Over the last two decades it has become apparent that adipose tissue macrophage (ATM) accumulation is a key feature of obesity-induced insulin resistance. Since both ATM accumulation and insulin resistance occur together, the prevaliing dogma is that inflammatory signals sent from ATM contribute, if not fully account, for the insulin resistance phenotype. This model is supported by countless studies, by both our group and others, where genetic manilpulation of myeloid cells in mice can either protect (1) or exacerbate (2) insulin resistance, depending upon the nature of the genetic manipulation. However, recent work from our group, suggests that ATM play no role in obesity-induced unsulin resistance (3). Moreover, work from the Scherer laboratory demonstrates that pro-inflammatory signaling in adipocytes is, in fact, required for proper adipose tissue remodeling and expansion (4). In this presentation, the complex roles of obesity-induced ATM wil be discussed.

1. Nicholls HT,et al. Haematopoietic cell restricted deletion of CD36 reduces high fat diet-induced macrophage infiltration and insulin resistance in adipose tissue. Diabetes 60:1100-1110, 2011.
2. Hevener AL, et al. Macrophage PPARg is required for normal skeletal muscle and hepatic insulin sensitivity and full antidiabetic effects of TZDs. J Clin Invest 117: 1658-1669, 2007.
3. Kraakman MJ, et al. Blocking IL-6 trans-signaling prevents high fat diet-induced adipose tissue macrophage recruitment and does not exacerbate weight gain, liver steatosis or insulin resistance. Cell Metab. 21: 403-416, 2015.
4. Wernstedt Asterholm et al. Addipocyte inflammation is essential for healthy adipose tissue expansion and remodeling. Cell Metab. 20: 103-118, 2014.