Global consumption of muscle foods (a tissue-based classification; eg, meat, fish, and poultry) is expected to rise in the coming decades, intensifying debates about the roles of these foods in health, disease, and environmental sustainability. From a nutritional perspective, foods, including muscle foods, are often discussed on the basis of their nutritional composition and expected medium- and long-term health effects, without considering the acute role of muscle foods in postprandial metabolism and how these effects can translate into long-term health outcomes. The present evidence-based narrative review synthesizes the current knowledge on how acute consumption of muscle foods influences postprandial metabolism and the implications for health and dietary recommendations. First, we analyzed global consumption trends and the environmental impacts of muscle foods using a nutrient density score (NDS) and greenhouse gas emission rates. Next, we reviewed human clinical studies examining postprandial responses, including glycemic, lipemic, aminoacidemic, and incretin responses to different muscle foods, considering the roles of digestibility, amino acid composition, and cooking methods. Evidence indicates that fish intake generally promotes more favorable postprandial metabolic profiles, including lower glycemic excursions and enhanced insulin sensitivity, whereas red meat intake tends to stimulate higher postprandial incretin secretion, likely reflecting differences in digestion kinetics and amino acid bioaccessibility. These findings highlight the importance of considering the impact of food systems on planetary health and the need to better understand the effects of muscle foods on postprandial metabolism as a crucial step towards dietary recommendations that considers environmental sustainability and human health.
Nutrition is increasingly recognized as a biologically active regulator of hematopoietic stem cell (HSC) function and transplant recovery. This review summarizes recent advances linking nutrient availability, metabolic signaling, and the gut-marrow axis to HSC maintenance and hematopoietic stem cell transplantation (HSCT) outcomes. Recent work supports a model in which nutrient sensing, glucose, amino acid and lipid metabolism, mitochondrial redox control, and microbiome-derived metabolites collectively shape HSC quiescence, regenerative capacity, immune recovery, and susceptibility to transplant-related complications. Dietary states such as caloric restriction, fasting, obesity, and high-fat diet exposure alter HSC behavior through metabolic, inflammatory, and niche-mediated pathways. In HSCT, nutritional status before and after transplantation appears to interact with mucosal injury, microbial disruption, graft-versus-host disease (GVHD), infection, and overall outcomes, although causal evidence remains limited. Nutrition should be viewed as more than a background component of supportive care in hematology. A better mechanistic understanding of how diet and metabolism influence HSC biology may help define biomarker-informed and clinically actionable nutritional strategies to improve transplant recovery.
Neonatal nutrition research is pivotal for optimizing long-term health outcomes in high-risk infants, particularly preterm and critically ill neonates, where the foundational "first 1000 days" concept increasingly links early nutritional interventions to lifelong neurodevelopmental, metabolic, and socio-economic trajectories. Despite substantial advances, translating this evolving pre-clinical knowledge base into consistent clinical improvements remains slow. This review synthesizes persistent barriers hindering progress in the field, including inconsistent definitions and reporting standards for nutritional intake and growth metrics, inadequate electronic health record infrastructure for automated nutrient calculations across parenteral and enteral sources, restrictive regulatory and consent frameworks that limit equitable enrollment in high-risk populations, and mounting institutional pressures that erode the physician-scientist pipeline. Natural variability in human milk further complicates precise nutritional delivery, where nutrient delivery scales predictably with caloric density, yet routine direct measurement remains underutilized. To accelerate meaningful advancements, the field requires standardized reporting guidelines, enhanced decision-support tools, innovative trial designs, and strengthened career support for physician-scientists. Addressing these interconnected barriers through collaboration, technological integration, and multi-level policy reform holds the potential to shift neonatal nutrition science from incremental gains to rapid improvements in infant survival, growth, and lifelong health.
Phenylketonuria and type 1 diabetes are lifelong metabolic disorders requiring complex and potentially conflicting nutritional strategies. Their coexistence is rare, yet management may become particularly challenging during transition from pediatric to adult care. We describe the case of a young adult with phenylketonuria who developed type 1 diabetes. A 27-year-old man with longstanding phenylketonuria was referred to an adult metabolic-diabetes center after the diagnosis of type 1 diabetes. Clinical, biochemical, nutritional, and continuous glucose monitoring data were reviewed. The intervention included structured therapeutic education, transition from fixed insulin doses to a dynamic regimen based on carbohydrate counting, and revision of medical nutrition therapy using phenylketonuria-adapted low-protein foods and sugar-free phenylalanine-free amino acid supplements. At diagnosis, HbA1c was 11.5%, with markedly reduced C-peptide levels and high titer anti-GAD antibodies. Initial diabetes management was associated with poor adherence to the phenylketonuria diet, increased intake of conventional protein sources, and elevated phenylalanine levels. After individualized insulin titration and nutritional intervention, HbA1c improved from 11.5% to 7.8%, phenylalanine levels decreased from 842 to 705 μmol/L, insulin requirement declined from 0.55 to 0.3 IU/kg/day, and continuous glucose monitoring showed improved glycemic control without increased hypoglycemia. The Glycemia Risk Index improved from high-risk Zone E to low-intermediate-risk Zone B. This case highlights the need for personalized multidisciplinary care integrating continuous glucose monitoring, carbohydrate counting, and phenylketonuria specific nutrition to optimize both metabolic conditions.
Heat-moisture-treated cassava roots (HMC) offer a promising nutritional strategy to enhance energy supply and nutrient utilization in fattening goats, primarily by modifying the starch structure to increase the resistant starch content. However, a comprehensive evaluation of its effects on performance, metabolism, and meat quality remains insufficiently characterized. In this study, we aimed to evaluate the effect of HMC inclusion in goat diets on growth, apparent nutrient digestibility, ruminal ecology, blood biochemistry, carcass yield, and meat quality. Twenty-four male crossbred Anglo-Nubian goats were randomly divided into four groups and fed diets containing 0, 100, 200, or 300 g/kg dry matter HMC for 60 days. All treatments were isonitrogenous and included ad libitum access to Napier grass. Dietary inclusion of 200 g/kg HMC increased the average daily gain and improved the feed-to-gain ratio without affecting total dry matter intake. The apparent nutrient digestibility was not significantly altered (p > 0.05) by the inclusion levels of HMC. Similarly, the ruminal pH remained stable across treatments. Blood glucose concentration declined with 200-300 g/kg HMC inclusion, whereas other biochemical indicators were unaltered. Although the proportion of lean meat was reduced, carcass dressing percentage improved with dietary 300 g/kg HMC. No differences were observed in chemical composition, color, shear force, or pH of meat among the groups. Moderate dietary inclusion of HMC, particularly 200 g/kg DM, enhanced growth and carcass yield in fattening goats without compromising meat quality. However, excessive use may reduce apparent protein digestibility and lean meat yield. Thus, HMC inclusion may serve as an effective nutritional strategy to optimize productivity in goat production systems. Future studies should investigate the applicability of these findings in sheep and other large ruminant species.
This study aims to investigate the association between niacin intake, paediatric obesity and metabolic dysfunction-associated steatotic liver disease in a diverse, large-scale population in the United States. This cross-sectional study used data from the National Health and Nutrition Examination Survey (NHANES) 2017-2020, including participants aged 12-19 years. Dietary niacin intake was assessed using two 24-h dietary recalls, with intake calculated as the average of both recalls. Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) was defined as hepatic steatosis plus at least one metabolic risk factor, including obesity, glucose intolerance, dyslipidemia, hypertriglyceridemia, or hypertension. Hepatic steatosis was identified using hepatic elastography (CAP ≥ 248 dB/m) or self-reported diagnosis. Participants lacking niacin or anthropometric data were excluded. Niacin intake was significantly lower in individuals with MASLD compared to those without (22 mg vs. 24 mg, p = 0.023). After adjusting for age, sex and race/ethnicity, individuals in the highest quartile of niacin intake (Q4) had significantly lower odds of MASLD (OR 0.55, 95% CI: 0.35-0.86) compared to those in the lowest quartile (Q1). Hispanic ethnicity remained an independent risk factor (OR 2.35, p < 0.001). Adolescents with MASLD had significantly higher BMI measures, diastolic blood pressure, liver enzymes and glucose metabolism markers (all p < 0.001). Lipid profiles were also reflective of dyslipidemia, with elevated triglycerides and LDL, and reduced HDL levels (all p < 0.001). Adolescents with MASLD demonstrated distinct demographic, metabolic and biochemical profiles, particularly higher rates among Hispanic youth and an association with lower niacin intake.
The use of life-support therapies like extracorporeal membrane oxygenation (ECMO), mechanical circulatory systems (MCS), and continuous renal replacement therapy (CRRT) creates a complex and dynamic metabolic environment that profoundly challenges nutritional management for these critically ill patients. Current existing guideline recommendations are largely based on expert opinions and observational data. No specific guidelines exist for this population. This mini-review synthesizes the current, limited evidence on the pathophysiological and metabolic alterations induced by ECMO, MCS, and CRRT and provides pragmatic recommendations for nutritional assessment and delivery. The key challenges include dramatic nutrient fluxes in the case of CRRT, a possible hypermetabolic state exacerbated by ECMO, fluid overload constraints, and drug-nutrient interactions. Practical strategies are proposed for calorie-protein targeting, micronutrient repletion, and monitoring, emphasizing a 'start low, advance carefully' approach within a multidisciplinary framework.
Enteric methane emissions from ruminants contribute significantly to agricultural greenhouse gases. Plant-derived phytochemicals such as grape seed proanthocyanidins (GSP) are promising natural antimethanogenic feed additives, yet their modes of action remain incompletely understood. This study aimed to comprehensively elucidate the microbiological and functional mechanisms underlying phytochemical-induced methane mitigation using integrative meta-omics. Both in vivo and in vitro experiments demonstrated that GSP supplementation significantly reduced methane emissions; in lactating dairy cows, GSP decreased methane emission intensity by 16.5% (g/kg energy-corrected milk). Metagenomic and metatranscriptomic analyses revealed a reprogramming of microbial communities, with decreased abundance and transcriptional activity of methanogenic archaea (e.g., Methanobrevibacter) and enhanced activity of alternative hydrogenotrophic bacteria (Selenomonas, Veillonella, Sharpea). Functionally, GSP elevated expression of genes involved in reductive acetogenesis (e.g., acsB), nitrate ammonification (narG, nrfA), and sulfate reduction (dsrA), thereby redirecting hydrogen flux away from methanogenesis. These shifts were accompanied by increased microbial carbohydrate metabolism and antioxidative responses. Our findings provide the first meta-omics-based mechanistic framework for understanding methanogenesis suppression by phytochemicals in ruminants. GSP modulates microbial composition and function to reroute reductant flows and suppress archaeal methanogenesis through enhanced bacterial electron sinks. This work highlights the potential of polyphenols to modulate the rumen microbiome for sustainable methane mitigation, supporting the development of next-generation feed additives.
Alcohol consumption is a cause of breast cancer (BC), yet the association between changes in alcohol consumption during adulthood and the risk of BC has been examined little. This study aimed to investigate the association between midlife changes in alcohol consumption and the risk of BC. Within the European Prospective Investigation into Cancer and Nutrition cohort including 123,679 women, changes in alcohol intake were obtained by comparing middle-aged participants' alcohol intake assessed at recruitment and during follow-up, 9.8 years (median) later. Missing information about follow-up alcohol intake and covariates was multiple imputed. In the primary analysis, changes in alcohol consumption were investigated continuously as a change in alcohol intake of 10 g/day, calculated by subtracting the baseline intake (g/day) from the follow-up intake (g/day) and divided by 10 in relation to the risk of subsequent postmenopausal BC, overall, and by hormonal receptor status: estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2). In a secondary analysis, changes in alcohol intake were categorized in nine combinations of three intake groups at baseline and follow-up (≤1 g/day, >1-8 g/day, and >8 g/day)., Multivariable Cox proportional hazards regression models were used to estimate hazard ratios (HRs) with 95% confidence intervals (CIs). During a median follow-up time of 4.0 years after the follow-up assessment, 2,173 cases of postmenopausal BC were diagnosed. No associations were observed between alcohol changes and BC risk (HR: 0.97, 95% CI 0.93, 1.01) per 10 g/day nor with ER-/PR-, ER+/PR, ER+/PR+, HER2-, or HER2+ specific BC. Changes in alcohol consumption during midlife were not associated with the risk of postmenopausal BC, either overall or by hormonal receptor status.
Folic acid (vitamin B9) plays a vital role in DNA synthesis, repair, and methylation, supporting both normal cellular functions and the proliferation of cancer cells. This review aims to explore the complex interplay between folic acid metabolism, antifolate chemotherapy (particularly methotrexate), and chemotherapy-induced malabsorption, with an emphasis on the need for nutritional interventions. A comprehensive literature review was conducted using databases such as PubMed, Scopus, and Google Scholar to identify studies addressing folic acid deficiency, chemotherapy-related malabsorption, methotrexate toxicity, and nutritional support strategies in cancer patients. Evidence indicates that methotrexate-induced inhibition of dihydrofolate reductase disrupts folate pathways, contributing to folic acid deficiency and malabsorption syndromes. This can lead to clinical complications such as anaemia, mucositis, immune suppression, and reduced treatment tolerance. Nutritional deficiencies further exacerbate drug toxicity and impair patient outcomes. While folic acid supplementation has shown benefit in reducing toxicity, its dosing must be carefully managed to avoid interference with chemotherapeutic efficacy. Folic acid deficiency and malabsorption are significant concerns in cancer therapy involving antifolate drugs. Targeted nutritional strategies, including judicious folic acid supplementation, are essential to improving patient outcomes and minimizing treatment-associated complications. Future clinical approaches should integrate personalized nutritional support alongside chemotherapy regimens.
With the growing demand for enhanced eating and the nutritional quality of rice, improving grain quality has become a central objective in modern breeding.1 However, translating reported quality-related loci, particularly favorable alleles from wild rice, into practical breeding programs remains challenging.2 This difficulty stems from the insufficient haplotype resolution in elite hybrid parental backgrounds and the absence of trackable, modular resources for effectively deploying introgressed segments. Here, we report the first telomere-to-telomere (T2T) gap-free genome assembly of high-quality Oryza sativa ssp. indica variety Youzhan 8 (Y8) with a size of 395.90 Mb and further reveal its abundant structural variation and the unique integration of Oryza sativa ssp. japonica haplotypes. Using a set of chromosome segment substitution lines (CSSLs) developed from a cross between Y8 and wild rice (Oryza rufipogon) and quantitative trait loci (QTL) mapping within this population, we identified a major locus for grain quality. We prioritized LOC_Os08g02094, a gene encoding a GDSL-like lipase involved in lipid metabolism, which supports its role as a regulator of both grain appearance and lipid content. Furthermore, a modular analysis of introgressed wild-rice segments indicated that a specific segment on chromosome 8, spanning the OsSSIIIa gene (bbbab), is associated with the relatively high taste value and a favorable grain morphology. Overall, our study delivers a foundational genomic resource and a clear molecular roadmap to support the design and breeding of rice varieties with improved agronomic performance and nutritional quality.
Background: Gastric cancer (GC) is characterized by late-stage diagnosis and a lack of reliable non-invasive biomarkers. This study aims to investigate the plasma bile acid (BA) profile to enhance the understanding of GC metabolism and identify potential diagnostic and prognostic tools. Methods: In a case-control design, 62 GC patients (stages I III) and 70 matched controls were recruited. Using liquid chromatography-tandem mass spectrometry (LC-MS/MS), the concentrations of 48 metabolites in plasma were measured. Statistical analysis included univariate tests, principal component analysis, and linear discriminant analysis (LDA). Results: GC patients showed a significantly lower CA/CDCA ratio and alterations in secondary and conjugated bile acids, including TLCA, GLCA, TDCA, GDCA, and GUDCA, suggesting involvement of the gut liver microbiome axis. The ability to distinguish between groups was moderate (AUC = 0.731). Furthermore, BA levels were negatively correlated with tumor stage, tumor size, and systemic inflammatory markers (CRP, mGPS), while they were positively correlated with nutritional and hematological markers such as albumin and hemoglobin. Conclusions: Gastric cancer is associated with a distinct circulating BA profile that reflects not only tumor-related metabolic remodeling, but also systemic inflammation, nutritional status, and disease burden. The reduced CA/CDCA ratio and alterations in secondary and conjugated bile acids support the involvement of the gut-liver-microbiome axis in GC biology. Although BA profiling alone showed moderate diagnostic performance, its integration with conventional tumor markers, inflammatory indices, and clinico-pathological parameters may improve multimodal biomarker panels for noninvasive patient stratification, disease assessment, and future prognostic evaluation.
Heart failure (HF) remains a leading cause of morbidity and mortality worldwide. The HbA1c/HDL-C ratio, a novel composite biomarker reflecting glycemic control and lipid metabolism, may be associated with HF risk, but its specific relationship remains underexplored. This study aimed to investigate the association between the HbA1c/HDL-C ratio and HF. We utilized samples from two sources: 1,360 inpatients from a cardiology department in 2020 and 101,316 participants from the National Health and Nutrition Examination Survey (NHANES) 1999-2018. Multivariate logistic regression, subgroup analyses, restricted cubic spline (RCS) regression, and receiver-operating characteristic (ROC) curve analysis were employed to examine the relationship. In an analysis of the NHANES sample including 48,922 participants, 1,598 individuals were identified as having HF, corresponding to a prevalence of 3.27%. In a separate clinical sample of 584 participants, 132 had HF, yielding an overall prevalence of 22.60%. After full adjustment, the HbA1c/HDL-C ratio demonstrated a consistent positive association with HF risk in both the NHANES sample (OR =1.07, 95% CI: 1.01-1.14; P = 0.033) and the clinical sample (OR = 1.15, 95% CI: 1.01-1.30; P = 0.029). Furthermore, a nonlinear relationship between the HbA1c/HDL-C ratio and HF risk was observed in both populations, with an inflection point identified at 6.21. Below this threshold (HbA1c/HDL-C < 6.21), the adjusted OR was 1.22 (95% CI: 1.09-1.37; P = 0.001) in the NHANES sample and 1.65 (95% CI: 1.20-2.28; P = 0.002) in the clinical sample. Above the inflection point (HbA1c/HDL-C ≥ 6.21), the association attenuated and became statistically nonsignificant. The ROC curve analysis also confirmed that the HbA1c/HDL-C ratio combination had more robust predictive power for heart failure than HbA1c and HDL-C alone (P < 0.05). This study found a nonlinear positive association between the HbA1c/HDL-C ratio and the risk of HF, identifying key threshold values.
Long-duration spaceflight poses risks to musculoskeletal health, yet articular cartilage remains understudied. This review explores how microgravity and radiation compromise its homeostasis. Mechanical unloading suppresses chondrocyte metabolism and disrupts extracellular matrix equilibrium. Concurrently, radiation, oxidative stress, and immune activation induce DNA damage, mitochondrial dysfunction, and senescence, exacerbating matrix degradation. We assess physical, nutritional, and pharmacological countermeasures, highlighting the need for integrated strategies protecting joints during space exploration.
Isovaleric acid (IVA) has been shown to benefit gut health, but its effects on broiler meat quality remain unclear. A total of 864 broilers were assigned to control or 0.05%, 0.1%, or 0.2% IVA groups to evaluate the effects of IVA supplementation on performance, blood biochemistry, immunity, gut microbiota, metabolome, and meat quality. IVA increased average daily gain and, at some doses, feed intake and villus height, while reducing feed conversion ratio. It also lowered serum blood urea nitrogen at 21 and 42 days and modulated inflammatory and immune indices. IVA improved meat quality by increasing breast and leg muscle protein content at 42 days, reducing drip loss and shear force, and improving color parameters. Microbiome analysis showed that IVA reduced Ace index and altered bacterial and fungal β-diversity at 21 days, whereas at 42 days it increased bacterial Shannon index and shifted community composition, while fungal α-diversity remained largely unchanged. Metabolomics revealed marked changes in lipid and amino acid metabolism. Integrative analysis identified Collinsella, norank_f__Ruminococcaceae, and unclassified_f__Oxalobacteraceae as key taxa associated with beneficial muscle metabolites. These findings highlight a gut microbiota-metabolome-muscle axis contributing to improved broiler meat quality and inform nutritional interventions in poultry production.
Grazing ruminants consuming CP- and phosphorus (P)-deficient pastures experience reduced voluntary feed intake and liveweight gain, indicating systemic metabolic changes. Because mitochondrial abundance reflects oxidative capacity and metabolic investment, altered mitochondrial content may provide insight into how sheep adapt to nutrient-deficiency-induced reduction of feed intake. This study aimed to determine whether reduced intake caused by CP and P deficiency, or by restriction of an otherwise adequate diet, alters tissue mitochondrial content in young sheep. Forty Merino wethers (7 months old, 23.7 ± 1.4 kg liveweight) underwent a 63-day feeding trial where they were fed one of five nutritional treatments (n = 8/treatment). Four treatment diets were fed ad libitum, with combinations of either high or low CP (110 and 55 g/kg DM) with high or low P (2.5 and 0.7 g/kg DM). Another treatment (Restricted) restricted intake of the High CP, High P diet to model hunger. Mitochondrial DNA copy number (mtDNA-CN) was quantified from rumen, duodenum, liver, heart, M. semitendinosus and M. soleus samples using a newly developed quantitative PCR test for sheep, as a high-throughput proxy for tissue mitochondrial content. This assay was validated against transmission electron microscopy (TEM), and mtDNA-CN correlated with TEM-derived mitochondrial content (ρ = 0.67, P < 0.01). Duodenum and rumen mtDNA-CN were also positively correlated (ρ = 0.41, P = 0.01), indicating functional metabolic relationships among these tissues. Liver mtDNA-CN was significantly higher in the wethers fed the High CP, High P diet than those fed nutrient-deficient and restricted diets (P < 0.02), with as much as a two-fold difference between this group and those fed the dual-deficient diet (High CP, High P v. Low CP, Low P). Wethers fed the High CP, High P diet also had 45% greater mitochondrial content in the M. semitendinosus compared to wethers fed the High CP, Low P and Low CP, High P diets (P < 0.03). Across individuals, liver mtDNA-CN was positively associated with liveweight gain after accounting for DM intake and diet (β = 34.7 ± 12.2 g/day, P < 0.01; ΔR2 = 0.017). These results show that hepatic mitochondrial content declines under both feed restriction and nutrient-deficiency-induced intake reduction, and that higher liver mitochondrial content is positively associated with growth. Together, the findings support the liver as a metabolically responsive tissue under nutritional constraint and suggest that reduced mitochondrial abundance may form part of the adaptive response to chronic energy deficit.
The study aimed to develop a high-protein plant-based beverage from cashew nut byproducts and evaluate its physicochemical, nutritional, sensory, and physiological properties. Three formulations were prepared using byproducts (partially defatted cashew nut cake and cashew nut protein concentrate) and submitted for sensory analysis. The formulation with the highest sensory acceptance was selected for evaluation. To assess satiety, three formulations, being isocaloric and nutritionally equivalent, were evaluated in an acute clinical trial: a test beverage made from cashew nut byproducts and control beverages from whey protein and cow's milk. Satiety was assessed using a 10-cm Visual Analog Scale (VAS) and subsequent food intake by dietary records. Gastrointestinal symptom questionnaires were applied to determine adverse effects. As a result, the vanilla-flavored beverage was most accepted by 81 panelists. It contained 35.39 g of protein per 400 mL and 62.68 mg/L of fructose. The beverage presented an amino acid profile including both essential and nonessential amino acids. Regarding physicochemical properties, oleic acid was the predominant fatty acid in the beverage (44%). The beverage also showed a DPPH value of 66.07 µmol TE/g, TEAC (ABTS) of 0.75 µmol TE/g, FRAP of 2.17 µmol TE/g, total phenolic content of 0.05 µmol GAE/g, total soluble solids of 1.336 °Brix, titratable acidity of 0.1013% malic acid, and a TSS/TA ratio of 13.72. In a randomized, blinded, crossover acute clinical trial with 27 healthy individuals, no significant differences were observed in satiety perception, subsequent energy intake, or gastrointestinal symptoms among the three beverages tested. The findings indicate that beverages from cashew nut byproducts are viable and sustainable alternatives.
Differences in body composition during childhood can influence long-term health, with notable links to cardiometabolic disorders in later life. While genetic associations with body composition traits are well-studied, less is known about the role of epigenetic mechanisms, particularly in low- and middle-income countries where the burden of cardiometabolic disease is high. We investigated links between DNA methylation and three compartments of body composition: fat mass, lean mass, and bone measures using data from children enrolled in the Epigenetic Mechanisms linking Pre-conceptional nutrition and Health Assessed in India and Sub-Saharan Africa (EMPHASIS) study. We conducted an epigenome-wide association study of 11 body composition traits assessed through dual-energy X-ray absorptiometry in children from India (mean [range] age = 5.8 [5-7] years; n = 686) and The Gambia (age = 9.0 [7-9] years; n = 284), with blood DNA methylation measured at ~ 800,000 CpGs sites on the Illumina EPIC array. Cohort-specific analysis identified 8 unique differentially methylated CpGs associated with traits across all three body composition compartments (p < 3.6 × 10-8), with none overlapping both cohorts. Cross-cohort meta-analysis revealed four CpGs associated with lean mass and bone area mapping to SOCS3 and ZBTB16. Region-level analyses identified 29 differentially methylated regions (DMRs) in India and 18 in The Gambia. 29 DMRs were identified in the meta-analysis, 25 of which were not detected in either cohort individually. Many DMRs were associated with more than one body composition trait. We report novel DNA methylation signatures associated with body composition traits in children from two low- and middle-income countries. Identified loci map to genes linked to inflammatory signalling, energy metabolism and cellular stress response pathways, highlighting a potential role for epigenetic mechanisms in shaping early-life body composition.
We examined whether the association between food insecurity and metabolic dysfunction-associated steatotic liver disease (MASLD) differs across different racial/ethnic groups and sex using data from the 2017-March 2020 National Health and Nutrition Examination Survey (NHANES). A total of 5076 participants aged ≥ 20 years who completed transient elastography examination for evaluation of MASLD were included. Logistic regression, odds ratios (ORs) and 95% confidence intervals (CIs) were used to estimate the association of food insecurity with MASLD. Adult food insecurity was associated with increased odds of MASLD (low/very low vs. full security: OR = 1.41, 95% CI 1.12-1.77). Although there was no significant interaction between food insecurity and race/ethnicity (p interaction = 0.23), the positive association between food insecurity and MASLD was limited among non-Hispanic Whites. Food insecurity was associated with higher odds of MASLD in women but not men, with an interaction between food insecurity and sex (p interaction = 0.049). Furthermore, mediation analyses suggested that added sugar intake and intake of whole fruits and non-potato vegetables partially mediated the association of food insecurity with MASLD. The partial mediating effects of these foods were observed only among non-Hispanic Whites but not observed in other racial/ethnic groups or across sex. Our results suggest that the positive association between food insecurity and MASLD may be dependent on race/ethnicity and sex. Increased consumption of whole fruits vegetables intake and reduced intake of added sugar may partially reduce the impact of food insecurity on MASLD development.
Phyllostachys pubescens (Moso bamboo) is a significant perennial crop species that provides valuable nutritional and industrial uses, as well as carbon sequestration. Due to its remarkable growth rate, bamboo offers an ideal system for studying organogenesis, particularly in monocots. Somatic embryogenesis (SE) serves as a useful technique for crop breeding and improvement. SE in moso bamboo (Phyllostachys pubescens) remains challenging due to limited knowledge of its transcriptional and metabolomic reprogramming. To address this, we optimized callus initiation (MS + 18.1 µM 2,4-D + 8.5 µM picloram), callus proliferation (MS + 12.5 µM 2,4-D + 8.5 µM picloram), and somatic embryogenesis (MS + 1.1 µM 2,4-D + 3.3 µM metatopolin), using nodal segments as explants. UHPLC-Q-TOF-MS-based metabolite profiling revealed distinct biochemical trajectories across developmental stages of P. pubescens. NEC (non-embryogenic callus) was enriched in flavonoids, alkaloids, and saponins, while in-vitro shoots showed flavonoids and glycosides enrichment, and ex-vitro shoots showed high accumulation of glycosides and terpenoids. In contrast, EC (embryogenic callus) showed elevated levels of fatty acid derivatives (α-ESA, 26-Methyl Nigranoate), phytoalexins (Wyerone acid), sesquiterpene (Alpha-santalal, Beta-guaiene), flavonoid glycosides, and plant hormones (Cis-Zeatin, Gibberellin A45), indicating a metabolically active state supporting somatic embryogenesis. Similarly, genes and transcription factors controlling cell differentiation and embryogenesis were upregulated during SE. This study provides a comprehensive resource to facilitate future genomic and genetic investigations aimed at deciphering the molecular basis of organogenesis and advancing research on somatic embryogenesis in bamboo.