Since there was no HFD or obesity to modify gut microbiota-derived glycine lipids in the chow-fed Apoe−/− model, our results suggest that in conditions where gut microbiome-derived TLR2 signals are lost (e.g., HFD-induced obesity), hyperlipidemia and changes in liver immune response may be exacerbated—although, the attenuated effects observed in chow-fed Apoe−/− mice may also be explained by genotype differences between the models. The gene discussed is APOE; the disease is obesity due to melanocortin 4 receptor deficiency.