson says.  

That suggests that a well-timed intervention in the inflammatory process might reverse some of the effects of diabetes. Some of the drugs that are already used to treat the disorder, like metformin, may work because they also dampen the inflammation response. In addition, preliminary research suggests that high CRP levels may indicate a greater risk of diabetes. But it's too early to say whether reducing CRP levels will actually keep diabetes at bay.