Inflammatory bowel disease (IBD), characterized by an abnormal immune response, includes two distinct types: Crohn’s disease (CD) and ulcerative colitis (UC). Extensive research has revealed that the pathogeny of IBD encompasses genetic factors, environmental factors, immune dysfunction, dysbiosis, and lifestyle choices. Furthermore, patients with IBD exhibit both local and systemic oxidative damage caused by the excessive presence of reactive oxygen species. This oxidative damage exacerbates immune response imbalances, intestinal mucosal damage, and dysbiosis in IBD patients. Meanwhile, the weaning period represents a crucial phase for pigs, during which they experience pronounced intestinal immune and inflammatory responses, leading to severe diarrhea and increased mortality rates. Pigs are highly similar to humans in terms of physiology and anatomy, making them a potential choice for simulating human IBD. Although the exact mechanism behind IBD and post-weaning diarrhea remains unclear, the oxidative damage, in its progression and pathogenesis, is well acknowledged. Besides conventional anti-inflammatory drugs, certain probiotics, particularly Lactobacillus and Bifidobacteria strains, have been found to possess antioxidant properties. These include the scavenging of reactive oxygen species, chelating metal ions to inhibit the Fenton reaction, and the regulation of host antioxidant enzymes. Consequently, numerous studies in the last two decades have committed to exploring the role of probiotics in alleviating IBD. Here, we sequentially discuss the oxidative damage in IBD and post-weaning diarrhea pathogenesis, the negative consequences of oxidative stress on IBD, the effectiveness of probiotics in IBD treatment, the application of probiotics in weaned piglets, and the potential antioxidant mechanisms of probiotics.
The immature immune system at birth and environmental stress increase the risk of infection in nursing pigs. Severe infection subsequently induces intestinal and respiratory diseases and even cause death of pigs. The nutritional and physiological conditions of sows directly affect the growth, development and disease resistance of the fetus and newborn. Many studies have shown that providing sows with nutrients such as functional oligosaccharides, oils, antioxidants, and trace elements could regulate immunity and the inflammatory response of piglets. Here, we reviewed the positive effects of certain nutrients on milk quality, immunoglobulin inflammatory response, oxidative stress, and intestinal microflora of sows, and further discuss the effects of these nutrients on immunity and the inflammatory response in the offspring.
Background The mammary gland is responsible for milk production and secretion, which is critical for neonatal health during lactation. Lactation efficiency is largely affected by energy status with unclear mechanism. Results In the current study, we found that synthesis of milk fat and protein was significantly inhibited under energy-deficient conditions, which is accompanied with AMP-activated protein kinase (AMPK) activation. Modulating the AMPK signaling pathway directly or indirectly affects the synthesis of milk fat and protein. Besides mammalian target of rapamycin complex 1 (mTORC1) signaling in the regulation of milk synthesis, we discovered that AMPK mainly regulates the synthesis of milk protein through prolactin signaling. Mechanistically, AMPK triggers the ubiquitination of prolactin receptor (PrlR) through regulating the activity of β-transducin repeat-containing protein (β-TrCP, an E3 ligase). Subsequently, PrlR is degraded by the endocytosis process of lysosomes, which further attenuates prolactin signaling. In addition, our results revealed that AMPK activation inhibits milk fat synthesis through decreasing and accelerating de novo synthesis and β-oxidation of fatty acids, respectively. To be precise, AMPK activation inhibits rate limiting enzymes and transcriptional regulatory factors involved in de novo fatty acid synthesis and decreases the acetylation process of peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α) to strengthen the oxidation of fatty acids. Conclusions Taken together, AMPK regulates the synthesis of milk not only depends on canonical mTORC1 signaling and key rate-limiting enzymes, but also through manipulating the degradation of PrlR and the acetylation of PGC-1α.
The maternal microbiome is essential for the healthy growth and development of offspring and has long-term effects later in life. Recent advances indicate that the maternal microbiome begins to regulate fetal health and development during pregnancy. Furthermore, the maternal microbiome continues to affect early microbial colonization via birth and breastfeeding. Compelling evidence indicates that the maternal microbiome is involved in the regulation of immune and brain development and affects the risk of related diseases. Modulating offspring development by maternal diet and probiotic intervention during pregnancy and breastfeeding could be a promising therapy in the future. In this review, we summarize and discuss the current understanding of maternal microbiota development, perinatal microbial metabolite transfer, mother-to-infant microbial transmission during/after birth and its association with immune and brain development as well as corresponding diseases.
BackgroundFat is a critical component in milk, which provided energy for the early growth and development of mammals. Milk fat is positively related to the concentration of acetate in the blood, while the underlying mechanism is still unclear.ObjectiveThis study is to investigate the effects of sodium acetate (NaAc) on milk fat synthesis in the mammary gland, and explored the underlying mechanism.MethodsIn vitro experiments were carried out in mouse mammary epithelial cell line (HC11) cells cultured with NaAc to explore the potential pathway of NaAc on milk fat synthesis. Furthermore, 24 pregnant mice (from d 18.5 of gestation to d 7 of lactation, exposed to 200 mM NaAc drinking water) were used as an in vivo model to verify the results.ResultsIn this study, we found that NaAc promoted milk fat synthesis and the expression of related genes and proteins in HC11 mammary epithelial cells with the activation of GPCR and mTORC1 signaling pathways (p < 0.05). Pretreatment with the mTORC1 inhibitors and G protein inhibitors attenuated the NaAc-induced milk fat synthesis in HC11 mammary epithelial cells (p < 0.05). Importantly, the effect of NaAc on milk synthesis was attenuated in GPR41 and GPR43 knockdown HC11 mammary epithelial cells (p < 0.05). This evidence indicates that NaAc might regulate milk fat synthesis through the GPR41/GPR43-mTORC1 pathway. Consistently, in in vivo experiment, dietary supplementation with NaAc significantly increased milk fat content and fat synthesis-related proteins in mice mammary glands with the activation of mTORC1 and GPCR signaling pathways at peak lactation (p < 0.05).ConclusionThe addition of NaAc promoted the increase of milk fat synthesis in HC11 mammary epithelial cells and mice mammary glands at peak lactation. Mechanistically, NaAc activates GPR41 and GPR43 receptors, leading to the activation of the mTORC1 signaling pathway to promote the synthesis of milk fat.
As one of the most important organs in animals, the intestine is responsible for nutrient absorption and acts as a barrier between the body and the environment. Intestinal physiology and function require the participation of energy. 5′‐adenosine monophosphate‐activated protein kinase (AMPK), a classical and highly expressed energy regulator in intestinal cells, regulates the process of nutrient absorption and barrier function and is also involved in the therapy of intestinal diseases. Studies have yielded findings that AMPK regulates the absorption of glucose, amino acids, and fatty acids in the intestine primarily by regulating transportation systems, as we detailed here. Moreover, AMPK is involved in the regulation of the intestinal mechanical barrier and immune barrier through manipulating the expression of tight junctions, antimicrobial peptides, and secretory immunoglobulins. In addition, AMPK also participates in the regulation of intestinal diseases, which indicates that AMPK is a promising therapeutic target for intestinal diseases and cancer. In this review, we summarized the current understanding regarding how AMPK regulates intestinal nutrient absorption, barrier function, and intestinal diseases.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.