A study out of Beth Israel Deaconess Medical Center has found that to restore normal glucose levels in type 1 diabetic mice, it’s not enough to halt the destruction of their beta cells. You also have to reverse the muscle and fat inflammation that prevents insulin from transferring glucose into those tissues.
The researchers started by giving diabetic mice a combination of three drugs that not only halted the immune destruction of their beta cells, but also relieved the inflammation in their muscle and fat tissues. They found that increasing insulin-producing beta cells and circulating insulin levels weren’t enough to achieve good blood sugars.
Instead, the restoration of good blood sugars was linked to relief from the inflammatory state that impaired the mice’s response to insulin. Both restoration of beta cells and relief from the inflammatory state in insulin-sensitive tissues were necessary to achieve permanent restoration of normal sugar levels.
Thus, this new triple-therapy regimen, possessing both tolerance-inducing and select anti-inflammatory properties, may represent a way to restore normal blood sugars and self-tolerance in type 1 diabetes. (The three drugs, in case you’d like to know, were rapamycin plus agonist IL-2-related and antagonist-type, mutant IL-15-related Ig fusion proteins (IL-2.Ig and mutIL-15.Ig.))
Sources: EurekAlert; Proceedings of the National Academy of Sciences, August 2007