Gut microbiome is crucial for lipid metabolism in humans and animals. However, how specific gut microbiota and their associated metabolites impact fat deposition remains unclear. In this study, we demonstrated that the colonic microbiome of lean and obese pigs differentially contributes to fat deposition, as evidenced by colonic microbiota transplantation experiments. Notably, the higher abundance of Bifidobacterium pseudocatenulatum was significantly associated with lower backfat thickness in lean pigs. Microbial‐derived lithocholic acid (LCA) species were also significantly enriched in lean pigs and positively correlated with the abundance of B. pseudocatenulatum . In a high‐fat diet (HFD)‐fed mice model, administration of live B. pseudocatenulatum decreased fat deposition and enhances colonic secondary bile acid biosynthesis. Importantly, pharmacological inhibition of the bile salt hydrolase (BSH), which mediates secondary bile acid biosynthesis, impaired the anti‐fat deposition effect of B. pseudocatenulatum in antibiotic‐pretreated, HFD‐fed mice. Furthermore, dietary LCA also decreased fat deposition in HFD‐fed rats and obese pig models. These findings provide mechanistic insights into the anti‐fat deposition role of B. pseudocatenulatum and identify BSH as a potential target for preventing excessive fat deposition in humans and animals.

The present study was performed to evaluate the antioxidant and intestinal protective effects of baicalin-copper on deoxynivalenol-challenged piglets. Forty weaned piglets were randomly divided into four groups and assigned to different diets: (1) basal diet (Con), (2) 4 mg/kg deoxynivalenol of basal diet (DON), (3) 5 g/kg baicalin-copper of basal diet (BCU); and (4)4mg/kgdeoxynivalenol+5g/kgbaicalin‐copperof basal diet (DBCU). The results showed that the ADFI and ADG of piglets in the DON group were markedly lower than those in the Con group, but the ADFI and ADG of the DBCU group were not significantly different from those of the Con group. In piglets fed a DON-contaminated diet, dietary supplementation with BCU significantly decreased the mRNA levels of P70S6K, 4E-BP1, and HSP70 in the liver, the protein expression of HO-1 in the jejunum, and the expression of p-Nrf2 and p-NF-κB in the ileum but increased Mn-SOD activity in serum. Dietary supplementation with BCU increased jejunal maltase, ZIP4 and MT mRNA levels, and serum concentrations of Arg, Val, Ile, Leu, Lys, and Tyr in DON-contaminated piglets. In summary, BCU can alleviate the growth impairment induced by DON and enhance antioxidant capacity and nutrition absorption in piglets fed DON-contaminated diets.

Background: Deoxynivalenol contamination is increasing worldwide, presenting great challenges to food security and causing great economic losses in the livestock industry. Objective: This study was conducted to determine the protective effect of baicalin zinc as a dietary supplement on pigs fed with a deoxynivalenol contaminated diet. Methods: A total of 40 weaned pigs (21 d of age; 6.13 ± 0.42 kg average BW) were randomly assigned (10 pigs/group) to 4 dietary treatments: basal diet (Con group), basal diet + 4 mg/kg DON (DON group), basal diet + 5 g/kg BZN (BZN group), and basal diet + 5 g/kg BZN + 4 mg/kg DON (DBZN group) for a 14-d period. Seven randomly-selected pigs from each treatment were killed for blood and tissue sampling. Results: The results showed that piglets challenged with DON exhibited significantly reduced levels of ADG, ADFI, and F/G (p < 0.05). BZN supplemented diets significantly suppressed the protein expression of p-Nrf2, p-NF-kB, and HO-1 in the jejunum of DON challenged piglets (p < 0.05). In liver, DON markedly increased the mRNA expression of P70S6K and HSP70 in piglets fed the basal diet, but significantly reduced that of HO-1, NQO-1, NF-kB, AMPKα2 and HSP70 in piglets fed the BZN supplemented diet (p < 0.05). Dietary supplementation with BZN markedly increased the T-AOC level of serum in weaned piglets (p < 0.05). In jejunum, dietary supplementation with BZN activated the mRNA expression of ZIP4 in piglets (p < 0.05), BZN supplementation significantly suppressed the activity of sucrose and increased the protein concentration in chyme (p < 0.05). Conclusion: BZN can play a protective role by reducing oxidative stress and enhancing nutrient absorption in pigs fed DON-contaminated diets.

The present experiment assessed the inflammatory responses, hormone secretion, and gut microbiota of weanling piglets administered baicalin-copper complex (BCU) or deoxynivalenol (DON) supplementation diets. Twenty-eight piglets were randomly assigned to four groups: control diet (Con group), a 4 mg DON/kg diet (DON group), a 5 g BCU/kg diet (BCU group), a 5 g BCU + 4 mg DON/kg diet (DBCU group). After 14 days, the results showed that dietary BCU supplementation remarkably increased the relative abundance of Clostrium bornimense and decreased the relative abundance of Lactobacillus in the DBCU group (p < 0.05). BCU decreased the serum concentration of IgG, IL-2, IFN-γ, and IgA in DON treated piglets (p < 0.05), and promoted the serum concentration of IL-1β, IgG, IL-2, IFN-γ, IgA, IL-6, IgM, and TNFα in normal piglets (p < 0.05). BCU increased the concentrations of serum IGF1, insulin, NPY, GLP-1, and GH, and decreased the concentrations of serum somatostatin in no DON treated piglets (p < 0.05). Dietary BCU supplementation significantly promoted the secretion of somatostatin, and inhibited the secretion of leptin in piglets challenged with DON (p < 0.05). BCU regulated the expression of food intake-related genes in the hypothalamus and pituitary of piglets. Collectively, dietary BCU supplementation alleviated inflammatory responses and regulated the secretion of appetite-regulating hormones and growth-axis hormones in DON challenged piglets, which was closely linked to changes of intestinal microbes.

Trimethylamine oxide (TMAO) is a microbiota-derived metabolite, and numerous studies have shown that it could regulate fat metabolism in humans and mice. However, few studies have focused on the effects of TMAO on fat deposition in growing-finishing pigs. This study aimed to investigate the effect of TMAO on fat deposition and intestinal microbiota in growing-finishing pigs. Sixteen growing pigs were randomly divided into 2 groups and fed with a basal diet with 0 or 1 g/kg TMAO for 149 d. The intestinal microbial profiles, fat deposition indexes, and fatty acid profiles were measured. These results showed that TMAO supplementation had a tendency to decrease lean body mass (P < 0.1) and significantly increased backfat thickness (P < 0.05), but it did not affect growth performance. TMAO significantly increased total protein (TP) concentration, and reduced alkaline phosphatase (ALP) concentration in serum (P < 0.05). TMAO increased the α diversity of the ileal microbiota community (P < 0.05), and it did not affect the colonic microbial community. TMAO supplementation significantly increased acetate content in the ileum, and Proteobacteria and Escherichia– S higella were significantly enriched in the TMAO group (P < 0.05). In addition, TMAO decreased fat content, as well as the ratio of linoleic acid, n-6 polyunsaturated fatty acids (PUFA), and PUFA in the liver (P < 0.05). On the contrary, TMAO increased intramuscular fat content of the longissimus dorsi muscle, whereas the C18:2n6c ratio was increased, and the n-6 PUFA:PUFA ratio was decreased (P < 0.05). In vitro, 1 mM TMAO treatment significantly upregulated the expression of FASN and SREBP1 in C2C12 cells (P < 0.05). Nevertheless, TMAO also increased adipocyte area and decreased the CPT-1B expression in subcutaneous fat (P < 0.05). Taken together, TMAO supplementation regulated ileal microbial composition and acetate production, and regulated fat distribution and fatty acid composition in growing-finishing pigs. These results provide new insights for understanding the role of TMAO in humans and animals.