White adipose tissue resident macrophages are required for adipogenesis and energy storage.

White adipose tissue (WAT) stores energy in the form of lipids. WAT macrophages cause adipose tissue inflammation and insulin resistance when intake exceeds expenditures, but their contribution to homeostasis remain poorly understood. Here, we show that two populations, ã and ä, of TNF-producing bone marrow-derived monocytic cells are transiently recruited to damaged adipocytes and mediate insulin resistance. In contrast, we identify a/ß yolk-sac derived resident macrophages that produce adipogenic growth factors, and form a niche required for adipogenesis as white adipocytes do not differentiate in their absence. Production of adipogenic growth factors by a/ß macrophages increases with lipid storage, but they do not contribute to inflammation. Thus the molecular identities and functions of resident macrophages and BM-derived cells are specified by their lineage rather than diet variation. These results identify an essential function of WAT resident macrophages in adipogenesis and energy homeostasis, separate from inflammation mediated by the recruitment of inflammatory leukocytes. Overall design: 5 immune populations were isolated from mice that were on 10 % and 45 % fat diets