Adiposity can increase as a consequence of the increased size of the adipocytes, as found in ER-α-ko mice [33], or increased numbers of adipocytes. This alternative, which is found in aromatase-deficient mice [34], derives from either increased proliferation or commitment of progenitor cells. Adipose tissue is comprised of adipocytes, supporting vasculature and macrophages [35]. The cross-sectional area of adipocytes doubles in WT mice fed the HFD for 11 weeks (Figure 2C) [36]. The decreased fat pad mass in the Cyp1b1-ko mice, relative to their WT counterparts, correlated with a decrease in adipocyte size (r2=0.97) (Figure 2D). The effect of Cyp1b1 deficiency is, therefore, targeted to lipid accumulation rather than to an increased number of adipocytes, thus representing a reversal of the ER-α-ko phenotype.
