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Review
. 2010:72:219-46.
doi: 10.1146/annurev-physiol-021909-135846.

Macrophages, inflammation, and insulin resistance

Jerrold M Olefsky  1 , Christopher K Glass
Affiliations
Review

Macrophages, inflammation, and insulin resistance

Jerrold M Olefsky et al. Annu Rev Physiol. 2010.

Abstract

Obesity induces an insulin-resistant state in adipose tissue, liver, and muscle and is a strong risk factor for the development of type 2 diabetes mellitus. Insulin resistance in the setting of obesity results from a combination of altered functions of insulin target cells and the accumulation of macrophages that secrete proinflammatory mediators. At the molecular level, insulin resistance is promoted by a transition in macrophage polarization from an alternative M2 activation state maintained by STAT6 and PPARs to a classical M1 activation state driven by NF-kappaB, AP1, and other signal-dependent transcription factors that play crucial roles in innate immunity VSports手机版. Strategies focused on inhibiting the inflammation/insulin resistance axis that otherwise preserve essential innate immune functions may hold promise for therapeutic intervention. .

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