Muir et al found the HFD leads to a rapid (within 3d) expansion of
adipose tissues of male mice and an increase in the proliferation of resident
macrophages. Only later, as obesity develops, are circulating monocyte
precursors recruited from the circulation into the tissue in a CCR2 dependent
manner where they become activated (M1-like, CD11c+) and drive inflammation and
tissue dysfunction. From 28–56 d of HFD, adipocyte size plateaus and
CD11c+ ATMs accumulate lipid droplets. The magnitude and time course of these
changes were more dramatic in eWAT than iWAT, but otherwise similar. The adipose
expansion was due to increased adipocytes size, with only an early transient
increase in preadipocyte proliferation and numbers, but this result does not
preclude the possibility that some were differentiated into adipocytes, as
illustrated. The results of Muir et al reinforce the importance of analyzing the
dynamic changes in the cross-talk among leukocytes, endothelial cells and
adipose progenitors in adipose tissue rsemodeling in response to acute and
chronic overnutrition.