Succinate is a circulating metabolite, and the relationship between abnormal changes in the physiological concentration of succinate and inflammatory diseases caused by the overreaction of certain immune cells has become a research focus. Recent investigations have shown that succinate produced by the gut microbiota has the potential to regulate host homeostasis and treat diseases such as inflammation. Gut microbes are important for maintaining intestinal homeostasis. Microbial metabolites serve as nutrients in energy metabolism, and act as signal molecules that stimulate host cell and organ function and affect the structural balance between symbiotic gut microorganisms. This review focuses on succinate as a metabolite of both host cells and gut microbes and its involvement in regulating the gut – immune tissue axis by activating intestinal mucosal cells, including macrophages, dendritic cells, and intestinal epithelial cells. We also examined its role as the mediator of microbiota – host crosstalk and its potential function in regulating intestinal microbiota homeostasis. This review explores feasible ways to moderate succinate levels and provides new insights into succinate as a potential target for microbial therapeutics for humans.

Flavonoids are natural plant-derived dietary bioactive compounds having a substantial impact on human health. Morin hydrate is a bioflavonoid mainly obtained from fruits, stem, and leaves of Moraceae family members' plants. Plenty of evidences supported that morin hydrate exerts its beneficial effects against various chronic and life-threatening degenerative diseases. Our current article discloses the recent advances that have been studied to explore the biological/pharmacological properties and molecular mechanisms to better understand the beneficial and multiple health benefits of morin hydrate. Indeed, Morin hydrate exerts free radical scavenging, antioxidant, anti-inflammatory, anti-cancerous, anti-microbial, antidiabetic, anti-arthritis, cardioprotective, neuroprotective, nephroprotective, and hepatoprotective effects. Moreover, morin hydrate exhibits its pharmacological activities by modulating various cellular signaling pathways such as Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-қB), Mitogen-activated protein kinase (MAPK), Janus kinases/ Signal transducer and activator of transcription proteins (JAKs/STATs), Kelch-like ECH-associated protein1/Nuclear erythroid-2-related factor (Keap1/Nrf2), Endoplasmic reticulum (ER), Mitochondrial-mediated apoptosis, Wnt/β-catenin, and Mechanistic target of rapamycin (mTOR). Most importantly, morin hydrate has the potential to modulate a variety of biological networks. Therefore, it can be predicted that this therapeutically potent compound could serve as a dietary agent for the expansion of human health and might be helpful for the development of the novel drug in the future. However, due to the lack of clinical trials, special human clinical trials are needed to address the effects of morin hydrate on various life-threatening disparities to recommend morin and/or morin-rich foods with other foods or bioactive dietary components, as well as dose-response interaction and safety profile.

The present study was conducted to investigate the effects of outdoor access on the growth performance and meat quality of broiler chickens. Thirty-f

Deoxynivalenol (DON) is a threatening mycotoxin primarily present in the agricultural environment, especially in food commodities and animal forages, and exerts significant global health hazards. Lycopene (LYC) is a potent antioxidant carotenoid mainly present in tomatoes and other fruits with enormous health benefits. The present study was designed to ascertain whether LYC could protect DON-induced intestinal epithelium oxidative injury by regulating Keap1/Nrf2 signaling in the intestine of mice. A total of forty-eight mice were randomly distributed into four groups (n = 12), Control (CON), 10 mg/kg BW LYC, 3 mg/kg BW DON, and 3 mg/kg DON + 10 mg/kg LYC BW (DON + LYC). The experimental groups were treated by intragastric administration for 11 days. Our results showed that LYC significantly increased average daily feed intake (ADFI), average daily gain (ADG), and repaired intestinal injury and barrier dysfunction, as evident by increased trans-epithelial electrical resistance (TEER) and decreased diamine oxidase (DAO) activity, as well as up-regulated tight junction proteins (occludin, claudin-1) under DON exposure. Furthermore, LYC treatment stabilized the functions of intestinal epithelial cells (Lgr5, PCNA, MUC2, LYZ, and Villin) under DON exposure. Additionally, LYC alleviated DON-induced oxidative stress by reducing ROS and MDA accumulation and enhancing the activity of antioxidant enzymes (CAT, T-SOD, T-AOC, and GSH-Px), which was linked with the activation of Nrf2 signaling and degradation of Keap1 expression. Conclusively, our findings demonstrated that LYC protects intestinal epithelium from oxidative injury by modulating the Keap1/Nrf2 signaling pathway under DON exposure. These novel findings could lead to future research into the therapeutic use of LYC to protect the DON-induced harmful effects in humans and/or animals.

As the first limiting amino acid, lysine (Lys) has been thought to promote muscle fiber hypertrophy by increasing protein synthesis. However, the functions of Lys seem far more complex than that. Despite the fact that satellite cells (SCs) play an important role in skeletal muscle growth, the communication between Lys and SCs remains unclear. In this study, we investigated whether SCs participate directly in Lys-induced skeletal muscle growth and whether the mammalian target of rapamycin complex 1 (mTORC1) pathway was activated both in vivo and in vitro to mediate SC functions in response to Lys supplementation. Subsequently, the skeletal muscle growth of piglets was controlled by dietary Lys supplementation. Isobaric tag for relative and absolute quantitation (iTRAQ) analysis showed activated SCs were required for longissimus dorsi muscle growth, and this effect was accompanied by mTORC1 pathway upregulation. Furthermore, SC proliferation was governed by medium Lys concentrations, and the mTORC1 pathway was significantly enhanced in vitro. After verifying that rapamycin inhibits the mTORC1 pathway and suppresses SC proliferation, we conclude that Lys is not only a molecular building block for protein synthesis but also a signal that activates SCs to manipulate muscle growth via the mTORC1 pathway.