Nutrition & Metabolism最新文献

Ketogenic supplements have gained much attention in exercise nutrition because they have the potential to enhance endurance, maximize metabolic efficiency, and provide an additional source of fuel during exercise. This review is an examination into the molecular process, physiological alteration, and overall impact of ketogenic supplementation on sport performance. Various forms of ketogenic supplements, including exogenous ketones, medium-chain triglyceride (MCT) oil, and ketone esters, are examined in terms of their ability to induce ketosis and influence cellular energy pathways. The influence of ketone bodies on ATP synthesis, mitochondrial function, and metabolic shifts from carbohydrates to fats is summarized with special attention to endurance and high-intensity exercise implications. Furthermore, the long-term physiological adaptations, including enhanced fat oxidation, improved recovery, and resistance to fatigue, are analyzed. While ketogenic supplementation offers potential performance benefits, it also presents challenges such as muscle glycogen depletion, gastrointestinal distress, and electrolyte imbalances. A risk-benefit analysis is provided, outlining strategies to optimize supplementation while minimizing adverse effects. Finally, gaps in current research and future directions for ketogenic supplementation in sports are explored, emphasizing the need for individualized approaches and further investigation into long-term effects.

Moyamoya disease (MMD) is a rare, progressive cerebrovascular disorder characterized by internal carotid artery stenosis and compensatory vascular network formation. While its pathogenesis remains unclear, multi-omics approaches provide crucial molecular insights. Genomic studies identify significant associations with the RNF213 p.R4810K variant and other susceptibility loci like HLA-DQA2 and GUCY1A3. Transcriptomics reveals dysregulation in extracellular matrix organization and mitochondrial oxidative phosphorylation, with specific markers such as AQP4 and non-coding RNAs (e.g., miR-107). Proteomic analyses highlight alterations in proteins including VEGF, apolipoproteins (APOC1, APOD), and ferroptosis-related pathways. Metabolomics identifies diagnostic amino acid markers (L-lysine, L-glutamate) and altered lysophosphatidylcholine (LPC 16:1) levels. Epigenomics implicates DNA methylation changes in genes like SOX6 and KCNMA1. Integrated multi-omics facilitates the development of multifaceted treatments, including revascularization surgery, targeted molecular therapies, and personalized interventions based on individual omics profiles, advancing precision medicine for MMD. This article outlines the omics techniques' application progress in MMD, discussing their pros and cons in disease analysis, prevention, and treatment, aiming to guide future research and inform clinical decisions.

Cardiovascular diseases (CVD) are one of the leading causes of death worldwide. Genetic factors, and various environmental factors, including nutrition and the composition of the gut microbiota, have been identified as important factors in the initiation of CVD. Among them, the pivotal role of the gut microbiota in modulating cholesterol metabolism and influencing cardiovascular outcomes has recently been highlighted. Extensive research has confirmed that the gut microbiota has direct and indirect regulatory effects on host cholesterol homeostasis. Recent studies have shown that the microbiota can influence blood cholesterol levels and thus the risk of CVD through various pathways, such as the production of certain metabolites such as bile acids (BAs), SCFAs, and TMAO, the activation of nuclear and membrane-bound receptors such as farnesoid X receptor (FXR), the regulation of gene expression involved in lipid metabolism and inflammatory responses, as well as microbial enzymatic pathways. These complex regulatory mechanisms make the gut microbiota a potential therapeutic target in cholesterol-related diseases and CVD. Microbiota-modulating strategies, including the use of probiotics, prebiotics, fecal microbiota transplantation (FMT), and selective antibiotics, have shown beneficial effects in previous studies. In this regard, in this study, we conducted an in-depth investigation of the regulatory effect of intestinal microbiota on cholesterol metabolism and their impact on the development and progression of atherosclerosis and CVD, and described potential therapeutic pathways based on the regulation of intestinal microbiota in CVD.

Background: To evaluate the association between the global diet quality score (GDQS) in children and adolescents and the incidence of metabolic syndrome (MetS) and its risk factors in youth.

Methods: In this secondary analysis, 1144 children and adolescents aged 6-19 years were selected from participants of the Tehran Lipid and Glucose Study and followed. Dietary data were gathered by a valid and reliable semi-quantitative food frequency questionnaire. Diet quality was computed using the GDQS. MetS was defined according to Cook 's criteria for participants aged < 19 years and the Iranian-modified National Cholesterol Education Program was used to define MetS for participants aged ≥ 19 years at baseline and follow-up years.

Results: The mean ± SD ages of 528 boys and 616 girls were 13.0 ± 3.76 and 14.0 ± 3.77, respectively. The incident cases of MetS included 108 and 51 person/years for males and females, respectively, with a median follow-up of 9.74 years. The MetS incidence was contrarily associated with quartiles of GDQS [HR: 1, 0.92 (0.77-1.09), 0.90(0.75-1.08), 0.77(0.63-0.95), P trend = 0.02]. There were inverse associations between GDQS and abdominal obesity [HR: 1, 0.86(0.70-1.04), 0.82(0.67-1.01), 0.75(0.60-0.94) P trend = 0.01], low high-density lipoprotein cholesterol [HR: 1, 0.85(0.70-1.02), 0.82(0.67-0.99), 0.74(0.60-0.92) P trend = 0.009], high blood pressure [HR: 1, 0.97(0.82-1.15), 0.99(0.82-1.18), 0.78(0.64-0.95) P trend = 0.02] incidence in the adjusted model. Individuals in the fourth quartile of GDQS have about 35% lower risk of high fasting blood glucose and high triglyceride incidence, compared to the first quartile.

Conclusion: Higher compliance with the GDQS in children and adolescents was associated with a reduced risk of MetS and its risk factors incidence in later years of life.

Background: Understanding the impact of food matrix, the combination of nutrients, bioactive compounds, and physical characteristics in a food product, on muscle protein synthesis (MPS), could provide insights on how to use different meals to promote muscle anabolism. The aim of this review was to explore the impact of the food matrix on MPS or whole-body PS.

Methods: PubMed, Scopus, Web of Science, and the Cochrane library were searched from inception until January 2024. A narrative synthesis was employed to synthesize the findings and the quality of the studies was assessed using the Cochrane risk-of-bias 2 tool for randomised trials (RoB 2). The study's protocol was registered in PROSPERO (International Prospective Register of Systematic Reviews; CRD42024503306).

Results: Only one study was eligible to be included in this review. MPS was 0.035 ± 0.004 %/hr in the minced beef group vs. 0.034 ± 0.003 %/hr in beef steak, postprandially, showing no significant differences between groups. Increased whole-body PS response was observed after the consumption of minced beef compared to beef steak (29 ± 2 mmol phenylalanine/kg vs. 19 ± 3 mmol phenylalanine/kg, respectively; P < 0.01). The overall risk of bias was considered low.

Conclusions: Future studies should use food products with identical nutrient composition to evaluate the influence of the food matrix on MPS and whole-body PS, considering that current trials have primarily focused on ensuring similar protein intakes across study arms.

Background: Omega-3 fatty acids are polyunsaturated fats that are essential for proper cell structure and function. The primary types of omega-3 fatty acids include alpha-linolenic acid (ALA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA). ALA is an essential fatty acid, meaning that humans and other mammals cannot produce it on their own and must obtain it from dietary sources. Research has firmly established the positive effects of omega-3 fatty acids in adults, showing benefits for cardiovascular health, brain function, mental health, inflammation, autoimmune diseases, and skin health. However, there is limited information regarding these effects in children. This narrative review evaluates the pre-clinical and clinical evidence for omega-3 polyunsaturated fatty acids, specifically eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), as complementary agents in pediatric oncology. It highlights their potential antioxidant and anti-inflammatory properties in optimizing clinical outcomes, enhancing chemotherapy safety, and improving the quality of life for pediatric patients. These benefits include the suppression of reactive oxygen species (ROS) production, which helps prevent cell damage related to oxidative stress and protects healthy cells from the harmful effects of chemotherapy. Enhancing the body's ability to neutralize ROS by promoting internal antioxidant systems may improve treatment tolerance and reduce side effects. Reducing toxicity by lowering inflammation and oxidative stress will enhance the safety and effectiveness of chemotherapy. Further large-scale clinical trials in the pediatric population are necessary to confirm the potential effects of n-3 fatty acids on chemotherapy toxicity.

Background: Neural stem cells (NSCs), crucial for brain function and repair, are disrupted by high-fructose diet (HFrD) in proliferation and survival, linking to neurogenesis impairment and neuropsychiatric risks. Mechanistic insights remain undefined.

Methods: Comprehensive behavioral assessments were conducted on HFrD mice, including the tail suspension test (TST) and sucrose preference test (SPT) for depressive-like behaviors, elevated plus maze (EPM) and open field test (OFT) for anxiety-like behaviors, as well as novel object recognition (NOR) and Morris water maze (MWM) for cognition. Hippocampal NSCs and newborn neurons were quantified by immunofluorescence, and fructose-treated NE-4C cells underwent RNA sequencing (RNA-seq) analysis coupled with measurements of proliferation, apoptosis and ferroptosis markers.

Results: HFrD mice showed depressive-like behaviors without anxiety-like behaviors, and exhibited impaired short-term memory in NOR but did not show impaired spatial memory in MWM. Decreased number of hippocampal NSCs and newborn neurons were observed, suggesting impaired neurogenesis. In vitro, fructose-treated NE-4c exhibited altered gene expression profiles, with PCA showing distinct clustering between treated and control groups. Further analysis (GO, KEGG, GSEA) indicated enrichment in energy metabolism pathways, including mitochondrial ATP synthesis (e.g., downregulated ATP5E, ATP5H). Consistently, intracellular ATP levels were elevated, indicating metabolic dysregulation. Further experiments demonstrated that high fructose promoted NSC proliferation via p53/Wnt pathways (upregulated CyclinA2, CDK1) while concurrently inducing apoptosis (BAX, P53 upregulation) and ferroptosis (reduced GPX4, elevated ROS, and lipid peroxidation).

Conclusion: This study elucidates the mechanistic link between HFrD-induced metabolic disruption and NSC dysfunction, providing novel insights into the pathogenesis of fructose-associated neuropsychiatric disorders.