Insulin Resistance: Due to Inflammation, Not Obesity

Filed in archive Developments , Research on November 10, 2007

Inflammation brought about by immune cells called macrophages are what UCSD (University of California, San Diego) School of Medicine researchers have discovered as the one leading to insulin resistance and type 2 diabetes - opposite to what has been previously associated to the said conditions: obesity.

In recent years, it has been theorized that chronic, low-grade tissue inflammation related to obesity contributes to insulin resistance, the major cause of Type 2 diabetes.

In research done in mouse models, the UCSD scientists proved that, by disabling the macrophage inflammatory pathway, insulin resistance and the resultant Type 2 diabetes can be prevented.

Findings of the said study are published as the feature article of the November 7 issue of Cell Metabolism.

Macrophages, found in white blood cells in the bone marrow, are key players in the immune response.

When these immune cells get into tissues, such as adipose (fat) or liver tissue, they release cytokines, which are chemical messenger molecules used by immune and nerve cells to communicate.

These cytokines cause the neighboring liver, muscle or fat cells to become insulin resistant, which in turn can lead to Type 2 diabetes.

The implication of the above new findings will hopefully pave the way to novel drug development in fighting obesity-related type 2 diabetes.

Find more details from University of California, San Diego.

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