Several key genes involved in fatty acid homeostasis were also suppressed extensively by the combination of HFD and Cyp1b1 deletion (Table 2). The largest response of this group involves the synergistic suppression of Scd1, which diverts fatty acids from oxidation to storage as triglycerides [16–17]. Malic enzyme 1 (Me1), acetyl-CoA carboxylase beta (Acacb), pyruvate dehydrogenase kinase 4 (Pdk4) and elongation of very long chain fatty acids protein 5 (Elovl5) are additional genes, which exhibit pivotal roles in stimulating fatty acid synthesis, that also decline selectively on the HFD [59–62]. The serum regulators of liver metabolism, insulin-like growth factor binding protein 1 (Igfbp1), which decreases IGF1 bioavailability, and fibroblast growth factor 21 (Fgf21), another important regulator of fatty acid metabolism [63–64], each demonstrated paralleled suppression with HFD and Cyp1b1 deletion. The expression levels of Igfbp1 and Fgf21 were highly correlated among the mice of the 4 treatment groups (r2=0.55) (data not shown).
