内容: The integration of artificial intelligence (AI) in precision exercise nutrition is reshaping how athletes optimize their dietary intake for performance, recovery, and overall well-being. This article discusses the intersection of AI technologies in formulating precision nutrition strategies tailored to distinct physiological and metabolic requirements of athletes. AI-based mechanisms, such as real-time diet monitoring, continuous glucose monitoring, and nutrient optimization systems, offer unique insights into the impact of AI on advancing precision nutrition applications through the involvement in analyzing complex datasets, merging genetic, metabolic and environmental factors, thereby contributing precise dietary recommendations that adjust to evolving necessities of an athlete. However, the obstacles presented by AI in this domain, including ethical considerations, data confidentiality, and the necessity for uniformity across diverse populations are also confronted. By using AI, athletes can attain greater precision in their nutrition plans, ultimately enhancing exercise performance and promoting fatigue or injury recovery in ways that traditional methods cannot rival. This article further culminates with an address on future trends, emphasizing the role of AI in boosting precision nutrition engagement for athletes, even common exercise enthusiasts.

内容: The global rise in obesity and its associated metabolic syndrome has garnered significant attention in recent years. Targeting the gut microbiota has been proposed as a promising strategy for the treatment of obesity and its related metabolic disorders. Bifidobacterium, one of the typical intestinal microorganisms in healthy individuals, has been recognized for its beneficial role in maintaining overall health. Numerous animal and human studies have elucidated the beneficial impact of bifidobacteria in maintaining the physiological and metabolic well-being of the host. Previous studies have found that bifidobacteria play a crucial role in regulating intestinal microbial communities and metabolism, as well as alleviating obesity by managing appetite, improving insulin resistance, modulating cholesterol and lipid metabolism, reshaping immune marker levels, and reducing inflammation. However, there remains a lack of comprehensive exploration into the potential correlation between bifidobacteria and obesity. By exploring the link between bifidobacteria and obesity based on recent research, this review aims to provide a theoretical foundation for elucidating the fundamental mechanisms underlying probiotic bifidobacteria intervention and promote the therapeutic applications of targeted regulation of microbial communities for obesity treatment.

内容: Atherosclerosis is the main cause of most cardiovascular diseases. Given the increasing morbidity and mortality in these diseases in recent years, it is important to investigate novel treatments and preventive strategies for atherosclerosis. Tea polyphenols (TPs), natural substances derived from tea, have a variety of functions such as anti-inflammation and antioxidants. Numerous studies have closely linked TPs and gut microbiota to the development of atherosclerosis. By retrieving EBSCO, PubMed, Wiley InterScience, and Google Scholar databases, our review selects relevant literature from 1998 to 2023 to summarize the mutual interaction between TPs and gut microbiota and their protective effect on atherosclerosis. Specifically, TPs influence the diversity and abundance of gut microbiota, which may relieve atherosclerosis by promoting the colonization of beneficial microbiota and inhibiting the colonization of harmful microbiota. Simultaneously, the involvement of gut microbiota in TPs metabolism not only increases the bioavailability of TPs but also generates active metabolites, like gallic acid and protocatechuic acid, which have been found to alleviate atherosclerosis. Furthermore, the review outlines recent advances and challenges in the utilization of gut microbes and TPs for the prevention and treatment of atherosclerosis. In general, the review reflects the great potential of the interaction between TPs and gut microbes in the prevention and treatment of atherosclerosis.

内容: Butyric acid, a representative short-chain fatty acid, has gained considerable attention due to its noteworthy health benefits and widespread application. Nonetheless, the majority of commercially available butyric acid is currently synthesized through environmentally harmful chemical synthesis methods, which pose a significant obstacle to the development of the butyric acid industry. Therefore, there is a need to develop cost-effective, efficient, and environmentally friendly methods for butyric acid production. This review commences with a systematic evaluation of the health effects and mechanisms of action of butyric acid. Subsequently, it outlines the advantages and disadvantages of different sources of butyric acid, including chemical synthesis and biosynthesis, along with their development trends. Finally, the review delves into high-efficiency strategies to enhance butyric acid production through targeted biosynthesis. This review not only serves as a valuable reference for researchers and practitioners interested in the diverse aspects of butyric acid but also offers insights into future trends in the development of butyric acid.

内容: Alcoholic liver disease (ALD), a pervasive global health concern, involves multifaceted pathological mechanisms including oxidative stress, lipid dysregulation and inflammatory responses, yet lacks effective multi-target therapies. Carnosic acid (CA), a natural diterpenoid with extensively characterized antioxidant and anti-inflammatory properties, remains underexplored for its systemic therapeutic potential in ALD. This study aimed to comprehensively investigate CA’s hepatoprotective efficacy and molecular mechanisms against ALD. Results demonstrated that CA significantly reduced serum total cholesterol, triglycerides, and transaminase levels in ALD mice, concurrently alleviating alcohol-induced histopathological damage. Network pharmacology identified 36 potential targets, with 10 core targets predominantly enriched in lipid metabolism, PPAR signaling and inflammatory response. Molecular docking revealed superior binding affinities of CA to core targets compared to silibinin, a reference hepatoprotectant. RT-qPCR validation further confirmed CA’s regulatory effects on apoptosis-related TP53/BCL2 axis, TNF-mediated inflammatory pathways and cytochrome P450 (CYP450) metabolic genes. Through a tripartite strategy integrating phenotypic validation, mechanistic prediction, and experimental confirmation, this study elucidates CA’s multi-target therapeutic actions against ALD via coordinated modulation of lipid homeostasis, oxidative stress and inflammatory pathways, providing the groundwork for future mechanism exploration.

内容: Central fatigue is closely linked to disruptions in the microbiota-gut-brain axis (MGBA), yet the molecular mechanisms involved remain largely unclear, and effective nutritional interventions are still limited. Tartary buckwheat polyphenols (TBP) have demonstrated potential in modulating the gut microbiota and supporting neuronal function. However, the specific pathways through which TBP exert their anti-fatigue effects are not fully understood. Clarifying these mechanisms is crucial for the development of precision dietary strategies to alleviate central fatigue. In this work, we established a mouse model of overexercise-induced central fatigue to systematically evaluate the effects of TBP through behavioral assessments, histological examination, neurotransmitter profiling, and inflammatory and oxidative stress marker analysis. The results showed that TBP significantly improved fatigue-related behaviors, alleviated intestinal and brain tissue damage, and modulated the expression of various neurotransmitters. Furthermore, TBP significantly reduced serum levels of pro-inflammatory cytokines (e.g., interleukin-1 beta, and tumor necrosis factor-alpha), and mitigated oxidative stress by enhancing glutathione peroxidase and catalase activity and reducing malondialdehyde levels. 16S rRNA sequencing revealed that TBP altered gut microbiota composition, promoting the abundance of beneficial taxa such as Lachnospiraceae, Lactobacillus, and Roseburia, while suppressing potentially harmful microbes. Short-chain fatty acids analysis further demonstrated that TBP modulated levels of acetic, propionic, and butyric acids, contributing to intestinal barrier integrity and energy homeostasis. Metabolomics analysis revealed that TBP influenced several key pathways, including alanine, aspartate, and glutamate metabolism, as well as neuroactive ligand-receptor interactions, thereby restoring the metabolic balance under central fatigue. Collectively, this work provides supportive evidence that TBP alleviates central fatigue through modulating the MGBA.

内容: Glucose plays a crucial role in maintaining human health as an indispensable source of energy in living organisms. Accurate monitoring of glucose levels in living organisms and detecting it in food is essential. In this study, gold nanoclusters (AuNCs) with unique aggregation-induced emission (AIE) effects were encapsulated within zeolite imidazole framework (ZIF-8) to fabricate a pH-responsive AuNCs@ZIF-8 fluorescent nanocomposite. The fluorescence intensity had significant sevenfold enhancement compared to AuNCs alone due to the structural domain-limiting effects exerted by ZIF-8, which effectively inhibited the rotations and vibrations of the AuNCs ligands. Based on the increased acidity generated by glucose catalytic oxidation via glucose oxidase (GOx), the subsequent degradation of ZIF-8 structure and the consequent reduction of AuNCs with AIE effects were achieved, and a rapid and efficient fluorescence quantification for glucose was performed. The constructed AuNCs@ZIF-8-based fluorescent probe demonstrated a favorable linear response to glucose, achieving a detection limit of 0.096 mmol/L and providing a rapid and efficient approach suitable for assessing glucose levels in both blood and beverage samples.

内容: Recently, ferroptosis has been found as a kind of cell death defined by the accumulation of reactive oxygen species (ROS) depending on iron and lipid peroxidation. A high-fat diet (HFD) may have the potential to trigger ferroptosis, resulting in liver injury. Apigenin is a natural flavonoid widely present in fruits and vegetables. In the study, we found HFD-fed could increase the iron level, malondialdehyde level, the expression of acyl-CoA synthetase long-chain family member 4 and transferrin receptor 1, decrease the glutathione level, the expression of glutathione peroxidase 4, ferritin heavy chain and ferroportin in C57BL mice. Further, conventional morphological hallmarks of ferroptosis were observed using transmission electron microscopy. However, apigenin treatment eliminated these harmful effects. Similar to in vivo results, we found apigenin could alleviate palmitic acid (PA)-induced ferroptosis in AML12 cells. Further, we found apigenin could promote PA-inhibited mitophagy and decrease intracellular ROS accumulation, thereby restoring PA-induced lysosomal membrane permeabilization (LMP). In the further mechanism study, we added relevant inhibitors. The results showed that apigenin could clear PA-induced damaged mitochondria through mitophagy, and reduce the leakage of free iron ions in lysosomes into the cytoplasm by restoring the permeability of lysosomes. Therefore, apigenin could inhibit ferroptosis induced by HFD and PA via suppressing lysosome iron efflux by reducing LMP and activating mitophagy in mice and AML12 cells.

内容: Diabetes mellitus (DM) is a severe chronic disease that results in high morbidity and mortality. DM causes endothelial injury (DEI) as a basis for cardiovascular complications of DM with few effective approaches developed for its intervention. Krill oil (KO) possesses anti-inflammatory and anti-oxidative activities, but its effect on DEI is unknown. Hence, the aims of this study were to investigate the effect and molecular mechanism of KO on DEI. To investigated the preventive effect of KO on DEI, streptozotocin and high-fat diet-induced type 2 diabetic mice were fed with KO for 6 months. RNA sequencing for endothelial cells (ECs) was used to explore the mechanism of KO’s protective function. To clarify the role of nuclear factor erythroid 2-related factor 2 (Nfe2l2 or NRF2) signaling in KO’s protection against DEI, Nfe2l2 gene-silenced ECs or knockout mice were treated with KO. Molecular docking assay and surface plasmon resonance assay were carried out to reveal binding between Kelch like ECH associated protein 1 (KEAP1) and major components of KO. KO significantly alleviated DEI and aortic pathological injury in the wild-type diabetic mice. RNA sequencing revealed that KO dramatically activated NRF2 antioxidant signaling in high glucose-challenged ECs, the effect of which was further confirmed in the diabetic aortas. Nfe2l2 gene deletion or silencing completely abolished KO’s protection against DEI in vivo and in vitro, demonstrating that NRF2 was required for KO’s action. Further, molecular docking assay and surface plasmon resonance assay identified that KO’s functional component astaxanthin (AST), but not docosahexaenoic acid and eicosapentaenoic acid, was able to bind the Kelch domain of KEAP1, promoting nuclear translocation of NRF2 which activated antioxidant gene expression. The comparison of the effects of KO and AST on endothelial NRF2 nuclear translocation suggested that KO might activate NRF2 at least partially through AST-KEAP1 interaction. KO activates NRF2 to prevent diabetic endothelial injury in part through AST-induced inhibition of KEAP1.

内容: Grape peel, as the by-product of grape wine, is rich in phenolic and proanthocyanidins. Obesity has become a serious global public health problem and supplementation of grape peel phenolics (GPP) may be an effective intervention method. From a dietary nutrition perspective, this study aims to investigate the effects of GPP on improving intestinal barrier function in high-fat diet-treated mice, and further explore the potential mechanism. The results showed that GPP supplementation obviously reduced body weight of mice, increased the abundance of beneficial bacteria (Akkermansia, g_Lachnospiraceae_NK4A136_group, Bacteroidetes and g_norank_f_Muribaculaceae), reduced the relative abundance of harmful bacteria (g_Coriobacteriaceae_UCG-002, g_Dubosiella and Romboutsia). Meanwhile, GPP could alleviate colonic barrier inflammation, facilitate the production of short-chain fatty acids and secondary bile acids, increase the mRNA and protein expression levels of intestinal tight junction proteins, and protect intestinal barrier integrity, especially in the LGPP group (100 mg/kg∙day GPP). Kyoto Encyclopedia of Genes and Genomes analysis on fecal metabolism indicated that GPP could effectively alleviate intestinal imbalance caused by obesity through targeting multiple shared pathways. Bile secretion and arachidonic acid are the key differential metabolic pathways, and 14 key differential metabolites were identified. In conclusion, GPP supplementation has the potential to alleviate obesity by regulating gut microbiota, improving gut barrier integrity, and modulating the related metabolites.