Changes of gut microbiota in pregnant sows induced by 5-Aminolevulinic acid.

Sow health is related to farm productivity and sustainability, but the increased resistance of bacteria to antibiotics in the pig industry has led to a decline in resistance to disease and environmental pollution. 5-Aminolevulinic acid (5-ALA) is considered a feed additive to replace antibiotics, but the effect of 5-ALA on gut microbiota has not been studied. In this study, we fed 12 healthy Landrace × Large White two-line hybrid sows with different concentrations of 5-ALA; blood and fecal samples were obtained after 110 days of pregnancy, and 16S rRNA amplicon sequencing was performed. The alpha diversity of the gut microbiota in sows was not significant among the sows fed different concentrations of 5-ALA. PCoA revealed a significant (P < 0.05) difference in the gut microbiota composition with different 5-ALA groups. LEfSe revealed that 5-ALA increased relative abundance of Streptococcus, while Myroides was enriched in CK group. Functional prediction of Tax4Fun showed that different concentrations of 5-ALA significantly (P < 0.05) increased the mean relative abundance of KEGG pathways involved in core microbiota cellular processes, environmental information processing, and genetic information processing. In summary, 5-ALA changed bacterial community composition of gut microbiota, reduced colonization of some pathogenes and increased the relative abundance of some probiotics. These results provide a theoretical basis for the healthy breeding of pigs.

Trimethylamine-N-oxide (TMAO)-induced atherosclerosis is associated with bile acid metabolism.

BACKGROUND: Recently, trimethylamine-N-oxide (TMAO) plasma levels have been proved to be associated with atherosclerosis development. Among the targets aimed to ameliorating atherosclerotic lesions, inducing bile acid synthesis to eliminate excess cholesterol in body is an effective way. Individual bile acid as endogenous ligands for the nuclear receptor has differential effects on regulating bile acid metabolism. It is unclear whether bile acid profiles are mechanistically linked to TMAO-induced development of atherosclerosis. METHODS: Male apoE-/- mice were fed with control diet containing 0.3% TMAO for 8 weeks. Aortic lesion development and serum lipid profiles were determined. Bile acid profiles in bile, liver and serum were measured by liquid chromatographic separation and mass spectrometric detection (LC-MS). Real-time PCRs were performed to analyze mRNA expression of genes related to hepatic bile acid metabolism. RESULTS: The total plaque areas in the aortas strongly increased 2-fold (P < 0.001) in TMAO administration mice. The levels of triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-c) in TMAO group were also significantly increased by 25.5% (P = 0.044), 31.2% (P = 0.006), 28.3% (P = 0.032), respectively. TMAO notably changed bile acid profiles, especially in serum, the most prominent inductions were tauromuricholic acid (TMCA), deoxycholic acid (DCA) and cholic acid (CA). Mechanically, TMAO inhibited hepatic bile acid synthesis by specifically repressing the classical bile acid synthesis pathway, which might be mediated by activation of small heterodimer partner (SHP) and farnesoid X receptor (FXR). CONCLUSIONS: These findings suggested that TMAO accelerated aortic lesion formation in apoE-/- mice by altering bile acid profiles, further activating nuclear receptor FXR and SHP to inhibit bile acid synthesis by reducing Cyp7a1 expression.

Comparative Analysis of EPA/DHA-PL Forage and Liposomes in Orotic Acid-Induced Nonalcoholic Fatty Liver Rats and Their Related Mechanisms.

Nonalcoholic fatty liver disease (NAFLD) has become one predictive factor of death from various illnesses. The present study was to comparatively investigate the effects of eicosapentaenoic acid-enriched and docosahexaenoic acid-enriched phospholipids forage (EPA-PL and DHA-PL) and liposomes (lipo-EPA and lipo-DHA) on NAFLD and demonstrate the possible protective mechanisms involved. The additive doses of EPA-PL and DHA-PL in all treatment groups were 1% of total diets, respectively. The results showed that Lipo-EPA could significantly improve hepatic function by down-regulating orotic acid-induced serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels by 55.6% and 34.2%, respectively (p < 0.01). Moreover, lipo-EPA exhibited excellent inhibition on the mRNA expression of SREBP-1c and FAS at the values of 0.454 ± 0.09 (p < 0.01) and 0.523 ± 0.08 (p < 0.01), respectively, thus ameliorating OA-induced NAFLD. Meanwhile, lipo-EPA could significantly suppress the SREBP-2 and HMGR levels (31.4% and 66.7%, p < 0.05, respectively). In addition, EPA-PL and lipo-DHA could also significantly suppress hepatic lipid accumulation mainly by enhancement of hepatic lipolysis and cholesterol efflux. Furthermore, DHA-PL played a certain role in inhibiting hepatic lipogenesis and accelerating cholesterol efflux. The results obtained in this work might contribute to the understanding of the biological activities of EPA/DHA-PL and liposomes and further investigation on its potential application values for food supplements.