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Insulin Resistance Linked to Inflammation of Fat Cells

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December, 2003 -- Two new studies found that obese fatty tissue is infiltrated by macrophages and that these infiltrating macrophages are an important source of inflammation in this tissue. Both studies found that the largest classes of genes significantly up regulated in obesity are macrophage and inflammatory genes in fatty tissue.

One of the studies (Chen), conducted in mice, reported that the up regulation of many inflammation and macrophage-specific genes precedes a dramatic increase in circulating insulin levels. This finding suggests that obesity-related insulin resistance is, at least in part, a chronic inflammatory disease that is initiated in fatty tissue.

The other study (Ferrante) that was conducted in humans provided evidence that human obesity is characterized by an accumulation of macrophages in fatty tissue. This was demonstrated by the association of macrophage accumulation in fatty tissue with body mass index.

The mechanism by which the inflammatory response in fatty tissue causes insulin resistance remains to be established. The findings of these two studies will prompt consideration of new models of the role of macrophages in the molecular changes that occur in fatty tissue in obesity.

References: Hong Chen, Chronic inflammation in fat plays a crucial role in the development of obesity-related insulin resistance View the PDF of this article. Anthony W. Ferrante, Jr., Obesity is associated with macrophage accumulation in adipose tissue

Commentary: Gökham S. Hotamisligil, Obesity-induced inflammatory changes in adipose tissue, View the PDF of this commentary

Source: Journal of Clinical Investigation (12/15/03)

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