| Title | Macrophages, inflammation, and insulin resistance. |
| Publication Type | Journal Article |
| Year of Publication | 2010 |
| Authors | Olefsky, JM, Glass CK |
| Journal | Annu Rev Physiol |
| Volume | 72 |
| Pagination | 219–246 |
| Date Published | Mar |
| Keywords | Adipose Tissue, Advanced, Animals, Anti-Inflammatory Agents, Diabetes Mellitus, genetics/pathology/physiopathology, genetics/physiology, Glycosylation End Products, Humans, Inflammation, Insulin Resistance, Liver, Macrophage Activation, Macrophages, metabolism/physiology, Mice, Muscle, Obesity, pathology, pathology/physiopathology, pharmacology/therapeutic use, physiology, physiopathology, PPAR gamma, Signal Transduction, Skeletal, Toll-Like Receptor 4, Transgenic, Type 2 |
| 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. Strategies focused on inhibiting the inflammation/insulin resistance axis that otherwise preserve essential innate immune functions may hold promise for therapeutic intervention. |
| URL | http://dx.doi.org/10.1146/annurev-physiol-021909-135846 |
| DOI | 10.1146/annurev-physiol-021909-135846 |
