Faculty Profiles

The major goal of the laboratory is to understand the links between obesity and inflammation.  The low grade chronic inflammation induced by obesity is a major contributor to the development of obesity-associated diseases such as cardiovascular disease and Type 2 diabetes.  Adipose tissue is a major source of inflammatory factors in obese humans and animal models and it has recently been showed that macrophages infiltrate adipose tissue in obesity and generate the majority of these proinflammatory factors.  Interestingly, these adipose tissue macrophages (ATMs) have been shown to be both necessary and sufficient to generate insulin resistance in obesity models.  We have shown that pro-inflammatory macrophages directly alter adipocyte insulin signaling and that ATMs can assume different activation states.  M2 or alternatively activated ATMs dominate in lean adipose tissue.  With high fat diet, a new population of M1 or classically activated macrophages invade adipose tissue and contribute to adipocyte dysfunction.  Our laboratory is interested in understanding the factors that regulate the switch from M2 to M1 ATMs in adipose tissue, how ATMs are trafficked into fat with different dietary exposure, how ATMs may relate to adipogenesis and angiogenesis in the fat pad, how ATMs differ between fat depots, and the molecular factors that govern the inflammatory activation of ATMs with obesity.  To answer these questions we employ a range of genetic, cell biological, microscopic and molecular techniques to examine the function of ATMs in obese mice as well as from human samples.  Understanding how ATMs function can provide novel insights into the pathogenesis of obesity-induced inflammation and can potentially identify novel ways to block these inflammatory changes as possible treatments for obesity-associated diseases such as diabetes.

Lumeng, C.N., DelProposto, J.B., Westcott, D. and Saltiel, A.R. Phenotypic switching of adipose tissue macrophages with obesity is generated by spatiotemporal differences in macrophage subtypes.  Diabetes, In Press, 2008.

Lumeng, C.N., Bodzin, J.L., and Saltiel, A.R.  Obesity induces a phenotypic switch in adipose tissue macrophage polarization.  Journal of Clinical Investigation, 117(1):175-184, 2007.

Lesniewski, L.A., Hosch, S.E., Neels, J.G., DeLuca, C., Pashmforoush, M., Lumeng, C.N., Chiang, S.H., Scadeng, M., Saltiel, A.R., and Olefsky, J.M.   Bone Marrow Specific CAP Gene Deletion Protects Against the Development of High Fat Diet-Induced Insulin Resistance. Nature Medicine, 13(4):455-62, 2007.

Lumeng, C.N., DeYoung, S.M., and Saltiel, A.R. Macrophages induce insulin resistance in adipocytes by altering expression of signaling and glucose transport proteins. American Journal of Physiology: Endocrinology and Metabolism. 292(1):E166-174. 2007.

Lumeng, C.N., DeYoung, S.M., Bodzin, J.L. and Saltiel, A.R. Increased inflammatory properties of adipose tissue macrophages recruited during diet induced obesity. Diabetes, 6(1):16-23, 2007.

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