Journal of Nutritional Biochemistry最新文献

{"title":"Associations between flavonoids intake and sleep disorders: A survey-weighted cross-section study from NHANES","authors":"Xiangjun Qi ,&nbsp;Caishan Fang ,&nbsp;Longyu Liu ,&nbsp;Jiayun Guo ,&nbsp;Yanlong Li ,&nbsp;Sun Chen ,&nbsp;Fuping Xu","doi":"10.1016/j.jnutbio.2025.109944","DOIUrl":"10.1016/j.jnutbio.2025.109944","url":null,"abstract":"<div><div>This study aimed to evaluate the associations between flavonoid intake and sleep disorders. A cross-sectional study was conducted using data from the National Health and Nutrition Examination Survey (2007–2010, 2017–2018). Intake data for 29 flavonoids were derived from the average of two 24-hour dietary recall interviews. Sleep disorders and sleep duration were the outcome measures. Dummy variables were used to account for missing covariate values. Survey-weighted generalized linear models and survey-weighted restricted cubic splines were applied to explore the associations between flavonoid intake and sleep disorders/sleep duration. Sensitivity and stratified analyses were performed to verify the robustness of results and examine potential subgroup differences. A total of 10,162 participants were included. After adjusting for covariates, isorhamnetin intake was inversely associated with sleep disorders. The odds ratios (OR) for sleep disorder were 0.944 (95% CI: 0.893–0.999) for continuous isorhamnetin intake and 0.754 (95% CI: 0.651–0.874; <em>P_trend</em>&lt;.001) for the highest tertile. Luteolin intake, both continuous and in tertiles, was also significantly inversely associated with sleep disorders (continuous OR = 0.903, 95% CI: 0.822–0.991; tertiles OR = 0.851, 95% CI: 0.732–0.989; <em>P_trend</em> = .031). Isorhamnetin intake, categorized by tertiles, was positively correlated with sleep duration (β = 0.125, 95% CI: 0.042–0.208; <em>P_trend</em> = .004), with a nonlinear relationship identified (<em>P_non-linear</em> = .0001). Sensitivity analysis confirmed the robustness of the results, and stratified analysis showed that luteolin's effect varied across different body mass index levels, while isorhamnetin's effect differed by age, gender, and race. Isorhamnetin and luteolin exhibit a significant negative correlation with sleep disorders. Isorhamnetin is linked to an increase in sleep duration. Additionally, both isorhamnetin and eriodictyol demonstrate a notable nonlinear relationship with sleep duration.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"143 ","pages":"Article 109944"},"PeriodicalIF":4.8,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144022912","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Enhanced citrate consumption increases colon permeability in C57BL/6J mice by affecting gut microbiota and activating HIF-1α","authors":"Emylle Costa-Bartuli ,&nbsp;Larissa Pereira Paixão ,&nbsp;Leticia Diniz Crepaldi ,&nbsp;Rhayane da Fonseca ,&nbsp;Mel Vianna ,&nbsp;Renata Moraes-Ribeiro ,&nbsp;Gabrielle Vitoria Lima ,&nbsp;José Xavier do Nascimento Junior ,&nbsp;Jessica Ristow Branco ,&nbsp;Carlos Alexandre Gonçalves Caldas ,&nbsp;Thiago Caetano Andrade Belo ,&nbsp;Christina M. Takiya ,&nbsp;Leonardo Augusto de Almeida ,&nbsp;Patricia Zancan ,&nbsp;Mauro Sola-Penna","doi":"10.1016/j.jnutbio.2025.109942","DOIUrl":"10.1016/j.jnutbio.2025.109942","url":null,"abstract":"<div><div>Citrate is a ubiquitously used food additive added to almost all industrialized alimentary product regardless the degree of processing. Indeed, citrate consumption has increased over the years since it is classified as a “generally recognized as safe” product, with no limitations to its use. Recently, we have shown that enhanced citrate consumption by mice impact physiology, impairing glucose tolerance and promoting low-grade systemic inflammation. Here, we treated mice for 24 hours or 12 weeks with standard chow diet enhanced with 40 mg citrate per gram of food, doubling its standard amount, and evaluated the colon of these animals and gut microbiota. Enhance citrate consumption for both 24 hours or 12 weeks promoted similar outcomes on mouse, as impairing glucose tolerance, thinning mucosal barrier and augmenting colon permeability and inflammation. Moreover, there is a robust change in gut microbiota population, that increased total bacteria with decreased variability, showing an obesogenic-like profile. Furthermore, enhanced citrate consumption upregulated the plasma membrane citrate transporter SLC13a5, HIF-1α and ATP: citrate lyase, boosting cytosolic citrate metabolism. In the end, we propose that enhanced citrate consumption increases cytosolic Acetyl-CoA formation, promoting lipid synthesis and acetylation of proteins and nucleic acids, and thus favoring epigenetic modifications.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"143 ","pages":"Article 109942"},"PeriodicalIF":4.8,"publicationDate":"2025-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144025075","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitochondrial fatty acid oxidation dysfunction impairs autophagic flux through ATP deficiency-caused lysosomal pH abnormity","authors":"Yan-Yu Zhang ,&nbsp;Ze-Dong Lv ,&nbsp;Mai Wang ,&nbsp;Jun-Xian Wang ,&nbsp;Samwel Mchele Limbu ,&nbsp;Fang Qiao ,&nbsp;Li-Qiao Chen ,&nbsp;Mei-Ling Zhang ,&nbsp;Yuan Luo ,&nbsp;Zhen-Yu Du","doi":"10.1016/j.jnutbio.2025.109943","DOIUrl":"10.1016/j.jnutbio.2025.109943","url":null,"abstract":"<div><div>Autophagy, a pivotal lysosomal degradation process, plays crucial roles in cellular homeostasis and energy metabolism. Mitochondrial fatty acid oxidation (FAO), a key mitochondrial function, is crucial for energy production. Generally, mitochondrial dysfunction exerts negative effects on autophagy, but the regulatory role of mitochondrial FAO dysfunction on the autophagic process remains unclear. The present study aimed to elucidate the role and mechanism of mitochondrial FAO in regulating autophagy process. We used Nile tilapia (<em>Oreochromis niloticus</em>) as a model and inhibited mitochondrial FAO by dietary mildronate feeding or knocking down carnitine palmitoyl transferase 1a. We found that mitochondrial FAO inhibition enhanced autophagy initiation and lysosomal proliferation accompanied by decreased autophagy degradation activity due to lysosomal acidification abnormity. Moreover, mitochondrial FAO inhibition decreased adenosine triphosphate (ATP) production and elevated adenosine monophosphate (AMP)/ATP promoted autophagy initiation via the AMP-activated protein kinase‑serine/threonine kinase 1 pathway. Furthermore, mitochondrial FAO inhibition upregulated peroxisome proliferator-activated receptor alpha and retinoid X receptor alpha protein expression, which promoted transcription factor EB mRNA and its protein expression. Meanwhile, mitochondrial FAO inhibition led to lysosomal alkalinization, which is due to a pH increase caused by v-ATPase V1/V0 imbalance and ATP deficiency from mitochondrial dysfunction. Collectively, our results highlight the role of mitochondrial FAO in maintaining lysosomal homeostasis and autophagic flux through stabilizing lysosomal acidification.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"143 ","pages":"Article 109943"},"PeriodicalIF":4.8,"publicationDate":"2025-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143976545","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"High-fat diet restriction to adult male mice maintains normal body weight but leads to liver impairment by disrupting mitochondrial oxidative phosphorylation","authors":"Chun‐Hsien Chiang ,&nbsp;Pu‐Sheng Hsu ,&nbsp;Shau‐Ping Lin ,&nbsp;Ching‐Yi Chen","doi":"10.1016/j.jnutbio.2025.109941","DOIUrl":"10.1016/j.jnutbio.2025.109941","url":null,"abstract":"<div><div>Dietary restriction (DR) delays aging and supports health primarily through its effects on mitochondrial function. Conversely, a high-fat diet (HFD) with excess calories promotes obesity and health risks via mitochondrial dysfunction. However, the role of an HFD in the benefits of DR remains unclear. This study investigated whether sustainable and intermittent DR with an HFD positively affects liver and heart health. Mice were assigned to four groups: chow diet <em>ad libitum</em> (CTR), HFD <em>ad libitum</em> (H), 60% HFD intake (HDR), and intermittent HFD restriction with weight cycling (WC). The results showed that the mice in the HDR and WC groups had reduced body weight, while animals in neither group had lower blood glucose levels compared to the H group. Hepatic steatosis, fibrosis, and NAFLD activity scores were similar in H, HDR, and WC mice but were higher than in CTR mice. The livers of mice in the HDR and WC groups also showed reduced ATP content and altered protein expressions related to mitochondrial dynamics. Liver in animals from the H group exhibited reduced LC3I expression and an increased LC3II to LC3I ratio compared with liver CTR. In contrast, livers of animals in the HDR and WC groups showed lower levels of p62, LC3I, and LC3II expression. Fibrosis was observed in the hearts of mice in the CTR and H groups, and DR did not reverse this damage. In conclusion, although HFD restriction maintained body weight, it adversely affected liver health by disrupting mitochondrial function. These findings emphasize the critical role of dietary fat in liver health when adopting calorie-restricted therapy.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"143 ","pages":"Article 109941"},"PeriodicalIF":4.8,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144025171","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Short-term methionine deprivation inhibits TCA cycle and regulates macrophage polarization through uncharged tRNA and PDHA1 phosphorylation","authors":"Xinyu Zhu ,&nbsp;Zinan Wang ,&nbsp;Xiaoyi Ye ,&nbsp;Puyang Liang ,&nbsp;Lingling Chen ,&nbsp;Jinzhu Chen ,&nbsp;Chenchen Li ,&nbsp;Jing Zhu ,&nbsp;Shixuan Zhuo ,&nbsp;Lanzexin Yang ,&nbsp;Lifeng Yang ,&nbsp;Yan Chen","doi":"10.1016/j.jnutbio.2025.109939","DOIUrl":"10.1016/j.jnutbio.2025.109939","url":null,"abstract":"<div><div>Methionine restriction diet has been extensively studied for its beneficial effects on metabolic health and aging. However, the impact of methionine deprivation on glucose metabolism <em>per se</em> and macrophage functions remains incompletely understood. In this study, we analyzed the functional roles of methionine deprivation on glucose flux and macrophage polarization. We used metabolic flux to investigate how methionine deprivation affected glucose metabolism. The functions of methionine deficiency on macrophage polarization and the underlying mechanisms were studied at both the cellular and animal levels. We found that short-term methionine deprivation represses the tricarboxylic acid (TCA) cycle in mitochondria, accompanied by rapid phosphorylation of the E1 subunit of pyruvate dehydrogenase (PDH) complex, PDHA1. This phosphorylation by methionine deprivation is dependent on increased levels of uncharged tRNA but is independent of GCN2. Furthermore, methionine deprivation promotes M1-like polarization of macrophages, consistent with metabolic reprogramming. Notably, the proinflammatory effect of methionine deprivation on macrophages is also mediated by PDHA1 phosphorylation and increases in uncharged tRNA, but independent of GCN2. Our study not only elucidates a direct regulatory role of methionine depletion on the TCA cycle but also reveals that such a regulation is tightly linked to the modulation of macrophage polarization.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"143 ","pages":"Article 109939"},"PeriodicalIF":4.8,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144023636","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ursolic acid attenuates sarcopenia through IL-17a-related gut-muscle axis in senile diabetic mice and myotube model","authors":"Meiling She ,&nbsp;Tianbai Li ,&nbsp;Lingli Zhou ,&nbsp;Zihao Deng ,&nbsp;Minna Huang ,&nbsp;Yan Yan ,&nbsp;Meng Zhang ,&nbsp;Yajun Yang ,&nbsp;Dongtao Wang","doi":"10.1016/j.jnutbio.2025.109940","DOIUrl":"10.1016/j.jnutbio.2025.109940","url":null,"abstract":"<div><div>Sarcopenia significantly impairs quality of life, especially in diabetic patients, where effective treatment options remain limited. The IL-17a-related gut-muscle axis suggests a potential role of the gut microbiota in the development of sarcopenia. Ursolic acid (UA) has shown promise as an anti-sarcopenic agent. Nevertheless, the relationship between UA and the IL-17a-related gut-muscle axis remains unclear. In this research, sarcopenia model was established using streptozotocin in vivo and in vitro with TNF-α-managed C2C12 myotubes. UA significantly altered the gut microbiota, notably increasing observed OTUs and the Shannon index of sarcopenic mice. Specifically, UA effectively mitigated the decrease of Bacteroides thetaiotaomicron and restored the total level of short-chain fatty acids, particularly reducing propionic acid and increasing isovaleric acid. Additionally, UA markedly improved muscle quality and function, as evidenced by increased body weight, grip strength, and muscle weight, as well as significantly decreased expression of Atrogin-1 and MuRF-1. Moreover, RNA sequencing results clearly indicated that UA suppressed the IL-17 signaling pathway in sarcopenic mice. Furthermore, UA alleviated oxidative stress and apoptosis in sarcopenic mice. Notably, UA inhibited the IL-17a pathway in sarcopenic mice by suppressing the heightened expression of the proteins. In vitro experiments further confirmed that UA inhibited TNF-α-induced myotube atrophy, reduced Atrogin-1 and MuRF-1 expression, and strongly suggested that IL-17a may be a key target of UA in combating myotube atrophy. The study emphasizes the importance of UA in alleviating sarcopenia, possibly through the IL-17a-related gut-muscle axis.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"143 ","pages":"Article 109940"},"PeriodicalIF":4.8,"publicationDate":"2025-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144021569","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of lactoferrin on high-fat and high-cholesterol diet-induced non-alcoholic fatty liver disease in mice","authors":"Li Ding ,&nbsp;Jin-si Chen ,&nbsp;Yi-fei Xing ,&nbsp;De-Ming Li ,&nbsp;An-Qi Fu ,&nbsp;Xing Tong ,&nbsp;Guo-Chong Chen ,&nbsp;Jia-Ying Xu ,&nbsp;Li-Qiang Qin","doi":"10.1016/j.jnutbio.2025.109938","DOIUrl":"10.1016/j.jnutbio.2025.109938","url":null,"abstract":"<div><div>Non-alcoholic fatty liver disease (NAFLD) is the most prevalent chronic liver disease, representing a growing public health burden. While previous studies indicated that lactoferrin (LF) alleviates hepatic lipid accumulation, a hallmark of NAFLD, the mechanisms involved are still elusive. Male C57BL/6 J mice were randomly divided into the control (CON), high-fat, high-cholesterol diet containing cholate (HFCCD), and HFCCD+LF groups and treated for 8 weeks' intervention. Liver and small intestine tissues were analyzed to investigate lipid metabolism and underlying mechanisms. Additionally, gut microbiota composition and short-chain fatty acid (SCFA) levels were assessed. HFCCD feeding induced hepatic steatosis, while LF intervention improved lipid metabolism by reducing fatty acid synthesis and increasing lipolysis in the liver. Mechanistically, LF downregulated the protein expression of serotonin receptor 2A (HTR2A), which is related to lipogenesis, and upregulated the protein expression of peroxisome proliferator-activated receptor α (PPARα), which is one of the pivotal lipolytic genes, and its downstream effector, carnitine palmitoyl transferase-1A (CPT-1A), in the liver. Additionally, LF increased the relative abundance of gut microbiota related to glycolipid metabolism, such as Adlercreutzia, and decreased the relative abundance of 5-HT-promoting gut microbiota, such as Clostridia. Furthermore, LF increased the levels of SCFAs, which positively correlated with the relative abundance of Adlercreutzia. Our study suggests that LF intervention alleviates HFCCD-induced NAFLD in mice, which is potentially associated with regulation of the HTR2A-PPARa-CPT-1A pathway and gut microbiota composition.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"143 ","pages":"Article 109938"},"PeriodicalIF":4.8,"publicationDate":"2025-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143988826","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Improvement of spatial memory dysfunction in type 2 diabetic mice through a low-carbohydrate and high-protein diet: Potential role of LRP6/Wnt3a signaling in the hippocampus","authors":"Takeru Shima ,&nbsp;Hayate Onishi ,&nbsp;Chiho Terashima","doi":"10.1016/j.jnutbio.2025.109937","DOIUrl":"10.1016/j.jnutbio.2025.109937","url":null,"abstract":"<div><div>Hippocampal dysfunction associated with type 2 diabetes mellitus (T2DM), including deficits in spatial learning and memory, represent a significant challenge to overall health. Dietary interventions are considered effective therapeutic approaches for managing metabolic parameters in T2DM, with a low-carbohydrate and high-protein (LC<img>HP) diet being a representative example. However, the impact of an LC<img>HP diet on hippocampal dysfunction in T2DM remains unclear. In this study, we examined the potential role of an LC<img>HP diet to alleviate spatial memory impairments. C57BL/6 J and ob/ob mice were assigned to either an LC<img>HP diet group (25.1 % carbohydrate, 57.2 % protein, and 17.7% fat as percentages of calories) or a control diet group (58.9% carbohydrate, 24.0% protein, and 17.1% fat as percentages of calories). After four weeks of dietary intervention, all mice underwent the Morris water maze test, followed by hippocampal mRNA expression analysis. The findings demonstrated that the LC<img>HP diet improved spatial memory performance in ob/ob mice. This dietary regimen mitigated the downregulation of hippocampal mRNA levels for low-density lipoprotein receptor-related protein 6 (<em>Lrp6</em>), IGF-1 receptor (<em>Igf1r</em>), and <em>Wnt3a</em> observed in ob/ob mice. These results suggest that modulating biochemical molecules may play a role in ameliorating memory deficits associated with T2DM through LC<img>HP dietary interventions, highlighting potential targets for developing nutritional strategies to address hippocampal dysfunction caused by T2DM.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"143 ","pages":"Article 109937"},"PeriodicalIF":4.8,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144064090","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reply to Dr. Chirumbolo’s letter to the editor","authors":"Bruce A Watkins ,&nbsp;Alyson E. Mitchell ,&nbsp;Andrew C. Shin ,&nbsp;Fereshteh Dehghani ,&nbsp;Chwan-Li Shen","doi":"10.1016/j.jnutbio.2025.109935","DOIUrl":"10.1016/j.jnutbio.2025.109935","url":null,"abstract":"","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"142 ","pages":"Article 109935"},"PeriodicalIF":4.8,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144064091","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association between nutritional and inflammatory status and mortality outcomes in patients with osteoporosis and osteopenia","authors":"Yazhou Liu ,&nbsp;Ying Yang ,&nbsp;Yuhao Li ,&nbsp;Wenbo Ding ,&nbsp;Xiaodong Yang","doi":"10.1016/j.jnutbio.2025.109936","DOIUrl":"10.1016/j.jnutbio.2025.109936","url":null,"abstract":"<div><div>Osteoporosis, characterized by reduced bone density and microarchitecture deterioration, is a significant global health concern, particularly among aging populations and those with malnutrition. Osteoporotic fractures affect up to 50% of women and 22% of men, making the optimization of assessment metrics crucial. Systemic inflammation, often linked to malnutrition, plays a key role in bone loss. The Advanced Lung Cancer Inflammation Index (ALI), a marker of inflammation and nutrition, shows potential in predicting prognosis but has been insufficiently studied in osteoporosis. This study uses NHANES data to explore ALI’s association with mortality in osteoporosis, suggesting its potential as a prognostic tool. Data from the National Health and Nutrition Examination Survey (NHANES) (2007-2023) were analyzed retrospectively. Kaplan-Meier survival curves were used to depict survival data, and the relationship between ALI and mortality was assessed through multivariable Cox regression analysis and restricted cubic spline plots. Subgroup and mediation analyses were also conducted. The study included 4,525 osteoporosis patients with 938 all-cause and 223 cardiovascular deaths. A linear negative correlation between ALI and both all-cause and cardiovascular mortality was observed. Mediation analysis showed that 4.9% and 6.6% of the associations between osteoporosis/osteoporotic fractures and mortality risk were mediated by ALI. Subgroup analyses indicated that ALI predicts mortality across genders and activity levels. This study highlights a linear negative correlation between ALI and both all-cause and cardiovascular mortality in osteoporosis patients.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"143 ","pages":"Article 109936"},"PeriodicalIF":4.8,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143947628","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}