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Another Disease, Another Utility of Vitamin D. 另一种疾病,维生素D的另一种用途
IF 3.8 3区 医学 Q2 NUTRITION & DIETETICS Pub Date : 2026-02-06 DOI: 10.1016/j.tjnut.2026.101390
Olivia Z B Ginnard
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引用次数: 0
Dietary Intake and Plasma Concentration of B vitamins in Relation to Incident Coronary Heart Disease in African American Adults: the Jackson Heart Study. 膳食摄入和血浆B族维生素浓度与非裔美国成年人冠心病发病率的关系:杰克逊心脏研究
IF 3.8 3区 医学 Q2 NUTRITION & DIETETICS Pub Date : 2026-02-04 DOI: 10.1016/j.tjnut.2026.101395
Cuiqiong Huo, Krisha Thiagarajah, Carmen D Tekwe, Katherine L Tucker, Aurelian Bidulescu

Background: B vitamin inadequacies are common in the US, particularly among African Americans. B vitamins play a key role in one-carbon metabolism, and poor status may influence cardiovascular health. We investigated associations of dietary intake of vitamins B6, B12, and folate, as well as plasma concentrations of vitamin B12 and folate, with incident coronary heart disease (CHD).

Methods: We analyzed data from the Jackson Heart Study (2000-2016), including 4,863 participants in the dietary analytic sample (309 CHD cases) and 4,906 in the plasma analytic sample (311 CHD cases). Dietary intake of B vitamins was energy-adjusted using the residual method. Cox proportional hazards regression with multiple imputation was applied to estimate hazard ratios (HRs) for incident CHD over a median of 13.8 years of follow-up (60,660 and 61,180 person-years in the dietary and plasma samples, respectively). Linearity of associations was evaluated using restricted cubic splines.

Results: In multivariable-adjusted models (per 1 SD), higher energy-adjusted dietary intake of vitamin B6 (HR = 1.07; 95% CI: 0.93-1.25), vitamin B12 (HR = 0.99; 95% CI: 0.87-1.12), or folate (HR = 0.97; 95% CI: 0.82-1.15) were not significantly associated with CHD risk. Similarly, plasma vitamin B12 (HR = 0.99; 95% CI: 0.84-1.18) and folate (HR = 0.97; 95% CI: 0.80-1.17) showed no statistically significant associations. Tests for non-linearity revealed no evidence of threshold or U-shaped relationships.

Conclusion: In this cohort of African American adults, neither dietary intake nor plasma concentrations of B vitamins were significantly associated with CHD risk. These findings do not support a strong association between B vitamin status and CHD risk in this cohort.

背景:B族维生素缺乏在美国很常见,尤其是非洲裔美国人。B族维生素在单碳代谢中起着关键作用,缺乏B族维生素可能会影响心血管健康。我们调查了膳食中维生素B6、B12和叶酸的摄入,以及维生素B12和叶酸的血浆浓度与冠心病(CHD)的关系。方法:我们分析了Jackson心脏研究(2000-2016)的数据,包括4863名参与者的饮食分析样本(309例冠心病患者)和4906名参与者的血浆分析样本(311例冠心病患者)。采用余量法对膳食B族维生素摄入量进行能量调节。采用Cox比例风险回归和多重归因来估计中位13.8年随访期间(饮食和血浆样本分别为60660和61180人年)冠心病发生的风险比(hr)。使用受限三次样条评估关联的线性。结果:在多变量调整模型(每1 SD)中,较高的能量调整膳食摄入维生素B6 (HR = 1.07; 95% CI: 0.93-1.25)、维生素B12 (HR = 0.99; 95% CI: 0.87-1.12)或叶酸(HR = 0.97; 95% CI: 0.82-1.15)与冠心病风险无显著相关性。同样,血浆维生素B12 (HR = 0.99; 95% CI: 0.84-1.18)和叶酸(HR = 0.97; 95% CI: 0.80-1.17)没有统计学上的显著相关性。非线性测试没有发现阈值或u型关系的证据。结论:在该非裔美国成年人队列中,饮食摄入和血浆B族维生素浓度与冠心病风险均无显著相关性。这些发现不支持在该队列中B族维生素水平与冠心病风险之间存在强关联。
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引用次数: 0
Maternal adiposity and DNA methylation of TfR2 and HJV genes in early pregnancy: mediating role of inflammation and consequences for iron status. 妊娠早期母体肥胖和TfR2和HJV基因的DNA甲基化:炎症的介导作用和铁状态的后果
IF 3.8 3区 医学 Q2 NUTRITION & DIETETICS Pub Date : 2026-02-04 DOI: 10.1016/j.tjnut.2026.101393
Sabrina P Demirdjian, Rachelle E Irwin, Paul D Thompson, Maria S Mulhern, Maeve A Kerr, Mark Ledwidge, Kazi L Rahman, Caroline Conway, Edna P Rodriguez, Mary T McCann

Background: Growing evidence shows that obesity influences iron status during pregnancy, however, it is unknown whether maternal obesity is associated with epigenetic changes in TfR2 and HJV.

Objective: To explore the association between adiposity and DNA methylation in TfR2 and HJV in early pregnancy and the mediating effect of inflammation on this association.

Methods: This cross-sectional study used data from a double-blind randomized controlled trial in singleton pregnant women with normal weight (BMI 18.5-24.9 kg/m2) and obesity (BMI ≥30.0 kg/m2). Maternal BMI, fat mass, visceral fat, iron/inflammatory markers and DNA methylation of TfR2 and HJV were measured at 12 gestational weeks (GW). Two primer sets were designed (TfR2 zone 1 and 2, (TfR2z1, TfR2z2); HJV zone 1 and 2 (HJVz1, HJVz2). An inflammation score was calculated using pro-inflammatory cytokines.

Results: 65 pregnant women were included, 34 with normal weight, and 31 with obesity. Compared to those of normal weight women, those with obesity showed: lower percentage of DNA methylation in TfR2z1 CpG sites 5, 6, 8-10 and the average in this zone (average CpG methylation 5.80 vs 6.92%, p=0.004); lower percentage of DNA methylation in TfR2z2 CpG sites 5 and 6 (12.5 vs 14.7%, p=0.035; 17.8 vs 20.1%, p=0.031); higher percentage methylation of DNA in HJVz1 CpG site 3 (HJVz1 CpG 3 45.3% vs 43.4%, p=0.010) and HJVz2 CpG site 2 and the average (HJVz2 CpG 2 43.2 vs 37.9%, p<0.001, average 65.9 vs 61.6%, p<0.001). Adjusting for covariates, TfR2z1 was negatively and HJVz2 positively associated with all adiposity measures (TfR2z1, BMI β=-0.288, p=0.030; HJVz2 β=0.459, p<0.001). Inflammation showed a mediating effect on the association between all adiposity measures and DNA methylation of HJVz1 (p=0.019).

Conclusions: Maternal adiposity is associated with epigenetic changes in the iron metabolism genes TfR2 and HJV in early pregnancy, part of which are inflammation-mediated changes in HJV.

背景:越来越多的证据表明,肥胖会影响妊娠期间铁的状态,然而,尚不清楚母亲肥胖是否与TfR2和HJV的表观遗传改变有关。目的:探讨妊娠早期TfR2和HJV DNA甲基化与肥胖的关系以及炎症在这一关系中的中介作用。方法:本横断面研究采用双盲随机对照试验数据,研究对象为体重正常(BMI 18.5 ~ 24.9 kg/m2)和肥胖(BMI≥30.0 kg/m2)的单胎孕妇。在妊娠12周(GW)时测量母体BMI、脂肪量、内脏脂肪、铁/炎症标志物以及TfR2和HJV的DNA甲基化。设计两组引物(TfR2区1和2,(TfR2z1, TfR2z2);HJV 1区和2区(HJVz1、HJVz2)。使用促炎细胞因子计算炎症评分。结果:纳入孕妇65例,体重正常34例,肥胖31例。与正常体重女性相比,肥胖女性TfR2z1 CpG位点5、6、8-10的DNA甲基化率较低,该区域的平均甲基化率为5.80比6.92% (p=0.004);TfR2z2 CpG位点5和6的DNA甲基化百分比较低(12.5 vs 14.7%, p=0.035; 17.8 vs 20.1%, p=0.031);HJVz1 CpG位点3的DNA甲基化率(45.3% vs 43.4%, p=0.010)和HJVz2 CpG位点2的DNA甲基化率高于平均水平(43.2 vs 37.9%)。结论:孕妇肥胖与妊娠早期铁代谢基因TfR2和HJV的表观遗传改变有关,其中部分是炎症介导的HJV改变。
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引用次数: 0
Dose Response Effects of Pecan Consumption on Blood Lipid Profiles in Adults with Excess Body Weight and/or Dyslipidemia: A Randomized Controlled Trial. 食用山核桃对超重和/或血脂异常成人血脂的剂量反应效应:一项随机对照试验
IF 3.8 3区 医学 Q2 NUTRITION & DIETETICS Pub Date : 2026-02-04 DOI: 10.1016/j.tjnut.2026.101396
Alyssa J Guadagni, Chad M Paton, Jamie A Cooper

Background: Consuming ≥20% of daily energy from pecans improves blood lipids and reduces dyslipidemia but exceeds dietary recommendations. The benefits of lower doses remain unclear.

Objective: Examine the effects of pecan consumption at doses of 6%, 13%, and 20% of total energy needs on fasting and postprandial blood lipids in adults with excess body weight and/or dyslipidemia, compared to the control. We hypothesized a dose-response relationship, with the 20% group showing the greatest lipid improvements, followed by 13% and 6%, and all would be better than the control.

Methods: This single-blind, randomized, controlled superiority trial enrolled 102 adults with excess body weight (BMI ≥28kg/m2) or dyslipidemia. Participants were randomized to 6% (n=26), 13% (n=26), or 20% (n=25) pecan-intake groups, or to a control group (n=25) that maintained a habitual, nut-free diet. Participants completed pre- and post-intervention visits, which included fasting lipid assessments and a high-fat meal challenge (17% of total energy), followed by 4-h postprandial blood draws.

Results: Change in total cholesterol, LDL cholesterol, Apolipoprotein B, non-HDL cholesterol, and TC/HDL cholesterol ratio all decreased from pre- to post-intervention in MID (-13.3±3.4, -12.7±3.3, -9.2±2.3, -13.9±3.2, and -0.3±0.1 mg/dL, respectively; p<0.05 for all) and HIGH (-12.7±3.6, -11.9±3.4, -7.8±1.9, -13.8±3.6, and -0.3±0.1 mg/dL, respectively; p<0.05 for all) vs. no change in LOW or CON. Change from baseline postprandial non-esterified fatty acids (NEFAs) decreased from pre-to-post intervention in MID (p=0.01) vs. no changes in CON, HIGH, or LOW (p>0.05 for all). Fasting triglycerides (TGs), fasting NEFAs, and postprandial TGs did not differ between groups (p>0.05 for all).

Conclusions: Pecan intake providing 20% and 13%, but not 6%, of daily energy improved fasting blood lipid profiles versus the control, with postprandial NEFA reductions observed only at 13%. These findings offer the first evidence that moderate doses of daily pecan consumption confer cardioprotective benefits.

Clinical trial registry: This trial was registered at clinicaltrials.gov as NCT05949879 and available from: https://clinicaltrials.gov/study/NCT05949879. The date of initial trial registration was July 18, 2023.

背景:每天从山核桃中摄入≥20%的能量可改善血脂并降低血脂异常,但超过了饮食推荐值。低剂量的益处尚不清楚。目的:研究与对照组相比,在体重超重和/或血脂异常的成年人中,核桃摄入剂量分别为总能量需求的6%、13%和20%时,对空腹和餐后血脂的影响。我们假设了一种剂量-反应关系,20%组显示出最大的脂质改善,其次是13%和6%,所有的都比对照组好。方法:这项单盲、随机、对照的优势试验招募了102名体重超重(BMI≥28kg/m2)或血脂异常的成年人。参与者被随机分为摄入6% (n=26)、13% (n=26)或20% (n=25)山核桃的组,或保持习惯性无坚果饮食的对照组(n=25)。参与者完成了干预前和干预后的访问,其中包括空腹脂质评估和高脂肪餐挑战(占总能量的17%),随后是餐后4小时抽血。结果:干预前后,总胆固醇、LDL胆固醇、载脂蛋白B、非HDL胆固醇、TC/HDL胆固醇比值均下降(分别为-13.3±3.4、-12.7±3.3、-9.2±2.3、-13.9±3.2、-0.3±0.1 mg/dL, p < 0.05)。各组间空腹甘油三酯(tg)、空腹NEFAs和餐后tg均无差异(p < 0.05)。结论:山核桃摄入量提供每日能量的20%和13%,而不是6%,与对照组相比,空腹血脂谱改善,餐后NEFA仅降低13%。这些发现提供了第一个证据,证明每天适量食用山核桃具有保护心脏的作用。临床试验注册:该试验在clinicaltrials.gov注册为NCT05949879,可从https://clinicaltrials.gov/study/NCT05949879获得。首次试验注册日期为2023年7月18日。
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引用次数: 0
Effect of gut microbiota from patients with uremia on body weight and micro-inflammation in rats. 尿毒症患者肠道菌群对大鼠体重和微炎症的影响。
IF 3.8 3区 医学 Q2 NUTRITION & DIETETICS Pub Date : 2026-02-04 DOI: 10.1016/j.tjnut.2026.101397
Yong-Zhan Liu, Xiang-Fei Cui, Si-Yu Mao

Background: Gut dysbiosis is associated with malnutrition and inflammation in chronic kidney disease (CKD); however, the causality remains unclear.

Objectives: This study aimed to determine whether fecal microbiota from patients with stage 5 CKD can directly induce nutritional impairment and inflammatory responses in recipient rats.

Methods: Fecal microbiota from patients with stage 5 CKD and healthy controls were transplanted into rats treated with antibiotics. After 2 weeks, we assessed nutritional parameters, inflammatory markers, and microbial composition.

Results: Compared with the healthy-FMT group, rats receiving CKD-derived microbiota exhibited a significant reduction in body weight (466.70 ± 12.60 g vs. 433.90 ± 20.10 g) and serum albumin concentrations (22.87 ± 5.43 g/L vs. 20.36 ± 7.51 g/L). In contrast, serum inflammatory markers were significantly elevated in the CKD-FMT group, including C-reactive protein (12.10 ± 3.10 vs. 15.40 ± 5.00 mg/L) and interleukin-6 (14.30 ± 1.80 vs. 18.80 ± 2.10 pg/L) (all p < 0.01). Microbial analysis revealed enrichment of Enterobacteriaceae and depletion of beneficial genera such as Lactobacillus and Ruminococcaceae.

Conclusions: Our results provide direct evidence that gut microbiota from patients with uremia can impair nutritional status and aggravate systemic inflammation in recipient rats, underscoring a pathogenic role of dysbiosis in CKD complications.

背景:慢性肾脏疾病(CKD)患者肠道生态失调与营养不良和炎症有关;然而,因果关系尚不清楚。目的:本研究旨在确定来自5期CKD患者的粪便微生物群是否可以直接诱导受体大鼠的营养损害和炎症反应。方法:将5期CKD患者和健康对照组的粪便微生物群移植到抗生素治疗的大鼠体内。2周后,我们评估了营养参数、炎症标志物和微生物组成。结果:与健康fmt组相比,接受ckd来源微生物群的大鼠体重(466.70±12.60 g vs. 433.90±20.10 g)和血清白蛋白浓度(22.87±5.43 g/L vs. 20.36±7.51 g/L)显著降低。相比之下,CKD-FMT组血清炎症标志物显著升高,包括c反应蛋白(12.10±3.10比15.40±5.00 mg/L)和白细胞介素-6(14.30±1.80比18.80±2.10 pg/L)(均p < 0.01)。微生物分析显示肠杆菌科的富集和有益菌如乳酸菌和瘤胃球菌科的减少。结论:我们的研究结果提供了直接证据,表明尿毒症患者的肠道微生物群可以损害受体大鼠的营养状况并加重全身炎症,强调了生态失调在CKD并发症中的致病作用。
{"title":"Effect of gut microbiota from patients with uremia on body weight and micro-inflammation in rats.","authors":"Yong-Zhan Liu, Xiang-Fei Cui, Si-Yu Mao","doi":"10.1016/j.tjnut.2026.101397","DOIUrl":"https://doi.org/10.1016/j.tjnut.2026.101397","url":null,"abstract":"<p><strong>Background: </strong>Gut dysbiosis is associated with malnutrition and inflammation in chronic kidney disease (CKD); however, the causality remains unclear.</p><p><strong>Objectives: </strong>This study aimed to determine whether fecal microbiota from patients with stage 5 CKD can directly induce nutritional impairment and inflammatory responses in recipient rats.</p><p><strong>Methods: </strong>Fecal microbiota from patients with stage 5 CKD and healthy controls were transplanted into rats treated with antibiotics. After 2 weeks, we assessed nutritional parameters, inflammatory markers, and microbial composition.</p><p><strong>Results: </strong>Compared with the healthy-FMT group, rats receiving CKD-derived microbiota exhibited a significant reduction in body weight (466.70 ± 12.60 g vs. 433.90 ± 20.10 g) and serum albumin concentrations (22.87 ± 5.43 g/L vs. 20.36 ± 7.51 g/L). In contrast, serum inflammatory markers were significantly elevated in the CKD-FMT group, including C-reactive protein (12.10 ± 3.10 vs. 15.40 ± 5.00 mg/L) and interleukin-6 (14.30 ± 1.80 vs. 18.80 ± 2.10 pg/L) (all p < 0.01). Microbial analysis revealed enrichment of Enterobacteriaceae and depletion of beneficial genera such as Lactobacillus and Ruminococcaceae.</p><p><strong>Conclusions: </strong>Our results provide direct evidence that gut microbiota from patients with uremia can impair nutritional status and aggravate systemic inflammation in recipient rats, underscoring a pathogenic role of dysbiosis in CKD complications.</p>","PeriodicalId":16620,"journal":{"name":"Journal of Nutrition","volume":" ","pages":"101397"},"PeriodicalIF":3.8,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146132175","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Untargeted Metabolomics Analysis of Human Milk from Breastfeeding Bangladeshi Women Reveals Amino Acid Metabolic Pathways Associated with Maternal Nutritional Status and Infant Growth. 对孟加拉国母乳喂养妇女母乳的非靶向代谢组学分析揭示了与母亲营养状况和婴儿生长相关的氨基酸代谢途径。
IF 3.8 3区 医学 Q2 NUTRITION & DIETETICS Pub Date : 2026-02-04 DOI: 10.1016/j.tjnut.2026.101394
Carmen Monthe-Dreze, Brij Bhushan, Chloe Andrews, Sara Cherkerzian, Wei Perng, Salahuddin Ahmed, Abdullah H Baqui, Nabidul Chowdury, Rasheda Khanam, Sayedur Rahman, Patricia A Sheridan, Gregory Michelotti, Camilia R Martin, Anne C C Lee, Sarbattama Sen
<p><strong>Background: </strong>Human milk (HM) contains bioactive constituents that continuously change throughout lactation and that are critical for optimal infant development. Yet, the temporal variation of the HM metabolome, its maternal nutritional determinants, and its links to infant outcomes remain insufficiently characterized in low middle-income countries (LMIC) where childhood disease burden and HM exposure are substantial, and maternal nutritional status is poor.</p><p><strong>Objective: </strong>We aimed to 1) characterize temporal changes in the HM metabolome, 2) quantify maternal nutritional status-related differences in HM metabolomic patterns, and 3) determine whether HM metabolomic patterns associated with maternal nutritional status are in turn associated with infant growth, in a cohort of rural Bangladeshi maternal-infant dyads.</p><p><strong>Methods: </strong>In a lactation cohort (n = 99, 6% preterm at 34-36 weeks), we characterized metabolites in HM samples at 2 (n = 94) and 5 (n = 88) months (mo) postpartum (PP) using untargeted metabolomics profiling. We performed a paired t-test to identify metabolites that differed between timepoints and principal component analysis to consolidate metabolites measured at each timepoint into "factors," representing metabolite patterns. We used linear regression models to determine associations between maternal nutritional predictors, factor scores at 2 and 5 mo, and infant growth outcomes, and performed metabolite set enrichment analysis (MSEA) to characterize relevant pathways. P-values were adjusted for multiple comparisons.</p><p><strong>Results: </strong>Among the 51 metabolites that differed in relative abundance across the two time-points, 37 (73%) metabolites decreased over time, mainly comprising of lipids (sphingolipids and phospholipids), and amino acids (AA). MSEA did not reveal specific metabolic pathways alterations over time. HM from mothers in the highest (vs. middle, ref) body mass index (BMI) tertile PP had significantly lower scores for a metabolomic pattern (factor 5) characterized by AA that enriched in six critical metabolic pathways (metabolism of glutathione, glutamate, alanine, glycine and serine, and aspartate; and the ammonia recycling pathway). In turn, lower scores for this profile were associated with greater (β 0.22; 95% CI: 0.00, 0.43) infant weight-for-age z-score at 3 mo but not 6 mo. Additionally, HM from undernourished mothers had lower scores for a metabolomic pattern (factor 4) characterized mainly by AA and acylcarnitines involved in branched chain AA and fatty acids metabolism, though MSEA were not significant. This pattern was not associated with infant growth.</p><p><strong>Conclusion: </strong>In this LMIC cohort, the abundance of several lipid and AA metabolites declined over time. Furthermore, HM metabolome differences in mothers with high BMI may underpin early weight gain in their infants. More studies from LMICs are needed to understand mat
背景:母乳(HM)含有生物活性成分,在整个哺乳期不断变化,对婴儿的最佳发育至关重要。然而,在儿童疾病负担和HM暴露严重、产妇营养状况较差的中低收入国家(LMIC), HM代谢组的时间变化、母体营养决定因素及其与婴儿结局的联系仍然没有充分表征。目的:我们的目的是1)表征HM代谢组的时间变化,2)量化HM代谢组模式中与母体营养状况相关的差异,以及3)确定与母体营养状况相关的HM代谢组模式是否反过来与婴儿生长有关,在孟加拉国农村的母婴双体队列中。方法:在一个哺乳期队列中(n = 99.6%,早产34-36周),我们使用非靶向代谢组学分析方法对产后2个月(n = 94)和5个月(n = 88)个月(PP)的HM样本中的代谢物进行了表征。我们进行了配对t检验,以确定不同时间点的代谢物,并进行主成分分析,将每个时间点测量的代谢物整合为代表代谢物模式的“因素”。我们使用线性回归模型来确定母亲营养预测因素、2个月和5个月时的因子评分与婴儿生长结局之间的关系,并进行代谢物集富集分析(MSEA)来表征相关途径。对多重比较的p值进行调整。结果:51种代谢物在两个时间点的相对丰度不同,其中37种(73%)代谢物随着时间的推移而减少,主要包括脂质(鞘脂和磷脂)和氨基酸(AA)。MSEA没有显示特定的代谢途径随时间的变化。体重指数(BMI)最高(相对于中等,参考)的PP母亲的HM在以AA为特征的代谢组学模式(因子5)上得分显著较低,该模式富集于六个关键代谢途径(谷胱甘肽、谷氨酸、丙氨酸、甘氨酸和丝氨酸以及天冬氨酸的代谢;以及氨循环途径)。反过来,在3个月(β 0.22; 95% CI: 0.00, 0.43)婴儿年龄体重z-得分越低,而在6个月(β 0.22; 95% CI: 0.00, 0.43)婴儿体重z-得分越高。此外,营养不良母亲的HM在代谢组学模式(因子4)方面得分越低,代谢组学模式主要以AA和酰基肉碱参与支链AA和脂肪酸代谢为特征,尽管MSEA并不显著。这种模式与婴儿生长无关。结论:在LMIC队列中,几种脂质和AA代谢物的丰度随着时间的推移而下降。此外,高BMI母亲的HM代谢组差异可能是其婴儿早期体重增加的基础。需要更多来自中低收入国家的研究来了解可能影响婴儿生长发育的母亲营养驱动的HM组成差异,以指导这些高危母乳喂养人群的干预措施。
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引用次数: 0
Computational Nutrition in Practice: Challenges and Opportunities from an Early-Career Perspective. 实践中的计算营养:从早期职业角度来看的挑战和机遇。
IF 3.8 3区 医学 Q2 NUTRITION & DIETETICS Pub Date : 2026-02-03 DOI: 10.1016/j.tjnut.2026.101387
Mattea Müller, Madeline Bartsch, Jan Voges

Computational approaches are transforming nutrition science by integrating data from wearables, digital health platforms, and multi-omics technologies to unravel complex diet-health interactions. Traditional statistical models cannot adequately capture the temporal, nonlinear, and individual variability inherent in such data. Computational nutrition, integrating data science, machine learning, and systems modeling, has therefore emerged as a distinct and rapidly developing field. Landmark studies have demonstrated its potential to improve dietary assessment, predict metabolic responses, and design personalized interventions. From an early-career perspective, however, the rise of computational nutrition also exposes structural and educational gaps. Early-career researchers (ECRs) often encounter fragmented training, limited mentorship, and restricted access to interoperable data and computational infrastructure. Empowering ECRs through integrated curricula, equitable data access, and recognition of interdisciplinary contributions will be essential for ensuring that computational nutrition evolves into a transparent, reproducible, and inclusive discipline capable of advancing both personalized and population-level nutrition.

通过整合来自可穿戴设备、数字健康平台和多组学技术的数据,计算方法正在改变营养科学,以揭示复杂的饮食与健康之间的相互作用。传统的统计模型不能充分捕捉这些数据中固有的时间、非线性和个体变异性。计算营养学,集成了数据科学、机器学习和系统建模,因此成为一个独特而迅速发展的领域。具有里程碑意义的研究已经证明了它在改善饮食评估、预测代谢反应和设计个性化干预方面的潜力。然而,从早期职业的角度来看,计算营养学的兴起也暴露了结构性和教育上的差距。早期职业研究人员(ecr)经常遇到零散的培训,有限的指导,以及限制访问可互操作的数据和计算基础设施。通过整合课程、公平的数据获取和对跨学科贡献的认可来增强计算营养学的能力,对于确保计算营养学发展成为一门透明、可复制和包容的学科,能够促进个性化和人口水平的营养至关重要。
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引用次数: 0
Letter to the Editor - "Relevant factors for the cardiovascular responses to dietary nitrate and nitrite". 致编辑的信-“饮食中硝酸盐和亚硝酸盐对心血管反应的相关因素”。
IF 3.8 3区 医学 Q2 NUTRITION & DIETETICS Pub Date : 2026-02-03 DOI: 10.1016/j.tjnut.2026.101384
Macario A Rebelo, Jose E Tanus-Santos
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引用次数: 0
Amino Acid Signaling in Skeletal Muscle Is Blunted by Prematurity in a Piglet Model 仔猪模型中骨骼肌氨基酸信号通路因早产而钝化。
IF 3.8 3区 医学 Q2 NUTRITION & DIETETICS Pub Date : 2026-02-01 DOI: 10.1016/j.tjnut.2025.101303
Antonio C Ramos dos Santos , Agus Suryawan , Ki Beom Jang , Rosemarie D Parada , Mahmoud A Mohammad , Marta L Fiorotto , Teresa A Davis

Background

Preterm (PT) infants are at increased risk for reduced postnatal lean mass accretion. We established that the feeding-induced stimulation of protein synthesis in skeletal muscle is blunted in piglets born PT compared with those born at term.

Objectives

We evaluated the extent to which key components of the amino acid–sensing pathways that regulate mechanistic target of rapamycin complex 1 (mTORC1) activation contribute to anabolic resistance in skeletal muscle of piglets born PT compared with those born term.

Methods

Piglets delivered by cesarean section 10 d PT (n = 23) or at term (n = 22) were administered total parenteral nutrition for 3 d. On day 4, euinsulinemic-euaminoacidemic-euglycemic (FAST group), hyperinsulinemic-euaminoacidemic-euglycemic (INS group), or euinsulinemic-hyperaminoacidemic-euglycemic (AA group) clamps were performed for 2 h. Abundances and activation of amino acid signaling components in skeletal muscle were analyzed by immunoblotting.

Results

Abundances of amino acid transporters LAT1/SLC7A5 (leucine), SLC38A9 (arginine), and SNAT2/SLC38A2 (glutamine) were unaffected by prematurity. Sestrin1- and Sestrin2-GATOR2 abundances were reduced (P < 0.05) by AA, consistent with leucine-induced dissociation of these inhibitory complexes; prematurity blunted this effect for Sestrin1-GATOR2 (P < 0.05). SAR1B, but not LARS-mTOR, leucine-sensor abundances were lower in PT than term animals (P < 0.05). TARS2 (threonine) and RAB1A (branched-chain amino acid) sensor abundances were lower in PT (P < 0.05). Arginine (CASTOR1-GATOR2), methionine (SAMTOR-GATOR1), and glutamine (ARF1) sensor abundances were unaffected by prematurity. AA-induced formations of RagA- and RagC-mTOR complexes were attenuated in PT compared with term piglets (P < 0.05). Both AA and INS stimulated mTORC1 phosphorylation, but these effects were blunted by prematurity.

Conclusions

PT birth impairs the abundance and activation of multiple amino acid–sensing components upstream of mTORC1 in skeletal muscle. This disruption attenuates amino acid–induced mTORC1-dependent translation initiation and protein synthesis and likely contributes to the anabolic resistance, reduced lean mass, and extrauterine growth faltering frequently observed in premature infants.
背景:早产儿产后瘦块增生减少的风险增加。我们证实,与足月仔猪相比,喂养诱导的骨骼肌蛋白质合成刺激在早产仔猪中减弱。目的:我们评估了与足月仔猪相比,早产儿(PT)骨骼肌中调节mTORC1激活的氨基酸感应通路的关键组分在多大程度上促进了合成代谢抵抗。方法:剖宫产10 d (n = 23)或T (n = 22)仔猪给予全肠外营养3 d。第4天,采用胰岛素-真氨基酸-正糖(FAST)钳夹、高胰岛素-真氨基酸-正糖(INS)钳夹或胰岛素-高氨基酸-正糖(AA)钳夹2 h。通过免疫印迹分析骨骼肌中氨基酸信号组分的丰度和激活情况。结果:氨基酸转运体LAT1/SLC7A5(亮氨酸)、SLC38A9(精氨酸)和SNAT2/SLC38A2(谷氨酰胺)的丰度不受早产影响。AA降低了Sestrin1-和Sestrin2-GATOR2的丰度(P < 0.05),这与亮氨酸诱导的这些抑制复合物解离一致;早产使Sestrin1-GATOR2的这种作用减弱(P < 0.05)。PT中SAR1B的亮氨酸传感器丰度低于T (P < 0.05),而LARS-mTOR的丰度不低于T (P < 0.05)。TARS2(苏氨酸)和RAB1A(支链氨基酸)传感器丰度在PT中较低(P < 0.05)。精氨酸(CASTOR1-GATOR2)、蛋氨酸(SAMTOR-GATOR1)和谷氨酰胺(ARF1)传感器丰度不受早产影响。与T相比,aa诱导的RagA-和RagC-mTOR复合物的形成在PT中减弱(P < 0.05)。AA和INS均刺激mTORC1磷酸化,但这些作用因早产而减弱。结论:早产会损害骨骼肌中mTORC1上游多个氨基酸敏感组分的丰度和激活。这种破坏减弱了氨基酸诱导的mtorc1依赖的翻译起始和蛋白质合成,并可能导致合成代谢抵抗、瘦体重减少和早产儿经常观察到的子宫外生长迟缓。
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引用次数: 0
Dietary Urolithin B Suppresses Lung Tumorigenesis Correlating with Autophagy Induction and Gut Microbiota Remodeling 膳食尿素B抑制与自噬诱导和肠道微生物群重塑相关的肺肿瘤发生。
IF 3.8 3区 医学 Q2 NUTRITION & DIETETICS Pub Date : 2026-02-01 DOI: 10.1016/j.tjnut.2025.101320
Jiacheng Sun , Xiaohan Li , Lemei Sun, Bingqi Chen, Jing Duan

Background

Urolithin B (UB) is a gut microbial metabolite derived from dietary ellagitannins found in foods such as pomegranates, berries, and nuts. Although UB has demonstrated antitumor potential, possibly through gut microbiota modulation, its specific role and underlying mechanisms in lung cancer remain unclear.

Objectives

This study aimed to investigate the antitumor effects of UB on lung cancer suppression and to explore the potential involvement of autophagy and gut microbiota in these effects.

Methods

We employed in vitro and in vivo approaches. Lung cancer cells were treated with UB at varying concentrations to assess proliferation and autophagy. Transcriptomic analysis was conducted to identify key regulatory pathways. A tumor-bearing mouse model was used to evaluate the effects of oral UB administration, and gut microbiota changes were analyzed via 16S rRNA sequencing.

Results

UB inhibited lung cancer cell growth in a dose- and time-dependent manner, primarily by inducing autophagy rather than apoptosis, as evidenced by increased microtubule-associated protein 1A/1B-light chain 3-II concentrations. Transcriptomic profiling and protein analysis revealed that UB treatment was associated with a change in the status of the AMP-activated protein kinase/mammalian target of rapamycin (AMPK/mTOR) pathway, a key regulator of autophagy. In vivo, oral UB administration significantly suppressed tumor growth, enhanced autophagic activity, and modulated the expression of autophagy-related proteins. Furthermore, 16S rRNA sequencing revealed that UB induced an enrichment of beneficial gut bacteria, including Lactobacillus and Desulfovibrio.

Conclusions

These findings highlight UB as a promising dietary-derived metabolite for lung cancer prevention and therapy. Our study suggests that UB exerts its antitumor effects in part through the induction of autophagy associated with the AMPK/mTOR pathway and concomitant modulation of the gut microbiota, emphasizing the critical role of food–gut interactions in cancer management.
背景:尿素B (UB)是一种肠道微生物代谢物,来源于石榴、浆果和坚果等食物中的鞣花单宁。虽然UB已经显示出抗肿瘤的潜力,可能是通过调节肠道微生物群,但其在肺癌中的具体作用和潜在机制尚不清楚。目的:本研究旨在研究UB对肺癌的抑制作用,并探讨自噬和肠道微生物群在这些作用中的潜在作用。方法:采用体外和体内两种方法。用不同浓度的UB处理肺癌细胞以评估其增殖和自噬。转录组学分析确定了关键的调控途径。采用荷瘤小鼠模型评价口服UB给药的效果,并通过16S rRNA测序分析肠道菌群的变化。结果:UB以剂量和时间依赖的方式抑制肺癌细胞的生长,主要是通过诱导自噬而不是凋亡,微管相关蛋白1A/ 1b -轻链3-II (LC3-II)水平的增加证明了这一点。转录组学分析和蛋白质分析显示,UB治疗与amp激活的蛋白激酶/哺乳动物雷帕霉素靶蛋白(AMPK/mTOR)通路状态的变化有关,AMPK/mTOR通路是自噬的关键调节因子。在体内,口服UB显著抑制肿瘤生长,增强自噬活性,调节自噬相关蛋白的表达。此外,16S rRNA测序显示,UB诱导了有益肠道细菌的富集,包括乳酸杆菌和Desulfovibrio。结论:这些发现突出了UB作为一种有前途的饮食衍生代谢物用于肺癌的预防和治疗。我们的研究表明,UB发挥其抗肿瘤作用部分是通过诱导与AMPK/mTOR通路相关的自噬以及伴随的肠道微生物群调节,强调了食物-肠道相互作用在癌症治疗中的关键作用。
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引用次数: 0
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Journal of Nutrition
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