Nutrition & Metabolism最新文献

Background: 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).

Methods: 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.

Results: 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).

Conclusions: 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.

Background: 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.

Methods: 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.

Results: 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.

Conclusions: 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.

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.

Background: 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.

Method: 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.

Results: 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.

Conclusions: 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.

Trial registration: This trial was registered at clinicaltrials.gov as NCT02194504.

Background: 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.

Methods: 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.

Results: 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.

Conclusion: 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.

Background: 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.

Methods: 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.

Results: 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.

Conclusions: 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.

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.

Background: Inflammatory Bowel Diseases (IBD) encompass chronic inflammatory conditions such as ulcerative colitis and Crohn's disease. This umbrella meta-analysis investigates the efficacy of probiotic supplementation in reducing relapse, recurrence, and maintaining remission in IBD patients.

Methods: We systematically searched PubMed, Scopus, and Web of Science up to November 2024 for meta-analyses evaluating probiotics in IBD. A random-effects model calculated pooled effect sizes. The methodological quality of included reviews was assessed using AMSTAR 2. Publication bias was evaluated through funnel plots, Egger's and Begg's tests, and corrected by trim-and-fill when appropriate.

Results: Twenty meta-analyses including 46 datasets were analyzed. Probiotics significantly reduced relapse risk compared to placebo (RR = 0.55; 95% CI, 0.22-0.88), but showed no significant effect compared to mesalazine. No consistent benefit was found for remission or recurrence; however, recurrence risk was reduced after correction for publication bias (RR:0.74;95%CI:0.51-0.97, P < 0.05). Subgroup analyses suggested greater benefit with lower probiotic doses (≤ 10¹⁰ Colony-Forming Units/day) and longer supplementation durations (≥ 8 weeks) regarding to relapse rate, although strain-specific effects could not be clarified.

Conclusion: Probiotic supplementation appears effective in reducing relapse compared to placebo, but shows no advantage over mesalazine and demonstrates benefit for recurrence only after adjusting for publication bias. These findings highlight a potential role for probiotics in IBD management, but interpretation should be cautious given the high heterogeneity and substantial overlap among included meta-analyses. Further high-quality, non-overlapping meta-analyses and randomized controlled trials are needed to determine the most effective probiotic regimens.

Background: The role of nutritional status in predicting prognosis in patients with sarcopenia has not been fully elucidated. This investigation sought to evaluate the link between prognostic nutritional index (PNI) and sarcopenia, as well as its influence on overall and cardiovascular death rates in adults diagnosed with sarcopenia.

Methods: This retrospective observational study utilized data from individuals aged 18 years and older extracted from the National Health and Nutrition Examination Survey (NHANES) during 1999-2004 and 2011-2018. The PNI calculation incorporated initial serum albumin measurements and complete lymphocyte numbers. To investigate the link between PNI and sarcopenia, researchers employed multiple analytical approaches, including multivariate logistic regression, stratified group evaluation, restricted cubic spline, and threshold and saturation effect analysis. The investigation utilized Cox regression modeling and Kaplan-Meier survival analysis to examine the link between PNI and both overall and cardiovascular-related mortality among subjects with sarcopenia.

Results: Among the 24,661 patients examined, sarcopenia was detected in 2760 individuals (11.19%). Throughout a median monitoring duration of 132.01 months, all-cause mortality claimed 959 (34.75%) subjects with sarcopenia, while cardiovascular-related fatalities accounted for 321 (33.47%) cases. Subjects in the uppermost PNI quartile (Q4) exhibited markedly decreased likelihood of sarcopenia (odds ratio [OR] 0.43, 95% confidence interval [CI] 0.37-0.49) and lower risks of both all-cause and cardiovascular mortality (hazard ratio [HR] 0.64, 95% CI 0.53-0.78; and 0.60, 95% CI 0.43-0.84, respectively) versus those in the lowermost quartile (Q1). These findings were consistent across subgroup analyses, restricted cubic spline, and threshold and saturation effect analysis.

Conclusions: The PNI is an independent predictor of sarcopenia, all-cause mortality, and cardiovascular mortality in U.S. adults. It can be a valuable tool for identifying individuals at elevated risk of unfavorable health outcomes.