Gut microbiota signatures and lipids metabolism profiles by exposure to polyene phosphatidylcholine.

The aim of the study was to address the causality links and identify specific features of the gut microbiota signatures contributing to host lipids metabolism in the presence or absence of polyene phosphatidylcholine (PPC) administration, and evaluate potential risk of PPC consumption. About 20 C57BL/6J mice were randomly allocated into two groups, normal diet group (CK) and PPC administration group (205.2 mg/kg). Compared with CK group, the contents of unsaturated fatty acids were increased and the saturated fatty acids were decreased in PPC group. The content of free fatty acids (FFA) and lipopolysaccharides (LPS) were significantly decreased (P < 0.05), and expression of carnitine palmitoyltransferase 1A (CPT1A), cluster of differentiation 36 (CD36), liver fatty acid binding protein (L-FABP), fatty acid transport protein 5 (FATP5), and fatty acid synthase (FASN) were significantly decreased in the mRNA and protein levels after treated by PPC (P < 0.05, P < 0.01). Also, we found that acetic acid in feces was significantly increased after consumption of PPC (P < 0.05). After PPC administration the relative abundances of Firmicutes and Clostridia were increased within the phylum level and the class level, respectively. Microbial abundances in genus level were dominated by Lachnospiraceae and Lachnospiraceae_NK4A136_group, whereas the proportion of sequences assigned to Bacteroidetes within the phylum level, class Bacteroidias and Mollicutes, order Anaeroplasmatalesl, genus Bacteroidales_S24-7_group were decreased in metagenomes of treated group with PPC and did not significantly influence on the accumulation of trimethylamine-N-oxide (TMAO). This study revealed that intake of PPC could regulate the gut microbiota signatures and lipids metabolism in mice without TMAO accumulations.