Serotonin, also known as 5-hydroxytryptamine (5-HT), is a metabolite of tryptophan and is reported to modulate the development and neurogenesis of the enteric nervous system, gut motility, secretion, inflammation, sensation, and epithelial development. Approximately 95% of 5-HT in the body is synthesized and secreted by enterochromaffin (EC) cells, the most common type of neuroendocrine cells in the gastrointestinal (GI) tract, through sensing signals from the intestinal lumen and the circulatory system. Gut microbiota, nutrients, and hormones are the main factors that play a vital role in regulating 5-HT secretion by EC cells. Apart from being an important neurotransmitter and a paracrine signaling molecule in the gut, gut-derived 5-HT was also shown to exert other biological functions (in autism and depression) far beyond the gut. Moreover, studies conducted on the regulation of 5-HT in the immune system demonstrated that 5-HT exerts anti-inflammatory and proinflammatory effects on the gut by binding to different receptors under intestinal inflammatory conditions. Understanding the regulatory mechanisms through which 5-HT participates in cell metabolism and physiology can provide potential therapeutic strategies for treating intestinal diseases. Herein, we review recent evidence to recapitulate the mechanisms of synthesis, secretion, regulation, and biofunction of 5-HT to improve the nutrition and health of humans.

Aging skin, wrinkles, pigmentation, and dryness are problems that plague people, and researchers are working to solve them. Recent studies have shown that intestinal microbiota homeostasis can influence skin health, demonstrating the existence of a gut–skin axis. Recently, improving skin health through probiotic interventions has been proposed, and micro-ecological skin care is becoming a popular concept. By regulating skin health and gut–skin axis interactions, probiotics can be used as potential management tools to suppress and improve skin diseases in multiple ways, including decreasing oxidative stress, suppressing inflammatory responses, and keeping immune effects. The purpose of this paper is to provide a comprehensive review of the application and mechanisms of probiotic-mediated gut microbiota homeostasis in skin care and to offer a theoretical basis for the application of probiotics in skin care.

Background: The milk fat globule membrane (MFGM) is a thin film that exists within the milk emulsion, suspended on the surface of milk fat globules, and comprises a diverse array of bioactive components. Recent advancements in MFGM research have sparked a growing interest in its biological characteristics and health-related functions. Thorough exploration and utilization of MFGM as a significant bioactive constituent in milk emulsion can profoundly impact human health in a positive manner. Scope and approach: This review comprehensively examines the current progress in understanding the structure, composition, physicochemical properties, methods of separation and purification, and biological activity of MFGM. Additionally, it underscores the vast potential of MFGM in the development of additives and drug delivery systems, with a particular focus on harnessing the surface activity and stability of proteins and phospholipids present on the MFGM for the production of natural emulsifiers and drug encapsulation materials. Key findings and conclusions: MFGM harbors numerous active substances that possess diverse physiological functions, including the promotion of digestion, maintenance of the intestinal mucosal barrier, and facilitation of nerve development. Typically employed as a dietary supplement in infant formula, MFGM’s exceptional surface activity has propelled its advancement toward becoming a natural emulsifier or encapsulation material. This surface activity is primarily derived from the amphiphilicity of polar lipids and the stability exhibited by highly glycosylated proteins.

Lipid metabolism plays crucial roles in cellular processes such as hormone synthesis, energy production, and fat storage. Older adults are at risk of the dysregulation of lipid metabolism, which is associated with progressive declines in the physiological function of various organs. With advancing age, digestion and absorption commonly change, thereby resulting in decreased nutrient uptake. However, in the elderly population, the accumulation of excess fat becomes more pronounced due to a decline in the body’s capacity to utilize lipids effectively. This is characterized by enhanced adipocyte synthesis and reduced breakdown, along with diminished peripheral tissue utilization capacity. Excessive lipid accumulation in the body, which manifests as hyperlipidemia and accumulated visceral fat, is linked to several chronic lipid-related diseases, including cardiovascular disease, type 2 diabetes, obesity, and nonalcoholic fatty liver disease. This review provides a summary of the altered lipid metabolism during aging, including lipid digestion, absorption, anabolism, and catabolism, as well as their associations with age-related chronic diseases, which aids in developing nutritional interventions for older adults to prevent or alleviate age-related chronic diseases.

Chronic kidney disease (CKD) is characterized by the accumulation of protein-bound uremic toxins (PBUTs), which play a pathophysiological role in renal fibrosis (a common pathological process resulting in CKD progression). Accumulation of the PBUT hippuric acid (HA) is positively correlated with disease progression in CKD patients, suggesting that HA may promote renal fibrosis. Oxidative stress is the most important factor affecting PBUTs nephrotoxicity. Herein, we assessed the ability of HA to promote kidney fibrosis by disrupting redox homeostasis. In HK-2 cells, HA increased fibrosis-related gene expression, extracellular matrix imbalance, and oxidative stress. Additionally, reactive oxygen species (ROS)-mediated TGFβ/SMAD signaling contributed to HA-induced fibrotic responses. HA disrupted antioxidant networks by decreasing the levels of nuclear factor erythroid 2-related factor 2 (NRF2), leading to ROS accumulation and fibrotic responses, as evidenced by NRF2 activation and knockdown. Moreover, NRF2 levels were reduced by NRF2 ubiquitination, which was regulated via increased interactions of Kelch-like ECH-associated protein 1 with Cullin 3 and NRF2. Finally, renal fibrosis and redox imbalance promoted by HA were confirmed in rats. Importantly, sulforaphane (NRF2 activator) reversed HA-promoted renal fibrosis. Thus, HA promotes renal fibrosis in CKD by disrupting NRF2-driven antioxidant system, indicating that NRF2 is a potential therapeutic target for CKD.

Oxidative stress, caused by the accumulation of reactive species, is associated with the initiation and progress of inflammatory bowel disease (IBD). The investigation of antioxidants to target overexpressed reactive species and modulate oxidant stress pathways becomes an important therapeutic option. Nowadays, antioxidative nanotechnology has emerged as a novel strategy. The nanocarriers have shown many advantages in comparison with conventional antioxidants, owing to their on-site accumulation, stability of antioxidants, and most importantly, intrinsic multiple reactive species scavenging or catalyzing properties. This review concludes an up-to-date summary of IBD nanomedicines according to the classification of the delivered antioxidants. Moreover, the concerns and future perspectives in this study field are also discussed.