It has been suggested that adipose tissue inflammation is related to insulin sensitivity, but whether this applies to different fat depots has not been examined. We hypothesized, that adipose tissue macrophage (ATM) burden is greater in abdominal than femoral fat because of the relationship between abdominal adiposity and insulin resistance.


We measured HOMA-IR and used immunohistochemistry to measure abdominal (n=85) and femoral (n=57) subcutaneous ATM burden per 100 adipocytes in 103 adults, including lean (n=28, 14 males), lower body obese (n=28, 5 males), and upper body obese (n=47, 16 males). CD68 was used to identify total macrophage, CD14 for pro-inflammatory (M1), and CD206 for anti-inflammatory (M2) macrophages.


ATM content in the abdominal and femoral depots was strongly correlated - CD68 (r=0.59, p=0.0001), CD14 (r=0.71, p=0.0001) and CD206 (r=0.62, p=0.0001). There were no differences in CD68 (p=0.26), CD14 (p=0.16) or CD206 (p=0.28) ATM between the abdominal and femoral depot in men. Females had significantly greater ATM in femoral than abdominal fat (CD68: 16.1±1.0 vs. 12.0±0.8 (p=0.005), CD14: 5.9±0.5 vs. 4.2±0.4 (p=0.03), CD206: 15.4±0.7 vs. 11.9±0.7 (p=0.003) per 100 adipocytes). There was no correlation between ATM burden and HOMA-IR for either depot or sex.


The ATM content of abdominal and femoral fat are strongly related, indicating that ATM infiltration affects both depots simultaneously. Contrary to our hypothesis, females have greater ATM burden in the femoral depot than the abdominal depot, whereas men had no difference between depots. Surprisingly, there was no relationship between ATM burden and HOMA-IR. Future studies should examine the relationship between ATM burden and other metabolic parameters associated with chronic disease.