Nutrition & Metabolism最新文献

{"title":"The association between dietary consumption of amino acids and the risk of non-alcoholic fatty liver disease: a case-control study.","authors":"Asieh Mansour, Mohammad Abdollahi, Maryam Mirahmad, Soudabe Motamed, Atie Sadat Khorasanian, Seyed Hossein Mirlohi, Hossein Poustchi, Elaheh Amini, Farnaz Tavakoli, Mohammad Reza Mohajeri-Tehrani, Sayed Mahmoud Sajjadi-Jazi, Azita Hekmatdoost","doi":"10.1186/s12986-025-00992-3","DOIUrl":"10.1186/s12986-025-00992-3","url":null,"abstract":"<p><strong>Background: </strong>Few studies, with inconsistent results, have been conducted to examine the effect of protein and amino acid consumption on non-alcoholic fatty liver disease (NAFLD). Therefore, this study aimed to assess the relationship between dietary intake of amino acids or groups of amino acids and the risk of NAFLD.</p><p><strong>Methods: </strong>This case-control study included 171 participants with NAFLD and 730 controls from Tehran, Iran. A validated Food frequency questionnaire (FFQ) with 168 items, was used to evaluate dietary information. Odds ratios (ORs) and corresponding confidence intervals (CIs) were calculated by regression models, adjusted for potential confounders including age, sex, body mass index (BMI), smoking status, physical activity, history of diabetes mellitus, and total energy intake.</p><p><strong>Results: </strong>The mean ± standard deviation (SD) age of participants was 43.26 ± 13.9 years. Intake of total protein and all amino acids was significantly higher in patients with NAFLD than in the control group (P < 0.001). Increased risk of developing NAFLD compared to the reference quartile was observed in the highest quartiles of dietary isoleucine (OR, 4.72; 95%CI, 1.57-14.19), tyrosine (OR, 5.11, 95%CI, 1.73-15.05), threonine (OR, 3.47; 95%CI, 1.16-10.33), and valine (OR, 4.51; 95%CI, 1.45-14.02) intake. Subgroup analysis by sex revealed that in the females, the OR for NAFLD were 0.36 (95%CI, 0.13-0.98) among those with the highest intake of non-essential amino acids, and 2.78 (95%CI, 1.02-7.50) among those with the highest intake of essential amino acids compared to those in the first quartile. However, there was no significant trend among male cases.</p><p><strong>Conclusion: </strong>Consumption of specific amino acids might be associated with odds of NAFLD.</p>","PeriodicalId":19196,"journal":{"name":"Nutrition & Metabolism","volume":"22 1","pages":"118"},"PeriodicalIF":4.1,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12512509/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145258660","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The efficacy of high-protein nutritional support on mortality, clinical outcomes, and nutritional adequacy in critically ill patients: a double‑center randomized controlled trial.","authors":"Mohaddeseh Badpeyma, Alireza Sedaghat, Ahmad Bagheri Moghaddam, Majid Khadem-Rezaiyan, Fatemeh Sistanian, Mohammad Bagherniya, Golnaz Ranjbar, Farzaneh Fazeli, Abdolreza Norouzy","doi":"10.1186/s12986-025-01003-1","DOIUrl":"10.1186/s12986-025-01003-1","url":null,"abstract":"<p><strong>Background: </strong>Although nutritional support is crucial in intensive care, the impact of protein intake remains unclear, emphasizing the need for further randomized controlled trials. This study aimed to evaluate the effects of high-protein versus conventional-protein nutritional support on clinical outcomes in critically ill patients, with 60-day mortality as the primary endpoint.</p><p><strong>Method: </strong>In this double-blind, two-arm, parallel-group randomized controlled trial, 56 adult patients admitted to the intensive care unit [1] were enrolled. Participants received either high-protein support (2.2 g/kg/day, actual body weight [ABW]) or conventional-protein support (1.0 g/kg/day, ABW) for 12 days. Both groups targeted 25 kcal/kg/day energy intake. Patients and data analysts were blinded. Mortality was assessed at ICU discharge, on days 28 and 60, and at hospital discharge. Hospital mortality was defined as any death occurring during the hospital stay, including both the ICU and post-ICU periods. Mid-arm circumference (MAC) was measured as an indicator of muscle attenuation.</p><p><strong>Results: </strong>Mean protein intake was 1.67 ± 0.33 vs. 0.93 ± 0.10 g/kg/day in high- vs. conventional-protein groups (P < 0.05). In-hospital mortality was significantly lower in the high-protein group (8 patients [28.6%]) compared to the conventional-protein group (16 patients [57.1%]; adjusted P = 0.049). Although 60-day mortality was also lower in the high-protein group (28.6% vs. 53.6%), the difference did not reach statistical significance (adjusted P = 0.07). A significant reduction in MAC attenuation was observed in the high-protein group (P < 0.001).</p><p><strong>Conclusion: </strong>High-protein intake (1.67 g/kg/day) significantly reduced in-hospital mortality and improved preservation of muscle mass. Although 60-day mortality reduction was not significant, the trend suggests a meaningful benefit warranting further study.</p><p><strong>Irct registration id: </strong>IRCT20180619040151N4.</p>","PeriodicalId":19196,"journal":{"name":"Nutrition & Metabolism","volume":"22 1","pages":"116"},"PeriodicalIF":4.1,"publicationDate":"2025-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12506466/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145252151","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"High-fat diet, intestinal microecology and bone loss.","authors":"Ning Wang, Xue Tong, Yi-Kai Li","doi":"10.1186/s12986-025-01013-z","DOIUrl":"10.1186/s12986-025-01013-z","url":null,"abstract":"<p><p>Bone, a vital component of the human body, plays a crucial role in maintaining mobility and systemic health. Growing evidence underscores the complex interplay between a high-fat diet (HFD), intestinal microecology, and bone loss. This review consolidates findings across three interconnected mechanisms: (1) HFD compromises bone homeostasis by reducing bone mineral density (BMD) and disrupting microarchitecture, driven by bone marrow adiposity, oxidative stress, and chronic inflammation; (2) HFD disrupts intestinal microecology through microbiota dysbiosis (e.g., elevated Firmicutes/Bacteroidetes ratio, depletion of Bifidobacterium), epithelial barrier impairment (e.g., suppressed Mucin2 secretion, downregulated tight junction proteins), and immune dysregulation (e.g., Th17/Treg imbalance, diminished IL-10 production); and (3) intestinal microecology imbalances exacerbate bone loss through microbial metabolite alterations (e.g., a deficiency of short-chain fatty acids impairing Treg-mediated Wnt10b signaling), systemic inflammation from barrier leakage, and intestinal immune cell trafficking (e.g., Th17 migration to bone marrow). These interconnected mechanisms point to an indirect pathway by which HFD contributes to bone loss through alterations in intestinal microecology. While this indirect relationship remains insufficiently validated, accumulating evidence highlights the important roles of HFD and intestinal microecology in bone regulation. This review aims to comprehensively examine the connections between HFD, intestinal microecology, and bone loss, with a focus on elucidating these potential mechanisms. Given diet's profound impact on intestinal microecology, optimizing dietary patterns to rebalance intestinal microecology offers a promising strategy for preventing and treating bone-related disorders.</p>","PeriodicalId":19196,"journal":{"name":"Nutrition & Metabolism","volume":"22 1","pages":"117"},"PeriodicalIF":4.1,"publicationDate":"2025-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12506283/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145252137","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of lipid accumulation product with the prevalence and incidence of sarcopenia: a nationwide study in Chinese.","authors":"Zhiyuan He, Jiangping Zeng, Wenquan Ding, Rui Xie, Ya Qian, Shenghao Wang, Wu Xu, Lixin Huang, Liyu Zhou, Dongqing You, Zijie Pei, Qian Wu","doi":"10.1186/s12986-025-01016-w","DOIUrl":"10.1186/s12986-025-01016-w","url":null,"abstract":"<p><strong>Background: </strong>Lipid accumulation product (LAP) has recently gained attention as a novel indicator of metabolic dysfunction. However, the association between LAP and sarcopenia, a metabolic condition characterized by loss of muscle mass, strength, and function, remains unclear. This study aimed to explore the relationship between LAP and both the prevalence and incidence of sarcopenia using data from the China Health and Retirement Longitudinal Study (CHARLS).</p><p><strong>Methods: </strong>Sarcopenia was defined according to the criteria established by the Asian Working Group for Sarcopenia in 2019. LAP was calculated using waist circumference and triglyceride levels. A cross-sectional analysis was performed with 7,004 participants from the baseline survey, utilizing logistic regression models to evaluate the association between LAP and sarcopenia prevalence. Additionally, a longitudinal cohort analysis involved 4,484 individuals who were free of sarcopenia at baseline and followed from 2011 to 2015. Cox proportional hazards models were employed to assess the longitudinal association between baseline LAP levels and incident sarcopenia. Furthermore, restricted cubic spline regression (RCS) and subgroup analyses were conducted to explore potential nonlinear relationships and differences across various subgroups. Receiver operating characteristic (ROC) curves was used to evaluate the discriminatory ability of LAP for identifying sarcopenia.</p><p><strong>Results: </strong>Cross-sectional analyses and RCS revealed a significant inverse linear relationship between LAP and the prevalence of sarcopenia [odds ratio (OR) = 0.95, 95% confidence interval (CI): 0.94-0.96]. Participants within the highest LAP tertile demonstrated substantially lower odds of sarcopenia compared to those in the lowest tertile (OR = 0.21, 95% CI: 0.14-0.31). Longitudinal analyses similarly indicated that elevated LAP levels were associated with reduced sarcopenia incidence, with the highest LAP tertile associated with notably decreased risk (HR = 0.17, 95% CI: 0.11-0.27). The nonlinear pattern identified through RCS analysis indicated significant risk reductions up to a LAP threshold of 27.577. Furthermore, subgroup analyses consistently supported this inverse association across various demographic and clinical subgroups. Finally, diagnostic performance of LAP was assessed using the ROC curve (0.763 ([CI]: 0.744-0.783) in the longitudinal study).</p><p><strong>Conclusions: </strong>Elevated LAP levels are inversely associated with both the prevalence and incidence of sarcopenia among middle-aged and elderly adults in China. These findings suggest LAP could serve as a useful metabolic indicator for predicting reduced sarcopenia risk, warranting additional studies to confirm and further elucidate these relationships.</p>","PeriodicalId":19196,"journal":{"name":"Nutrition & Metabolism","volume":"22 1","pages":"115"},"PeriodicalIF":4.1,"publicationDate":"2025-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12506364/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145244729","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Choosing sweeteners wisely-nutrigenetic study on childhood obesity.","authors":"Daniel Wang Qiu, Chia-Min Kuo, Shih-Yuan Hsu, Emily Chia-Yu Su, San-Yuan Wang, Jia-Woei Hou, Meng-Che Tsai, Chen Yang, Yang-Ching Chen","doi":"10.1186/s12986-025-01015-x","DOIUrl":"10.1186/s12986-025-01015-x","url":null,"abstract":"<p><strong>Background: </strong>This study investigated the association of specific sweet-taste and obesity-related genes with sweetener consumption patterns among children and the interaction between these genetic factors and sweetener intake on the risk of childhood obesity. By leveraging data from the Taiwanese Pubertal Longitudinal Study (TPLS), the current study minimized the influence of environmental confounders commonly encountered in adult studies, offering a more precise understanding of these relationships in pediatric and adolescent populations.</p><p><strong>Methods: </strong>Participants in the TPLS underwent genetic sampling, anthropometric measurements, puberty stage assessments, dietary recall, and measurements of relevant lifestyle variables. Nonnutritive sweetener (NNS) intake was assessed using the validated Nonnutritive Sweetener Food Frequency Questionnaire (NNS-FFQ). The statistical analysis employs logistic regression to investigate the correlations between genotypes and sweetener consumption, while accounting for potential confounders such as parental education and household income. Simultaneously, the study examines gene-sweetener interactions to assess the association between specific alleles and particular sweetener consumption patterns.</p><p><strong>Results: </strong>Higher consumption of specific artificial sweeteners-acesulfame potassium, sucralose, and steviol-was associated with lower body mass index (BMI) Z-scores and reduced body fat percentage. The interaction analyses indicated a significantly positive association of the interaction between sucralose consumption and sweet-taste genes on the waist-hip ratio. Genetic analysis revealed significant associations between obesity-related genes (e.g., ADCY9 and TFAP2B) and sweet-taste receptor genes (e.g., TAS1R2 and TAS1R3) with sweetener consumption, which may influence susceptibility to obesity. Notably, rs7498665 was significantly associated with BMI Z-scores, underscoring its role in obesity predisposition.</p><p><strong>Conclusions: </strong>These findings highlight the genetic underpinnings of sweetener consumption and its interactive effects with genetic variants on childhood obesity risk, providing valuable insights for promoting public health and developing personalized nutrition strategies. Future research involving larger samples and consideration of genetic and environmental factors is required to develop personalized nutrition strategies aimed at effectively combating childhood obesity.</p>","PeriodicalId":19196,"journal":{"name":"Nutrition & Metabolism","volume":"22 1","pages":"114"},"PeriodicalIF":4.1,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12502141/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145239412","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vitamin D and bone health: from physiological function to disease association.","authors":"Yu Liu, Wei Wang, Yusheng Yang, Jiezhong Deng, Zehua Zhang","doi":"10.1186/s12986-025-01011-1","DOIUrl":"10.1186/s12986-025-01011-1","url":null,"abstract":"<p><p>Vitamin D (VD) is a pleiotropic secosteroid hormone with well-established roles in calcium homeostasis, bone metabolism, and emerging functions in immune regulation, inflammation, and chronic disease modulation. In this paper, we provide a comprehensive summary of the current research on the significance of VD for bone health, with emphasis on its mechanism of action and its clinical significance in bone health. This review starts with an overview of VD metabolism, with emphasis on the enzyme transformation of vitamin D3 (VD3) and vitamin D2 (VD2) into the active 1,25-dihydroxyvitamin D (1α,25(OH)₂D) and their genomic and non-genomic signaling pathways through the Vitamin D receptor (VDR). Then, we discuss how VDR polymorphisms affect disease susceptibility and the dual role of VD in promoting innate immunity as well as inhibiting over-adaptive immunity. Our main focus is placed on VD's involvement in bone destruction diseases, including osteoarthritis (OA), osteoporosis (OP), rheumatoid arthritis (RA), and bone tuberculosis. For OA, there is conflicting evidence on whether VD supplementation reduces cartilage degradation or pain. In OP, vitamin D deficiency aggravates bone loss, but the effectiveness of supplementation is dependent on baseline and calcium supplementation. For RA, the immunomodulatory effects of VD may decrease the activity of the disease, whereas in tuberculosis, VD increases the clearance of macrophage-mediated mycobacterial clearance, although the clinical study data are still inconclusive. This review underscores VD as a critical mediator of bone-immune crosstalk while calling for rigorous translational research to clarify its therapeutic potential across diverse diseases.</p>","PeriodicalId":19196,"journal":{"name":"Nutrition & Metabolism","volume":"22 1","pages":"113"},"PeriodicalIF":4.1,"publicationDate":"2025-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12490156/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145213269","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mixed-meal challenge differentially modulates metabolic pathways in adipose tissue in healthy abdominally obese subjects with high versus low liver fat: a secondary analysis of a randomized clinical trial.","authors":"Yan Fang, Guido J E J Hooiveld, Lydia A Afman","doi":"10.1186/s12986-025-01010-2","DOIUrl":"10.1186/s12986-025-01010-2","url":null,"abstract":"<p><strong>Background: </strong>Increased liver fat increases the risk of chronic metabolic diseases. This study is an exploratory secondary analysis aimed at (1) investigating whether transcriptomic responses of abdominal subcutaneous adipose tissue (SAT) to a high-fat-high-glucose meal challenge differ according to varying levels of liver fat accumulation and (2) identifying pathways in abdominal SAT metabolism that may be related to liver fat accumulation. We examined differences in abdominal SAT gene expression and pathway activity both at fasting and in response to a mixed-meal challenge, comparing individuals with varying levels of liver fat.</p><p><strong>Method: </strong>From the subset of 66 of 110 middle-aged participants of a previous intervention study, we grouped participants by tertiles of intrahepatic lipids (IHL) into high liver fat group (n = 22, IHL: 8.0%-32.6%), middle liver fat group (n = 22, IHL: 2.5%-8.0%) and low liver fat group (n = 22, IHL: 0.1%-2.5%). Participants received a high-fat-high-glucose mixed-meal challenge (3833 kJ). Abdominal SAT samples were collected before and 4 h after the challenge for microarray gene expression analysis.</p><p><strong>Results: </strong>At fasting, 87 gene sets were differently expressed (FDR < 0.25) between the high and the low liver fat group, and 66 gene sets were differently expressed between the high and middle liver fat group, pathways related to energy metabolism were lower expressed in the high compared to the low liver fat group. Postprandially, 17 gene sets responded differently to the mixed meal challenge, of which 7 changed within the high liver fat group, 2 changed within the middle liver fat group and 4 within the low liver fat group. The challenge increased the expression of genes involved in oxidative phosphorylation more in the high compared to the low liver fat group.</p><p><strong>Conclusions: </strong>Compared to individuals with low liver fat, individuals with high liver fat have lower gene expression but a higher response of energy-related pathways in abdominal SAT at fasting and after a high-fat-high-glucose challenge. Whether this is the cause or consequence of increased liver fat storage or an early stage of insulin resistance needs to be investigated.</p><p><strong>Trial registration: </strong>This trial was registered at clinicaltrials.gov as NCT02194504.</p>","PeriodicalId":19196,"journal":{"name":"Nutrition & Metabolism","volume":"22 1","pages":"112"},"PeriodicalIF":4.1,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12486747/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145207060","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dietary carotenoids and breast cancer risk: evidence from a large population-based incident case-control study.","authors":"Bahar Darouei, Torsten Bohn, Farhad Vahid, Reza Amani-Beni, Shaghayegh Haghjooy Javanmard, Kazem Zendehdel, Ibrahim Abdollahpour","doi":"10.1186/s12986-025-01007-x","DOIUrl":"10.1186/s12986-025-01007-x","url":null,"abstract":"<p><strong>Background: </strong>Although mechanistic studies suggest protective roles for carotenoids against breast cancer (BC), human studies yield inconsistent findings. Few have comprehensively evaluated dietary intake of individual and grouped carotenoids in relation to BC risk.</p><p><strong>Methods: </strong>This population-based case-control study recruited 600 patients with newly diagnosed BC and 600 healthy controls. Dietary carotenoid intake was assessed using a validated 168-item food frequency questionnaire. The intake levels of α-carotene, β-carotene, β-cryptoxanthin, lutein/zeaxanthin, lycopene, astaxanthin, phytoene, phytofluene, neoxanthin, violaxanthin, and total carotenoids were categorized into quartiles. Logistic regression models were employed to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for BC risk, controlling for potential confounders.</p><p><strong>Results: </strong>Higher intake of lycopene, phytoene, phytofluene, total non-provitamin A and provitamin A, β-carotene, lutein/zeaxanthin, as well as total carotenoids was significantly associated with reduced BC risk Lycopene showed the strongest inverse association (Q4 vs. Q1: OR = 0.23; 95% CI: 0.14-0.37). Total provitamin A (Q4 OR = 0.46; 95% CI: 0.29-0.75) and total non-provitamin A carotenoids (Q4 OR = 0.25; 95% CI: 0.15-0.41) also showed strong protective associations. Total carotenoid (Q4 OR = 0.34, 95% CI: 0.20-0.56, p < 0.001) intake also showed inverse associations across all quartiles. Conversely, α-carotene, β-cryptoxanthin, astaxanthin, neoxanthin, and violaxanthin displayed weaker or inconsistent associations.</p><p><strong>Conclusion: </strong>These findings support an inverse association between dietary intake of specific carotenoids, particularly lycopene, lutein/zeaxanthin, and colorless carotenoids (phytoene and phytofluene) and BC risk. Promoting a carotenoid-rich diet may represent a feasible strategy for BC prevention.</p>","PeriodicalId":19196,"journal":{"name":"Nutrition & Metabolism","volume":"22 1","pages":"107"},"PeriodicalIF":4.1,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12487211/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145200507","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dietary polyunsaturated fatty acid intake and all-cause and cardiovascular mortality in patients with COPD.","authors":"Yang Zhang, Xiao Liang, Shuai Luo, Zhizhe Zhang, Pinglang Zhou, Zhiyang Zhou, Yihan Yang","doi":"10.1186/s12986-025-01006-y","DOIUrl":"10.1186/s12986-025-01006-y","url":null,"abstract":"<p><strong>Background: </strong>Chronic obstructive pulmonary disease (COPD) patients face increased mortality risk, particularly from cardiovascular causes. While polyunsaturated fatty acids (PUFAs) have shown cardiovascular benefits in general populations, their impact on COPD mortality remains unexplored.</p><p><strong>Methods: </strong>This prospective cohort study analyzed 2,102 COPD patients from NHANES (1999-2018). PUFA intake was assessed through 24-hour dietary recalls and categorized into tertiles. Associations with all-cause and cardiovascular mortality were evaluated using Cox regression models, restricted cubic splines (RCS), and weighted quantile sum (WQS) regression. Comprehensive subgroup and sensitivity analyses confirmed result robustness.</p><p><strong>Results: </strong>During 9.08 years of follow-up, 603 deaths (28.7%) occurred, including 190 (9.0%) from cardiovascular disease. Compared to the lowest tertile, the highest tertile of total PUFA (HR: 0.70, 95% CI: 0.53-0.91), N-3 PUFA (HR: 0.67, 95% CI: 0.52-0.87), and N-6 PUFA (HR: 0.74, 95% CI: 0.57-0.97) intake was associated with lower all-cause mortality. For cardiovascular mortality, higher intake of total PUFA (HR: 0.55, 95% CI: 0.33-0.90), N-3 PUFA (HR: 0.56, 95% CI: 0.36-0.89), and N-6 PUFA (HR: 0.57, 95% CI: 0.34-0.93) showed significant protective effects. RCS analyses revealed non-linear associations with significant threshold effects. WQS analysis identified two plant-derived PUFA-α-linolenic acid (ALA) and linoleic acid (LA) as the primary contributors to mortality reduction. All sensitivity analyses confirmed the stability and consistency of our main findings.</p><p><strong>Conclusions: </strong>Higher dietary PUFA intake is associated with lower all-cause and cardiovascular mortality among COPD patients, suggesting that increasing dietary PUFA, particularly from plant sources, may help reduce COPD-related mortality risk.</p>","PeriodicalId":19196,"journal":{"name":"Nutrition & Metabolism","volume":"22 1","pages":"108"},"PeriodicalIF":4.1,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12487311/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145200530","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"mTOR-autophagy axis regulation by intermittent fasting promotes skeletal muscle growth and differentiation.","authors":"Chen Xinyan, Wu Yajie, He Shangfan, Yang Yuefei, Li Junwei, Zhu Jiaqiao, Ju Huiming","doi":"10.1186/s12986-025-01001-3","DOIUrl":"10.1186/s12986-025-01001-3","url":null,"abstract":"<p><p>Intermittent fasting (IF) as a dietary intervention with potential health benefits has garnered significant attention in recent years. This study investigated the effects of varying fasting intensities on skeletal muscle growth using mouse models. Compared to the normal-diet (ND) control group, short-term fasting induced feeding amount-dependent alterations in skeletal muscle autophagy markers, characterized by elevated LC3B expression, reduced p62 levels, and decreased p-mTOR/mTOR ratio. Notably, short-term mild fasting (sMF) significantly upregulated myogenic (MYH, MyoD) and adipogenic (LPL, PPARγ) differentiation markers, whereas short-term severe fasting (sSF) suppressed myogenic markers without significantly affecting adipogenic factors. Pharmacological modulation using 3-methyladenine (3-MA) and rapamycin (RAPA) confirmed the critical role of autophagy in myogenic and adipogenic processes. Multi-cycle IF studies revealed that intermittent mild fasting (IMF) enhanced metabolic efficiency (evidenced by increased feed conversion ratio), elevated organ indices of gastrocnemius and quadriceps femoris muscles, and reduced groin fat. IMF also promoted intramuscular adipogenesis and myofiber remodeling. In contrast, intermittent severe fasting (ISF) impaired glucose tolerance, decreased triglyceride levels and aspartate aminotransferase (AST) activity, inhibited myofiber growth, and exhibited no significant effect on intramuscular adipogenesis. Our findings demonstrate that IMF enhances skeletal muscle mass and reduces visceral adiposity through mTOR-autophagy axis, providing an optimized fasting regimen for metabolic health and body composition regulation.</p>","PeriodicalId":19196,"journal":{"name":"Nutrition & Metabolism","volume":"22 1","pages":"109"},"PeriodicalIF":4.1,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12486585/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145200502","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}