Dr. Steve Shoelson, professor of medicine at Harvard Medical School and a researcher at Joslin Diabetes Center has been investigating the role of inflammation in the development of insulin resistance and type 2 diabetes.He notes:
1. "Epidemiologists have found that patients with type 2 diabetes and cardiovascular disease have slightly elevated levels of inflammatory markers in their bloodstream, raising the possibility that inflammation might be associated with the development of these diseases."Here's the study which supports that last point:
2. "Proinflammatory cytokines such as TNF-α and IL-6 promote insulin resistance in experimental models."
3. "A third series of investigations really provided a breakthrough for our understanding. Drawing upon earlier studies suggesting that anti-inflammatory salicylates reverse hyperglycemia in diabetic patients, we identified the NF-κB pathway as a target of this effect and found it to be activated by obesity. We found that activation of the inflammatory NF-κB pathway in fat and liver by weight gain leads to the production of inflammatory mediators that cause both local and systemic insulin resistance."
Local And Systemic Insulin Resistance Resulting From Hepatic Activation Of IKK-Beta And NF-Kappab, Nature Medicine, February 2005
It investigated the effect of activation of this inflammatory pathway on both transgenic mice (bred to exhibit type 2 diabetes), and mice fed a high-fat diet. It concluded:
"These findings indicate that lipid accumulation in the liver leads to subacute hepatic 'inflammation' through NF-kappaB activation and downstream cytokine production. This causes insulin resistance both locally in liver and systemically."Of note:
"Oral salicylate* therapy reversed insulin resistance in LIKK mice."* Salicylate is an anti-inflammatory drug similar to the active component in aspirin (acetylsalicylic acid)
