Both 18:0 LPC and 18:1 LPC serum levels decline in the Cyp1b1-ko mice described in Figure 1, whereas the introduction of human CYP1B1 restored both serum LPC content and low adiposity [38]. This diacyl GPC activation of PPARα is likely to depend on an exchangeable pool. The phosphatidyl choline transport protein, PCTP, not only has this exchange function, but also partners with Acot13 to suppress mitochondrial oxidation of fatty acids [55] (Figure 8A). Pctp gene expression and serum 18:0/16:0 LPC each correlate with these adiposity changes (Figures 8B and 8E). Serum 18:1 LPC decreases in Cyp1b1-ko mice in parallel with the loss of Scd1. This suppression plays an important role in this extra-hepatic control by Cyp1b1 deletion, since normal DIO is restored when Scd1 levels are increased by adenoviral transfection [38].
