Macrophages, inflammation, and insulin resistance

JM Olefsky, CK Glass - Annual review of physiology, 2010 - annualreviews.org
Annual review of physiology, 2010annualreviews.org
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 …
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-κB, AP1, and other signal-dependent transcription factors that play crucial roles in innate immunity. 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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