Minqi Wang

The incidence of non-alcoholic fatty liver disease has proportionally escalated alongside the global epidemic of obesity. Monobutyrin (MB), a food additive found in butter and cod liver oil, possesses lipid-regulating properties. This study aimed to explore the alleviating effect of MB on liver oxidative injury and lipid metabolism in obese mice induced by a high-fat diet (HFD). The results showed that MB administration (1 or 2 g/kg body weight (BW)) for 8 weeks significantly reduced body weight, improved hepatic lipid metabolism via activation of the peroxisome proliferator-activated receptor α (PPARα) signaling pathway, and stabilized liver mitochondrial ultrastructure to alleviate oxidative liver injury by triggering mitochondrial autophagy through regulation of microtubule-associated protein 1A/1B-light chain 3 (LC3) and ubiquitin-binding protein (P62) in mice. Moreover, MB might increase the abundance of beneficial bacteria, promote short-chain fatty acid levels, and alleviate high-fat induced obesity via the gut-liver axis. These findings provide a novel insight into MB as an intervention strategy for hepatic metabolic disorders.

Porcine small intestinal epithelial cell line (IPEC-J2) is a good research model exploring the impact of feed additives on intestinal epithelial cells. Monobutyrin (MB), as a derivative of butyric acid (BA), overcomes the shortcomings of BA. MB can maintain intestinal barrier function in animals, but its underlying regulatory mechanism is unknown. Thus, we used IPEC-J2 cells as the research object. We were using real-time fluorescence quantitative PCR, western blot, immunofluorescence, and transcriptomics technology to explore the effect of MB on the barrier function of IPEC-J2 cells and its regulatory mechanism. The results found that MB treatment could cause IPEC-J2 cells to occur a response to hypoxia at the transcriptional level, thereby increasing the expression of hypoxia-inducible factor 1 and phospho-extracellular signal-regulated kinase 1/2 protein and improving the expression of tight junction proteins. Therefore, MB can alleviate the activation of the NF-κB signaling pathway. In addition, MB mitigates the damage to cell transmembrane glycoproteins, microvilli, and tight junctions caused by lipopolysaccharides (LPS) stimulation, thus resisting the effects of LPS. As a dietary supplement, MB has good application prospects in maintaining the intestinal epithelial barrier function of animals.

In this study, we investigated the effect of monobutyrin (MB) on the gut microbiota and intestinal health of weaned mice. MB was administered via gavage to 21-day-old weaned mice. Samples of small intestinal and ileal contents were collected on day 1, day 7, and day 21 post-administration. Seven days of MB administration enhanced the mucin layer and morphological structure of the intestine and the integrity of the intestinal brush border. Both MB and sodium butyrate (SB) accelerated tight junction development. Compared to SB, MB modulated intestinal T cells in a distinct manner. MB increased the ratio of Treg cells in the small intestine upon the cessation of weaning. After 21 days of MB administration, enhancement of the villus structure of the ileum was observed. MB increased the proportion of Th17 cells in the ileum. MB facilitated the transition of the small intestinal microbiota toward an adult microbial community structure and enhanced the complexity of the microbial community structure. An increase in Th17 cells enhanced intestinal barrier function. The regulatory effect of MB on Th17 cells may occur through the intestinal microbiota. Therefore, MB can potentially be used to promote intestinal barrier function, especially for weaning animals, with promising application prospects.

Obesity and its complications constitute a main threat to global human health. The purpose of this investigation was to explore the influences of Clostridium tyrobutyricum (Ct) on lipid metabolism, intestinal barrier function, and intestinal microbiome in obese mice induced by a high-fat diet (HFD). After establishing the obesity model, 10⁷ CFU/mL and 10⁸ CFU/mL C. tyrobutyricum were used to intervene in HFD-fed mice by gavage for six weeks, and indexes related to obesity were measured. In the liver of HFD-fed mice, the results revealed that C. tyrobutyricum reduced liver weight and the levels of triglyceride (TG), total cholesterol (TC), and nonesterified fatty acid (NEFA), along with decreasing red lipid droplets and fat vacuoles. After C. tyrobutyricum intervention, the mRNA expression of peroxisome proliferator-activated receptor-γ (PPARγ) was downregulated, and AMP-activated protein kinase (AMPK), peroxisome proliferator-activated receptor-α (PPARα), adipose triglyceride lipase (ATGL), and hormone-sensitive lipase (HSL) were upregulated in the liver. Additionally, C. tyrobutyricum alleviated intestinal morphology injury caused by HFD, decreased the expression of tumor necrosis factor-α (TNF-α), interleukin 6 (IL-6), and IL-1β in the colon, and upregulated tight junction protein expression. In addition, 16S rRNA sequencing revealed that C. tyrobutyricum increases the diversity of intestinal microbiota. Overall, C. tyrobutyricum improved HFD-induced lipid metabolism disorders, preserved the intestinal barrier’s integrity, and modulated the structure of the intestinal microbiome. These findings provide a novel insight into the role of C. tyrobutyricum as a probiotic in regulating lipid metabolism.

Rice husk, as a cellulose-rich by-product in agriculture, has been considered as a low-cost substrate for the production of bioethanol and chemicals. In this study, rice husk was pretreated with an alkali, followed by cellulose and β-glucosidase hydrolysis optimized by an orthogonal experiment and response surface methodology (RSM), respectively. Under the optimal treatment conditions, a hydrolysate containing a high reducing sugar yield (77.85%) was obtained from the rice husk. Then, the hydrolysate was used as a carbon substrate for butyric acid production through Clostridium tyrobutyricum Δpta fermentation. Compared to free-cell fermentation, higher concentrations of butyric acid (50.01 g/L vs. 40.8 g/L and 49.03 g/L vs. 27.49 g/L) were observed in immobilized-cell fermentation for the carbon source of glucose and hydrolysate, respectively. A final butyric acid concentration of 16.91 g/L, a yield of 0.31 g/g, and an overall productivity of 0.35 g/L/h from rice husk hydrolysate were obtained in the repeated-fed-batch mode. Taken together, rice husk hydrolysate can be effectively utilized for the bioproduction of butyrate with immobilized-cell fermentation.

This study investigates the attenuating effects of butyrate glycerides (BG) on intestinal inflammatory responses and barrier dysfunction induced by LPS stimulation. An initial dose-response test was carried out to identify the optimal dose of BG for further testing. The mice were given intragastric administration of BG at different doses followed by lipopolysaccharide (LPS) intraperitoneal injection. The small intestinal morphology and cytokine mRNA expression were measured. With 1.5 g/kg BW BG administration, it was possible to alleviate the injury of duodenal morphology, attenuate ileum villus height reduction and promote IL-10 mRNA expression. Therefore, the optimal dosage of 1.5 g/kg BW BG was selected for the main experiment. The ultrastructure image of jejunum and ileum epithelial cells, mRNA expression, the level of cytokine and immunofluorescence in the ileum were analyzed. The results showed that BG maintain the ileac brush border, tight junction structures and protein expression. BG attenuated the increased inflammatory cytokines, TLR4 and JNK mRNA expression. Taken together, 1.5 g/kg BW BG administration maintained intestinal barrier function and reduced intestinal and body inflammation responses induced by LPS in mice. The mechanism by which BG alleviated intestinal inflammatory response and maintained intestinal barrier function may be related to the JNK signaling pathway.

Antibiotics used to be supplemented to animal feeds as growth promoter and as an effective strategy to reduce the burden of pathogenic bacteria present in the gastro-intestinal tract. However, in-feed antibiotics also kill bacteria that may be beneficial to the animal. Secondly, unrestricted use of antibiotics enhanced the antibiotic resistance in pathogenic bacteria. To overcome above problems, scientists are taking a great deal of measures to develop alternatives of antibiotics. There is convincing evidence that probiotics could replace in-feed antibiotics in poultry production. Because they have beneficial effects on growth performance, meat quality, bone health and eggshell quality in poultry. Better immune responses, healthier intestinal microflora and morphology which help the birds to resist against disease attack were also identified with the supplementation of probiotics. Probiotics establish cross-feeding between different bacterial strains of gut ecosystem and reduce the blood cholesterol level via bile salt hydrolase activity. The action mode of probiotics was also updated according to recently published literatures, i.e antimicrobial substances generation or toxin reduction. This comprehensive review of probiotics is aimed to highlight the beneficial effects of probiotics as a potential alternative strategy to replace the antibiotics in poultry.

This study was conducted to investigate the protective effect of chitosan oligosaccharide (COS) against lipopolysaccharide (LPS)-induced intestinal injury. The results demonstrated that COS improved the mucosal morphology of the jejunum and colon in LPS-challenged mice. COS alleviated the LPS-induced down-regulation of tight junction protein expressions and reduction of goblet cells number and mucin expression. The mRNA expressions of anti-microbial peptides secreted by the intestinal cells were also up-regulated by COS. Additionally, COS decreased pro-inflammatory cytokine production and neutrophil recruitment in the jejunum and colon of LPS-treated mice. COS ameliorated intestinal oxidative stress through up-regulating the mRNA expressions of nuclear factor E2-related factor 2 and downstream antioxidant enzymes genes. Correlation analysis indicated that the beneficial effects of COS on intestinal barrier function were associated with its anti-inflammatory activities and antioxidant capacity. Our study provides evidence for the application of COS to the prevention of intestinal barrier dysfunction caused by the stress of a LPS challenge.