Medium-chain fatty acid glycerides have been shown to provide energy for rapid oxidation in the body. The study was conducted to investigate the effects of dietary supplementation with medium-chain fatty acid glyceride on the growth performance and intestinal health of weaned piglets fed with a low-protein diet. Nighty healthy weaned piglets were randomly divided into five treatments: NP (Normal protein treatment, normal-protein diet no antibiotics included); NC (Negative control, low-protein diet no antibiotics included); PC (Positive control, low-protein diet +75 mg/kg quinocetone, 20 mg/kg virginiamycin and 50 mg/kg aureomycin); MCT (tricaprylin + tricaprin treatment, low-protein diet + tricaprylin + tricaprin); GML (glycerol monolaurate treatment, low-protein diet + glycerol monolaurate). The results showed that the average daily feed intake (ADFI) of the MCT treatment was significantly higher than that of the NP, NC treatments (p < 0.05). In the jejunum, the villus height of the GML treatment was significantly lower than that of the PC treatment (p < 0.05), and the number of goblet cells in the GML treatment was higher than that in the NC treatment (p < 0.05). Compared with the NC treatment, the MCT treatment significantly increased the level of claudin-1, Zonula occludens-1(ZO-1), while the GML treatment significantly increased the level of claudin-1, occludin, ZO-1 (p < 0.05). In the ileum, the level of ZO-1 in the GML treatment was significantly higher than that in the NP, NC, PC treatments (p < 0.05). Compared with the NC treatment, the GML treatment significantly increased the level of Secretory immunoglobulin A (SIgA) in the ileum and serum, while the MCT treatment significantly increased the level of SIgA and decreased the level of interleukin-6 (IL-6) in the ileum (p < 0.05). These results showed that the addition of medium-chain fatty acid glycerides to a low-protein diet could improve the growth performance and intestinal functional barrier of weaned piglets and also improve the immune function of weaned piglets.

Obesity is a global health challenge that has received increasing attention in contemporary research. The gut microbiota has been implicated in the development of obesity, primarily through its involvement in regulating various host metabolic processes. Recent research suggests that epigenetic modifications may serve as crucial pathways through which the gut microbiota and its metabolites contribute to the pathogenesis of obesity and other metabolic disorders. Hence, understanding the interplay between gut microbiota and epigenetic mechanisms is crucial for elucidating the impact of obesity on the host. This review primarily focuses on the understanding of the relationship between the gut microbiota and its metabolites with epigenetic mechanisms in several obesity-related pathogenic mechanisms, including energy dysregulation, metabolic inflammation, and maternal inheritance. These findings could serve as novel therapeutic targets for probiotics, prebiotics, and fecal microbiota transplantation tools in treating metabolic disruptions. It may also aid in developing therapeutic strategies that modulate the gut microbiota, thereby regulating the metabolic characteristics of obesity.

Early weaning stress impairs the development of gastrointestinal barrier function, causing immune system dysfunctions, reduction in feed intake, and growth retardation. Autophagy was hypothesized to be a key underlying cellular process in these dysfunctions. We conjectured that rapamycin (RAPA) and chloroquine (CQ), as two autophagy-modifying agents, regulate the autophagy process and may produce deleterious or beneficial effects on intestinal health and growth. To explore the effect of autophagy on early weaning stress in piglets, 18 early-weaned piglets were assigned to three treatments (each treatment of six piglets) and treated with an equal volume of RAPA, CQ, or saline. The degree of autophagy and serum concentrations of immunoglobulins and cytokines, as well as intestinal morphology and tight junction protein expression, were evaluated. Compared with the control treatment, RAPA-treated piglets exhibited activated autophagy and had decreased final body weight (BW) and average daily gain (ADG) (p < 0.05), impaired intestinal morphology and tight junction function, and higher inflammatory responses. The CQ-treated piglets showed higher final BW, ADG, jejuna and ileal villus height, and lower autophagy and inflammation, compared with control piglets (p < 0.05). Throughout the experiment, CQ treatment was beneficial to alleviate early weaning stress and intestinal and immune system dysfunction.

Phosphatidylethanolamine (PE), a multifunctional phospholipid, is necessary for neonate development. This study aimed to explore the impact of the regulation of exogenous PE on postnatal growth retardation (PGR) by improving intestinal barrier function. Thirty-two neonatal pigs were divided into four groups according to their body weight (BW 2.79 ± 0.50 kg or 1.88 ± 0.40 kg) at 7 days old, CON-NBW, PE-NBW, CON-PGR, and PE-PGR. PE was supplemented to NBW piglets and PGR piglets during lactation and post-weaning periods. Compared with the NBW piglets, the growth performance of PGR piglets was lower, while PE improved the poor growth performance. PGR piglets showed injured intestinal morphology, as evidenced by the reduced ratio of villus height to crypt depth (VH/CD) and goblet cell numbers in the jejunum and ileum. PE recovered the intestinal barrier injury by increasing VH/CD and goblet cell numbers. The decreased MUC2 mRNA and protein expressions were observed in the small intestine of PGR piglets, and PE remarkably increased the expression of MUC2. Mechanistically, PE increased the goblet cell differentiation promoting gene spdef mRNA levels and reduced the mRNA expressions involved in endoplasmic reticulum stress in the jejunal and ileal mucosa of PGR piglets. Overall, we found that PE alleviated growth retardation by regulating intestinal health and generalized its application in neonates.

Abnormal hepatic energy metabolism limits the growth and development of piglets. We hypothesized that β-hydroxybutyrate (BHB) might improve the growth performance of piglets by maintaining hepatic caloric homeostasis. A total of 30 litters of newborn piglets were tracked, and 30 postnatal growth retardation (PGR) piglets and 40 healthy piglets were selected to treat with normal saline with or without BHB (25 mg/kg/days) at 7-d-old. At the age of 42 days, 8 piglets in each group were sacrificed, and serum and liver were collected. Compared with the healthy-control group piglets, PGR piglets showed lower body weight (BW) and liver weight (p < 0.05), and exhibited liver injury and higher inflammatory response. The contents of serum and hepatic BHB were lower (p < 0.05), and gene expression related to hepatic ketone body production were down-regulated in PGR piglets (p < 0.05). While BHB treatment increased BW and serum BHB levels, but decreased hepatic BHB levels in PGR piglets (p < 0.05). BHB alleviated the liver injury by inhibiting the apoptosis and inflammation in liver of PGR piglets (p < 0.05). Compared with the healthy-control group piglets, liver glycogen content and serum triglyceride level of PGR piglets were increased (p < 0.05), liver gluconeogenesis gene and lipogenesis gene expression were increased (p < 0.05), and liver NAD⁺level was decreased (p < 0.05). BHB supplementation increased the ATP levels in serum and liver (p < 0.05), whereas decreased the serum glucose, cholesterol, triglyceride and high-density lipoprotein cholesterol levels and glucose and lipid metabolism in liver of PGR piglets (p < 0.05). Therefore, BHB treatment might alleviate the liver injury and inflammation, and improve hepatic energy metabolism by regulating glucose and lipid metabolism, thereby improving the growth performance of PGR piglets.

肠道干细胞通过增殖和分化沿隐窝-绒毛轴不断地向上迁移，构成全部肠上皮细胞，是生命早期肠道发育的结构基础。肠道微生物可通过其表面分子或者代谢物调控肠道干细胞的命运与功能，继而影响肠道发育轨迹。本文综述了肠道干细胞稳恒及上皮更新作用驱动幼龄动物肠道发育，修复肠道稳态。重点解析了肠道微生物表面鞭毛蛋白、肽聚糖、脂多糖以及微生物三大代谢产物短链脂肪酸、色氨酸代谢物、次级胆汁酸对肠道干细胞增殖与分化的调控机制。探讨了益生菌、益生元等营养物质及菌群移植对肠道干细胞发育的促进作用，为研究生命早期微生物菌群与肠道发育互作提供参考。