Nutrition & Metabolism最新文献

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.

Background: Parasitic infections possess comparable risk factors to obesity. In addition, obesity impairs innate and adaptive immunity subsequently increasing vulnerability to infectious diseases.

Aim: The study investigated the leptin/leptin receptors, obesity-parasites mutual relationship and the effect of parasitic infections on immune metabolism, microbiota, and tumorigenesis in the context of obesity.

Methodology: To implement the current review, articles were gathered using the Egyptian Knowledge Bank (EKB), Web of Science, PubMed, and Google Scholar.

Conclusion: Leptin enhances anti-parasitic immunity. Obesity favors intestinal colonization of Blastocystis sp., Dientamoeba fragilis, Entamoeba coli, and Giardia intestinalis. Adipocytes act as a niche and a food source for Trypanosoma cruzi, Trypanosoma brucei, and Plasmodium. In addition, Toxoplasma gondii relies on the circulatory cholesterol to thrive. Obesity provokes low-grade chronic inflammation and metabolic syndrome. Yet, Nippostrongylus brasiliensis and Fasciola hepatica attempted to alleviate inflammation and metabolic syndrome. Hookworm improves insulin resistance. However, parasites such as Schistosoma mansoni, Trichuris suis, Taenia pisiformis, Entamoeba histolytica, Trypanosoma cruzi, and Trypanosoma brucei, and Toxoplasma aggravated metabolic immune metabolic syndrome. Obesity hampered immunity against Leishmania sp.. and Plasmodium sp. is diabetogenic. Giardia infection and Heligmosoides polygyrus infections induce dysbiosis in obesity. Obesity and parasites like Trichomonas vaginalis, S. haematobium, S. mansoni, Clonorchis sinensis, Opishorchis viverrini showed similar cancer types. Yet, Toxoplasma gondii and Echinococcus granulosus have anti-tumorigenic effects. Obesity/high-fat diet hinders Schistosoma mansoni, Trichuris muris, and Entamoeba histolytica infections. Also, Blastocystis sp., Dientamoeba fragilis, Giardia intestinalis, Trichinella spiralis, and Schistosoma appeared to have ameliorative effects in obesity.

Background: Untargeted metabolomic analysis provides novel insights into the relationship between sodium intake and cardiometabolic risk. This study examined cross-sectional associations between estimated sodium intake and plasma metabolite profiles in a large Swedish cohort.

Methods: This cross-sectional analysis was conducted in the in the SCAPIS cohort (mean age 50-64 years, n = 8,957). Sodium intake was estimated using the Kawasaki formula (est24hNa) from urine samples. Plasma metabolites were measured using ultrahigh performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) (Metabolon Inc^®), identifying 713 metabolites grouped into eight biochemical classes (CC). Principal component analysis (PCA) was conducted for each CC, and the first principal component (PC1) was used as the response variable, with est24hNa, age, sex, and cardiovascular risk factors as predictors in restricted cubic spline models. ANOVA and pathway enrichment analyses were performed to explore associations.

Results: Est24hNa was significantly associated with the lipid and energy CC. Lower est24hNa was linked to higher concentrations of free fatty acids and citric acid cycle intermediates, suggesting enhanced beta-oxidation. Bonferroni-adjusted analyses revealed 231 metabolites significantly associated with est24hNa, with 2 S,3R-dihydroxybutyrate (β = -0.13, p = 2.28 × 10^- 37) showing the strongest association. Lipid subgroups including phosphatidylcholines, lysophospholipids, bile acids, and plasmalogens were positively associated with est24hNa. Pathway enrichment suggested links to branched-chain amino acid metabolism and biosynthesis of unsaturated fatty acids.

Conclusions: Lower salt intake was associated with a metabolic profile indicative of increased beta-oxidation, while higher salt intake was linked to lipid species previously implicated in atherosclerosis. These findings highlight potential metabolic pathways through which salt intake may influence cardiovascular health and merit further evaluation in longitudinal studies.

Background: Frailty syndrome poses significant challenges in older populations. Understanding the genetic and biochemical factors associated with frailty is essential for effective management strategies.

Methods: In this study, Thai older adults (≥ 60 years, n = 170) were assessed for physical parameters, levels of B vitamins, creatinine, and homocysteine. The polymorphisms of methylenetetrahydrofolate reductase (MTHFR) (677 C > T) and Transcobalamin II (TCN2) 776G > C were identified. Global DNA methylation (global DNAm) was assessed using a colorimetric assay.

Results: Participants were categorised into robust (n = 61), pre-frail (n = 62), and frail (n = 47) groups by Fried criteria and Kihon checklist. The physical parameters, including chair stand, functional reach, gait speed, and handgrip strength, showed highly significant differences among the groups (p < 0.01). Significant differences in folate and vitamin B₆ concentrations were observed between MTHFR and TCN2 genotypes, respectively. In addition, global DNAm levels were significantly lower in pre-frail individuals, particularly among those carrying the MTHFR C677T genotype, compared to both robust and frail groups. Notably, lower global DNAm was associated with a higher likelihood of being classified as pre-frail rather than frail, and a lower likelihood of being pre-frail compared to robust individuals. Moreover, correlation analyses revealed significant associations among physical parameters, clinical characteristics, and global DNAm.

Conclusions: This study demonstrated the interplay between genetic variants, micronutrient status, and epigenetic modifications in the context of frailty among older adults. These findings highlight the potential of epigenetic and metabolic markers in identifying early frailty, though longitudinal and mechanistic studies are needed to further clarify causal pathways.

Trial registration: This study was duly registered with the Thai Clinical Trial under the identifier TCTR20240626002 (date of registration: 21/06/2024).

Background: The coexistence of sarcopenia and obesity has been established as a pivotal factor driving the pathological progression of metabolic dysfunction-associated steatotic liver disease (MASLD). This study systematically evaluates the prevalence and risk of MASLD in patients with sarcopenic obesity (SO).

Method: A comprehensive literature search was conducted in PubMed, Cochrane Library, EMBASE, Web of Science and SCOPUS up to March 2025. All studies investigating the association between SO and MASLD were included in this meta-analysis. Two independent reviewers performed screening and data extraction. ORs and 95% CIs were calculated using random effect models. Subgroup analysis was used to identify the sources of heterogeneity. Heterogeneity was assessed using Cochran's Q test and quantified via the I² statistic. Quality assessment and publication bias (by Funnel plots and Egger's test) evaluation were also performed.

Results: Thirteen studies involving 35,373 SO patients (from six countries) were included after screening. Odds ratios (ORs) of the included studies were combined by random effect model. The pooled results revealed that 63.4% of SO patients had MASLD. Compared to non-SO individuals, SO was significantly associated with an increased risk of MASLD (OR = 4.45, 95% confidence interval (CI): 2.57-7.72, P < 0.001). Females exhibited a higher MASLD risk than males (OR = 4.22, 95% CI: 2.10-8.50 vs. OR = 7.56, 95% CI: 2.39-23.92). Substantial heterogeneity was observed across pooled results and subgroups. Additionally, SO patients had a 2.34-fold higher risk of MASLD-related fibrosis than non-SO individuals (OR = 2.34, 95% CI: 1.78-3.08, P < 0.001).

Conclusion: SO may be closely associated with a high prevalence of MASLD and accelerated fibrosis progression. These findings highlight SO as a potential high-risk population for MASLD, underscoring the need for targeted screening and intervention strategies. However, more high-quality research with unified definitions and different races is needed.

Background: The association of sugar sweetened beverages (SSBs) and coronary artery disease (CAD) has not been well-established in Asians, where SSBs are the leading ultra-processed food product.

Objective: We aim to examine the association between SSBs and premature CAD (PCAD) in Iranian adults.

Design: Case-control.

Participants: A multi-centric study of Iranians including 2006 PCAD and 1131 healthy individuals as control group.

Main outcome measures: Dietary intakes were assessed using a validated food frequency questionnaire (FFQ). SSBs consist of artificial juice and sugar -sweetened drinks. The PCAD was determined based on the results of angiography and the occlusion percent of vessels.

Statistical analysis: The odds of PCAD across the quartiles of SSBs were assessed by binary logistic regression.

Results: The mean (SD) age of participants and SSB consumption was 51.5 years and 46.9 g/d, respectively. In the fully-adjusted model, compared with participants in the first quartile, those in the fourth quartile had higher risk of PCAD (OR = 1.50, 95% CI: 1.12, 2.00; P trend = 0.044). Consistently, SSB consumption was directly associated with the severity of PCAD. The higher SSB consumption, the greater risk for the severe PCAD (OR Q4 vs. Q1 = 1.34, 95% CI: 1.06, 1.68; P < 0.001).

Conclusion: This study demonstrated that higher consumption of SSB might be associated with higher risk of PCAD. However, more prospective cohort studies are necessary to confirm this association.