Deficiency of the hemoglobin-haptoglobin receptor, CD163, worsens insulin sensitivity in obese male mice.

Loss of CD163 mediates a phenotypic switch in M2-like macrophages towards a pro-inflammatory state.CD163 is involved in free hemoglobin uptake and catabolism as well as oxidative metabolism, specifically in M2-like macrophages.In inguinal white adipose tissue (iWAT) of CD163 defficient mice, macrophage iron is reduced; while concomitantly, adipocyte and other immune cell iron content is increased.Loss of CD163 provokes glucose intolerance and insulin resistance in obese male mice.