Grape seed proanthocyanidin improves intestinal inflammation in canine through regulating gut microbiota and bile acid compositions.

Although certain progress has been made in treating canine inflammatory bowel disease (IBD), a large proportion of dogs have a poor prognosis and may develop resistance and side effects. Therefore, it is of great significance to prevent or alleviate canine IBD through nutritional intervention. Plant polyphenol can interact with intestinal bacteria and has important prospects in the intestinal health improvement. This study evaluated the effect of grape seed proanthocyanidin (GSP), a plant-derived natural polyphenol, on Labrador Retrievers with mild IBD. In Experiment 1 of this study, GSP alleviated persistent intestinal inflammation in canines by improving inflammatory indexes and reducing intestinal permeability. Moreover, GSP treatment increased the abundance of bacteria with potential anti-inflammatory properties and engaging bile acid metabolism, including Ruminococcaceae, Faecalibacterium, Ruminococcus_torques_group, and Lachnospiraceae_NK4A136_group. Notably, targeted metabolomic analysis identified elevated productions of fecal chenodeoxycholic acid and its microbial transformation product lithocholic acid, which might contribute to relieving canine intestinal inflammation. Further, in Experiment 2, fecal microbiota transplantation was used to determine whether gut microbiota is a potential mechanism for GSP efficacy. Dogs with mild IBD received the fecal microbiota from the group administered GSP and mirrored the improvement effects of GSP, which results verified that gut microbial alteration could be an underlying mechanism for GSP efficiency on canine IBD. Our findings highlight that the mechanism of the GSP function on canine IBD is mediated by altering gut microbial composition and improving bile acid metabolism. This study proposes a natural polyphenol-based dietary strategy for improving canine intestinal health.

Effects of Avenanthramide on the Small Intestinal Damage through Hsp70-NF-κB Signaling in an Ovalbumin-Induced Food Allergy Model.

A food allergy is caused by an abnormal immune reaction and can induce serious intestinal inflammation and tissue damage. Currently, the avoidance of food allergens is still the most effective way to prevent or reduce allergic symptoms, so the development of new strategies to treat allergies is important. Avenanthramide (AVA) is a bioactive polyphenol derived from oats with a wide range of biological activities; however, it is still not clear whether or how AVA alleviates intestinal damage under allergic situations. The aim of this study was to explore the effect of AVA on the small intestinal damage in an ovalbumin (OVA)-induced food allergy model and its mechanism. In experiment 1, 10 mg/kg bw and 20 mg/kg bw doses of AVA both decreased the serum levels of OVA-specific IgE, histamine, and prostaglandin D induced by OVA. The AVA administration relieved inflammation indicated by the lower serum concentrations of pro-inflammatory cytokines including interleukin-1ß, IL-6, and tumor necrosis factor-α. The levels of tight junction proteins including Claudin-1, ZO-1, and Occludin in the jejunum were elevated after AVA administration, accompanied by the improved intestinal morphology. Furthermore, AVA elevated the protein expression of heat shock protein 70 (Hsp70) and inhibited the phosphorylation of nuclear factor kappa-B (NF-κB), thus the apoptozole, which a Hsp70 inhibitor, was applied in experiment 2 to assess the contribution of Hsp70-NF-κB signaling to the effects of AVA. In the experiment 2, the inhibition of Hsp70 signaling treatment abolished the beneficial effects of AVA on the small intestinal damage and other allergic symptoms in mice challenged with OVA. Taken together, our results indicated that AVA exerted an intestinal protection role in the OVA-induced allergy, the mechanism of which was partly mediated by the Hsp70-NF-κB signaling.

Short-term changes in dietary fat levels and starch sources affect weight management, glucose and lipid metabolism, and gut microbiota in adult cats.

A 2 × 2 factorial randomized design was utilized to investigate the effects of fat level (8% or 16% fat on a fed basis) and starch source (pea starch or corn starch) on body weight, glycolipid metabolism, hematology, and fecal microbiota in cats. The study lasted for 28 d and included a low fat and pea starch diet (LFPS), a high fat and pea starch diet, a low fat and corn starch diet, and a high fat and corn starch diet. In this study, hematological analysis showed that all cats were healthy. The apparent total tract digestibility of gross energy, crude protein, and crude fat was above 85% in the four diets. After 28 d, cats fed the high fat diets (HF) gained an average of 50 g more than those fed the low fat diets (LF). The hematological results showed that the HF diets increased the body inflammation in cats, while the LFPS group improved the glucolipid metabolism. The levels of glucose and insulin were lower in cats fed the LF diets than those in cats fed the HF diets (P < 0.05). Meanwhile, compared with the LF, the concentrations of total cholesterol, triglyceride, and high-density lipoprotein cholesterol in serum were greater in the cats fed the HF diets (P < 0.05). Additionally, both fat level and starch source influenced the fecal microbiota, with the relative abundance of beneficial bacteria, such as Blautia being significantly greater in the LFPS group than in the other three groups (P < 0.05). Reducing energy density and using pea starch in foods are both valuable design additions to aid in the management of weight control and improve gut health in cats. This study highlights the importance of fat level and starch in weight management in cats.

Obesity is a common problem in domestic cats. Fat in dry-extruded pet food may be a risk factor for feline obesity. Additionally, the utilization of various carbohydrates in domestic cats has garnered attention. This study explored the impact of varying fat levels and starch sources on body weight, glucose metabolism, and gut microbiota composition in healthy adult cats. Our findings suggest that the LF diets are beneficial for weight management, inflammation reduction, and blood sugar regulation in cats. Moreover, adding pea starch can positively affect the gut microbiota by increasing beneficial bacteria.

Chitosan Enhances Intestinal Health in Cats by Altering the Composition of Gut Microbiota and Metabolites.

The interaction between gut microbiota and the health of the host has gained increasing attention. Chitosan is a natural alkaline polysaccharide with a wide range of beneficial effects. However, rare studies have been observed on the effects of dietary chitosan supplementation on intestinal health in cats. A total of 30 cats with mild diarrhea were divided into three groups, receiving a basic diet with 0 (CON), 500 (L-CS) or 2000 (H-CS) mg/kg chitosan. Samples of blood and feces were collected and analyzed for serology and gut microbiota composition. The results demonstrated that chitosan alleviated symptoms of diarrhea, with enhanced antioxidant capability and decreased inflammatory biomarker levels in serum. Chitosan reshaped the composition of gut microbiota in cats that the beneficial bacteria Allobaculum was significantly increased in the H-CS group. Acetate and butyrate contents in feces were significantly higher in the H-CS group in comparison to the CON group (p < 0.05). In conclusion, the addition of dietary chitosan in cats enhanced intestinal health by modulating their intestinal microbes and improved microbiota-derived SCFA production. Our results provided insights into the role of chitosan in the gut microbiota of felines.

Avenanthramide Improves Colonic Damage Induced by Food Allergies in Mice through Altering Gut Microbiota and Regulating Hsp70-NF-κB Signaling.

Food allergies can cause intestinal damage that can exacerbate allergic symptoms, and gut microbiota have been shown to influence allergic development. This study was intended to investigate the effects of Avenanthramide (AVA) on colonic damage induced by food allergy and its mechanism. In Exp. 1, AVA administrations alleviated colonic inflammation in mice challenged with ovalbumin, as shown by decreased concentrations of TNF-α, IL-25 and IL-33. Additionally, the AVA supplementations improved intestinal barrier damage by elevating occludin, ZO-1 and claudin-1 levels. Moreover, AVA inhibited NF-κB phosphorylation and enhanced heat shock protein 70 (Hsp70) expression in the colon. In Exp. 2, apoptozole as a Hsp70 inhibitor was used to explore the Hsp70-NF-κB signaling contribution to AVA function. The AVA additions increased the productions of acetate and butyrate, but decreased propionate. Notably, AVA reduced the colonic abundance of propionate-producing microbes such as Muribaculaceae, but elevated butyrate-producing microbes including Roseburia, Blautia, and Lachnospiraceae_NK4A136_group. Microbial alteration could be responsible for the increased butyrate, and thus the up-regulated Hsp70. However, apoptozole treatment eliminated the effects of AVA. Our study revealed that AVA improved colonic injury and inflammation induced by food allergies, and this mechanism may be mediated by the increased microbial-derived butyrate and involved in the Hsp70-NF-κB signaling.

Comparison of the Effects of Enzymolysis Seaweed Powder and Saccharomyces boulardii on Intestinal Health and Microbiota Composition in Kittens.

Kittens are prone to intestinal health problems as their intestines are not completely developed. Seaweed is rich in plant polysaccharides and bioactive substances that are highly beneficial to gut health. However, the effects of seaweed on cat gut health have not been assessed. This study compared the effects of dietary supplementation with enzymolysis seaweed powder and Saccharomyces boulardii on the intestinal health of kittens. In total, 30 Ragdoll kittens (age: 6 months; weight: 1.50 ± 0.29 kg) were assigned to three treatment groups for a 4-week feeding trial. The dietary treatment given was as follows: (1) basal diet (CON); (2) CON + enzymolysis seaweed powder (20 g/kg of feed) mixed evenly with the diet (SE); and (3) CON + Saccharomyces boulardii (2 × 1010 CFU/kg of feed) mixed evenly with the diet (SB). Compared with the CON and SB groups, dietary supplementation with the enzymolysis seaweed powder improved the immune and antioxidant capacity and also reduced the intestinal permeability and inflammation levels of kittens. The relative abundance of Bacteroidetes, Lachnospiraceae, Prevotellaceae, and Faecalibacterium in the SE group was higher than those in the CON and SB groups (p ≤ 0.05), while the relative abundance of Desulfobacterota, Sutterellaceae, and Erysipelatoclostridium in the SB group was lower than that in the SE group (p ≤ 0.05). Moreover, enzymolysis seaweed powder did not alter the level of intestinal SCFAs in kittens. Conclusively, supplementing kitten diet with enzymolysis seaweed powder can promote intestinal health by enhancing the gut barrier function and optimizing the microbiota composition. Our findings provide new perspectives on the application of enzymolysis seaweed powder.

Dietary lysolecithin supplementation improves growth performance of weaned piglets via improving nutrients absorption, lipid metabolism, and redox status.

Lysolecithin is widely used as emulsifier to improve the digestibility and retention of fat. The current study aimed to investigate the effects of dietary lysolecithin supplementation on growth performance, nutrients absorption, lipid metabolism, and redox status of weaned pigs. A total of 60 weaned piglets were assigned into 2 dietary treatments in a randomized complete block design, receiving basal diet with 0 or 1,000 mg/kg lysolecithin for a period of 28 d. Each dietary treatment had 10 replicates with 3 piglets per replicate. Growth performance and fecal score were monitored during trial. Samples of blood, ileum, and liver tissues were collected and analyzed for serology, intestinal histomorphology, and lipid metabolism-related gene and protein expressions. Dietary lysolecithin supplementation increased average daily gain (+15%, P < 0.05) and tended to increase average daily feed intake (+14%, P = 0.08) in overall experimental period. At final, the average body weight of piglets in lysolecithin group was 10% greater than that of control group (P = 0.09). In addition, dietary lysolecithin supplementation improved the ability of nutrients absorption as indicated by the higher d-xylose level in plasma (P < 0.05). Moreover, piglets from lysolecithin group had higher concentration of high-density lipoprotein (P < 0.05), but lower triglyceride (P < 0.05) in plasma. The inclusion of lysolecithin in diet increased the level of reduced glutathione (GSH) and GSH to oxidized glutathione (GSSG) ratio in plasma and liver (P < 0.05), but attenuated the levels of malondialdehyde and GSSG in ileum (P < 0.05). The upregulation of lipogenesis-related genes (FAS and ACC), downregulation of lipolysis (PNPLA2 and PABP1), and lipid mobilization (PGC-1α and SRIT1) genes were observed in lysolecithin relative to control piglets. Compared with control group, dietary lysolecithin supplementation upregulated protein expressions of GPX4, SREBP1, and LPL in liver and LPL in ileum (P < 0.05). Collectively, our study indicates that dietary lysolecithin supplementation improved growth performance of weaned piglets, which may be associated with the improved nutrients absorption, redox status, and lipid metabolism.

Early weaning has been widely adopted to maximize productivity for swine production. However, the weaned piglets suffer from insufficient energy intake due to the reduced feed intake caused by weaning stress, which compromises the growth rate of piglets. In the present study, dietary lysolecithin supplementation increased average daily gain and average daily feed intake in overall experimental period, thereby showed positive effect on final body weight of weaned piglets. In addition, lysolecithin supplementation improved adipogenesis and anti-oxidant capacity, but suppressed lipolysis and pro-oxidant factors.

Grape Seed Proanthocyanidin Alleviates Intestinal Inflammation Through Gut Microbiota-Bile Acid Crosstalk in Mice.

Regulation of gut microbiota and modulation of bile acid (BA) composition are potential strategies for the treatment of intestinal inflammation. This study aimed to investigate the effect of grape seed proanthocyanidin (GSP) on intestinal inflammation and to understand its mechanism. C57BL/6J male mice (7-8 weeks old) were used in experiments. Antibiotics were applied to deplete gut microbiota to evaluate the contribution of gut microbiota to the effect of dietary GSP. Intestinal-specific farnesoid X receptor (FXR) inhibitor was used to analyze the role of FXR signaling. In this study, GSP alleviated intestinal inflammation induced by LPS and altered the gut microbiota accompanied by increased abundance of hydroxysteroid dehydrogenase (HSD) producing microbes. GSP activated the intestinal FXR signaling pathway and increased gene expression of enzymes of the alternative BA synthetic pathway, which associated with elevated levels of chenodeoxycholic acid (CDCA) and lithocholic acid (LCA) in liver and feces. However, gut microbiota depletion by antibiotics removed those effects of GSP on mice injected with LPS. In addition, the protective effect of GSP on mice challenged with LPS was weakened by the inhibition of intestinal FXR signaling. Further, the mixture of CDCA and LCA mirrored the effects of GSP in mice injected with LPS, which might verify the efficiency of CDCA and LCA on intestinal inflammation. Taken together, our results indicated that GSP exerted an intestinal protection role in the inflammation induced by LPS, and these effects were mediated by regulating gut microbiota-BA crosstalk.