The analyses of serum LPC levels in these mice showed that Cyp1b1 deletion exerts a general suppression effect that was reversed by a human CYP1B1 transgene [38]. These LPC levels are of additional interest since the minor phosphatidyl choline, 16:0/18:1 diacyl glycerophosphatidyl choline (diacyl GPC), is a selective activator of PPARα. Thus, the 16:0 LPC and 18:1 LPC are potential indicators of suppression of diacyl GPC and of endogenous liver PPARα activity. The relationship between these genes with respect to synthesis of diacyl GPC, LPC and triglycerides versus fatty acid oxidation is shown in Figure 8A. Serum 18:0 LPC [38] or the ratio to the largely constant 16:0 LPC (18:0/16:0; preferred measure) provides an accessible marker of both adiposity and hepatic steatosis, and is suppressed on both LFD and HFD in Cyp1b1-ko mice (Figure 8B). The 18:1 LPC levels decline on a HFD and are further attenuated when combined with Cyp1b1 deletion (Figure 8C), paralleling changes in Scd1 expression in the same mice (Figure 8D).
