January 16, 2013

Improving Metabolic Function by Dumping the JNK

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junkIt’s an undisputed fact that junk clutters the environment – unless you’re a hoarder. Whether it’s at the office or your bank account, you need organization. The findings of researchers point to JNK as a contributing factor to obesity-induced insulin resistance and inflammation.

Sparing you the medical jargon, we can accept that this “JNK” signaling pathway contributes to inflammation and plays a key role in the metabolic response to obesity. This, in turn, leads to insulin resistance, a key player in Type 2 diabetes.  The costars in the leading role of JNK are macrophages.

The study began with mice that had a JNK deficiency in macrophages. As with any good experiment, the researchers had a control group to compare with the JNK deficient microphage mice. Both groups were fed a high fat diet. Both groups became obese. However, the mice with  JNK-deficient macrophages remained insulin-sensitive.

In this study, apparently less is more. Specifically, the macrophage-specific JNK deficiency against insulin resistance limited the inflammation to the  tissues causing the telltale insulin resistance. This is a very good approach but at what cost to the rest of the pro-inflammatory response?

The pro-inflammatory response is very necessary at times. The main functions of inflammation are to destroy the agent causing injury,  to limit the effects of the agent on the rest of the body, and to repair or replace damaged tissue. It has been said that one man’s junk is another man’s treasure. The real tresure here is figuring how to make your macrophages JNK-deficient in the right way.

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