Perturbation of the lipid metabolism and intestinal inflammation in growing pigs with low birth weight is associated with the alterations of gut microbiota

摘要

Low birth weight (LBW) is accompanied by metabolic dysfunction, chronic inflammation and gut microbiota perturbation in piglets during early life. Regulating gut microbiota structure can indirectly or directly affect gut health and the host's metabolism. However, whether gut microbiota dysbiosis impact lipid metabolism and inflammation progression in the LBW pigs later in life is unclear. In the present study, we investigated the role of gut microbiota on homeostasis in organisms using young pigs as a model. The plasma concentrations of High-density lipoproteins (HDL—C) and pro-inflammatory cytokines such as Interleukin 6 (IL-6), Tumor necrosis factor alpha (TNF-a) and Interleukin 18 (IL-18) were increased in LBW pigs. The bacterial composition was modified dramatically in LBW group in association with an increase in propionate, butyrate and Short-chain fatty acids (SCFAs) in the ileal digesta. LBW impaired intestine results in damaged Fatty acid-binding protein 1 {FABP2) and Fatty acid-binding protein 4 (FABP4) expressions, and the inhibition of Free fatty acid receptor 1 (FFAR1), Free fatty acid receptor 2 (FFAR2) and G protein-coupled receptor 119 (GPR119) expressions, causing inefficient SCFAs absorption. Meanwhile, the physical barrier and chemical barrier related to functional gene expressions of Occludin, Claudin-1, Mucin 1 (ML/C1) and Mucin 2 (MUC2) in both ileum and colon were decreased in the LBW pigs. The genera of Blautia, Bifidobacterium, Subdoligranulum and Coprococcus 3 in the ileum were correlated positively with lipid metabolic dysfunction and pro-inflammatory response in LBW pigs. Collectively, the gut microbiota is critical for perturbation of lipid metabolism and inflammatory progression in LBW pigs, which suggests the interventions for modulating bacterial communities may be therapeutically beneficial for metabolic diseases and chronic inflammation.