Nutrition & Metabolism最新文献

Objective: Metabolic dysfunction-associated steatotic liver disease (MASLD) and subclinical carotid atherosclerosis (SCA) share common roots in systemic inflammation and metabolic dysregulation. Hepatic fibrosis mirrors the intensity of these disturbances; however, its association with SCA in younger adults remains unclear.

Methods: A total of 14 567 MASLD patients were enrolled from the health examination center of Northern Jiangsu People's Hospital. Participant stratification into SCA and non-SCA groups was based on carotid ultrasound findings. Variable selection was performed using Least Absolute Shrinkage and Selection Operator (LASSO) regression. The associations between the selected indicators and SCA risk were subsequently evaluated through multivariate logistic regression, restricted cubic spline (RCS) analysis, subgroup analysis, receiver operating characteristic (ROC) curves, and mediation analysis.

Results: Both LASSO and multivariate logistic regression analyses demonstrated that elevated NAFLD Fibrosis Score (NFS) and Fibrosis-4 (FIB-4) levels were positively correlated with the prevalence of SCA in patients with MASLD (P for trend < 0.001). Mediation analysis indicated that the Red-cell Distribution Width-to-Albumin Ratio (RAR) significantly mediated this association, with the mediated proportion ranging from 28.6% to 44.6% (P < 0·05). Subgroup analysis identified a significant interaction between age and the association of both fibrosis scores with SCA (P for interaction < 0.05). Subsequently, RCS analysis demonstrated significant positive non-linear associations between NFS/FIB-4 and SCA risk specifically in patients aged under 50 years (P for non-linear < 0.001). The area under the ROC curve (AUC) indicated that both scores had fair predictive value for SCA in this younger subgroup.

Conclusion: This study confirms that elevated NFS and FIB-4 levels are significantly associated with an increased risk of SCA in MASLD patients, demonstrating a distinct non-linear relationship and fair predictive value, particularly in individuals under 50 years of age.

Background: Overweight and obesity are widespread in Mexico, often linked to dyslipidemia and higher cardiovascular risk. The search for safe and effective treatments has promoted interest in natural supplements such as Ashwagandha (Withania somnifera), recognized for its adaptogenic and potential lipid-lowering properties.

Objective: To assess the impact of Ashwagandha supplementation on serum lipid profiles and anthropometric parameters in Mexican adults with overweight and obesity.

Methods: A double-blind, randomized, placebo-controlled pilot clinical trial was carried out with 43 adults (n = 17 in the control group and n = 21 in the intervention group) over 40 days. Participants followed a monitored diet and received one daily capsule containing 500 mg of Ashwagandha or a placebo, in addition to a guided unrestricted dietary plan. Anthropometric and biochemical measurements were taken at baseline and after the intervention. In silico analysis was also performed to examine the binding affinity of Ashwagandha bioactive compounds to key proteins involved in lipid metabolism.

Results: Ashwagandha supplementation did not produce statistically significant changes in body weight, body mass index (BMI), or waist circumference (WC). However, significant reductions were observed in triglyceride and VLDL-c levels (p = 0.0082 and p = 0.0321, respectively). In silico results supported these findings, showing favorable interactions between compounds such as withanolide A and lipid metabolism targets, including AMPK, CETP, and LPL.

Conclusions: Ashwagandha supplementation improved serum lipid profiles in adults with overweight and obesity, suggesting potential lipid-lowering effects when combined with a prescribed dietary plan. Also, it was possible to elucidate some metabolic pathways in which Ashwagandha composition has an influence on producing the reported effects. Further long-term studies with controlled dietary intake are needed to confirm these findings and clarify the underlying molecular mechanisms.

Aging induces structural and functional alterations in the kidneys, including changes in renal morphology and progressive decline in renal function. During aging, the gut microbiota undergoes profound shifts in composition and activity, transitioning from predominantly commensal to more pathogenic communities. Renal dysfunction further exacerbates this process by reducing toxin clearance and promoting the accumulation of uremic metabolites, which disrupt gut microbial balance. In turn, gut dysbiosis impairs kidney function, creating a self-perpetuating cycle of microbial imbalance and renal damage. Hence, breaking this vicious cycle of dysbiosis and kidney damage is important. This review sheds light on the bidirectional relationship between gut microbiota and kidney aging. It also highlights the potential of microbiota-targeted interventions to restore microbial balance and delay the onset of age-related issues.

Introduction: Acne vulgaris is chronic skin condition with considerable physical, psychological, social, and economic impacts. Adherence to Western diets with a high glycemic index and dairy content has been linked to acne. However, the associations between acne and the Mediterranean diet (MD), a non-Western diet, have not been reviewed. This review aimed to examine the associations between adherence to the MD and the development and severity of acne vulgaris.

Materials and methods: PubMed, Embase, and Web of Science databases were searched for studies examining the association between adherence to the MD and acne vulgaris. Data were extracted by two independent reviewers. The risk of bias was assessed using the Newcastle‒Ottawa Scale, and the quality of evidence was assessed using the GRADE tool. The Meta-analyses were conducted using a random-effects model to pool the odds ratio (OR) and correlation coefficient.

Results: Five case‒control studies were included, with 765 participants, 340 cases, and 425 controls. The meta-analysis found that higher adherence to the MD was not significantly associated with lower odds of acne development (OR 0.32, CI = 0.08-1.28), with high heterogeneity (Q test p = .02, I2 = 75%). The second meta-analysis of correlational studies found a significant negative correlation between adherence to the MD and acne severity (correlation coefficient= -0.29, CI= -0.55 to -0.03), with high heterogeneity (Q test p = .008, I2 = 79%). Higher consumption of vegetables was significantly associated with lower odds of acne development (OR = 0.46, 95% CI, 0.29-0.74). The quality of evidence for the associations with both acne development and severity was low.

Conclusions: This review found that higher adherence to the Mediterranean diet was significantly correlated with less severe acne, while the association with acne development was not significant. Due to the low number of studies, small sample size, and methodological limitations, more well-designed studies are needed to strengthen the evidence base.

Background: Metabolic Syndrome (MetS) involves several cardiovascular risk factors, with hypertension being a critical component that significantly impacts cardiovascular outcomes. As guidelines support blood pressure control in populations with high cardiovascular risk factors, we evaluated BP control in MetS patients.

Methods: We conducted a cross-sectional analysis of probability samples of adults aged ≥ 18 years with MetS from the National Health and Nutrition Examination Survey (NHANES) from 1999 to 2020 to assess changes in BP control. MetS was identified by meeting at least three of the following criteria: (1) waist circumference ≥ 102 cm in men and ≥ 88 cm in women; (2) fasting glucose ≥ 100 mg/dl; (3) BP ≥ 130/85 mmHg; (4) triglycerides ≥ 150 mg/dl; and (5) high-density lipoprotein cholesterol (HDL-C) < 40 mg/dl in men and < 50 mg/dl in women. BP control was defined as systolic BP < 130 mmHg and diastolic BP < 80 mmHg. All analyses accounted for differences between survey years, complex sampling design, and survey weights.

Results: From 1999-2002 to 2015-2020, the prevalence of MetS increased from 19% to 24% (P < 0.001). Among MetS patients, the proportion of those self-reporting hypertension or taking BP medications increased from 65% in 1999-2002 to 72% in 2015-2020 (P = 0.001). Over time, both the use and quantity of antihypertensive medications increased significantly, and according to current guidelines, BP control among MetS patients has improved significantly. Similar trends were observed across subgroups stratified by gender, diabetes status, and CKD status.

Conclusion: BP management in MetS patients showed significant improvement from 1999 to 2020, with increasing control rates despite fluctuations.

Background: This study aimed to explore the causal relationships between 1,400 plasma metabolites and various chronic liver conditions, including liver fibrosis or cirrhosis, liver carcinoma, hepatic failure, and metabolic liver disorders.

Methods: This study used a two-sample Mendelian randomization (MR) method. Forward analysis focused on associations with four liver disease categories, whereas reverse analysis examined links with specific metabolites or ratios. Five MR methods were applied, primarily the inverse variance weighted (IVW) method. The IVW, Egger, and Weighted Median analyses showed p-values < 0.05 with positive directions, suggesting strong positive effects. The IVW analysis alone indicated a potential positive effect with p-value < 0.05. Sensitivity analyses ensured the results' robustness and validity.

Results: In the forward causal analysis, we identified 252 potential causal associations, 13 of which were notably strong. Specifically, six plasma metabolites and metabolic ratios were found to increase the risk of fibrosis/cirrhosis, while the other three were associated with an increased likelihood of liver cancer. Additionally, three were positively correlated with metabolic liver disease risk and one was inversely related to liver failure risk. In contrast, reverse causal analysis revealed that fibrosis/cirrhosis was linked to ten plasma metabolites and metabolic ratios, whereas liver cancer was associated with three plasma metabolites and metabolic ratios.

Conclusion: Our findings underscore the significant association between an elevated glucose-to-mannose ratio and a range of liver conditions, including fibrosis/cirrhosis, metabolic liver disease, and hepatoma, thereby highlighting the crucial role of glucose metabolism in liver disease.

Background: Given the limited understanding of how dietary amino acid intake affects metabolic dysfunction-associated fatty liver disease (MAFLD), we examined the potential relationship between dietary amino acid patterns and the odds of MAFLD in children and adolescents with overweight and obesity.

Methods: This cross-sectional study was conducted on participants aged 6 to 18 years with a WHO body mass index (BMI)-for-age z-score ≥ 1. MAFLD diagnosis followed established consensus definitions. Principal component factor analyses were conducted based on eighteen amino acids. Logistic regression models, adjusted for potential confounders, were used to estimate the odds of MAFLD across amino acid profile score quartiles.

Results: A total of 505 (52.9% boys) with mean ± SD age and BMI-for-age-Z-score of 10.0 ± 2.3 and 2.70 ± 1.01, respectively, were enrolled. Three major amino acid profiles were characterized: (1) higher loads by branched chain, lysine, tyrosine, threonine, methionine, histidine, alanine, and aspartic acid; (2) higher loads of proline, serine, glutamic acid, and phenylalanine; (3) higher loads of tryptophan, arginine, glycine, and cysteine. After adjusting for all potential confounders, participants in the highest quartile of the first amino acid profile tended to be associated with increased odds of MAFLD (OR:2.14; 95%CI:0.97-4.77). There was no significant association for the second and third profiles.

Conclusions: These novel data suggest that the amino acid composition of an individual's diet may modify their odds of MAFLD.

Background: Niemann-Pick C1-like 1 (NPC1L1) mediates cholesterol absorption and plays major roles in cholesterol homeostasis. Our previous study showed that curcumin reduced NPC1L1 expression and cholesterol absorption in Caco-2 cells. This study aimed to investigate whether curcumin could prevent hypercholesterolemia by transcriptionally suppressing intestinal and hepatic NPC1L1 expression via inhibition of sterol regulatory element binding protein-2 (SREBP-2) and hepatocyte nuclear factor 1α (HNF1α) transcriptional activity.

Methods: Male hamsters were fed a high-fat diet (HFD) with or without 0.1% w/w curcumin for 12 weeks. Additionally, Caco-2 cells and HepG2 cells were treated with 6, 12, 25, or 50 µmol/L curcumin for 24 h. The cholesterol absorption was determined with 22-NBD-cholesterol assay, the promoter activity of NPC1L1 and the transcriptional activity of SREBP-2 and HNF1α were determined with luciferase assay, and the gene expression of NPC1L1, SREBP-2, and HNF1α and the nuclear abundance of SREBP-2 and HNF1α were measured by RT-qPCR and Western blotting, respectively.

Results: Compared to HFD-fed hamsters, curcumin supplementation significantly lowered cholesterol levels in the serum (20.2%,) and liver (26.1%), and increased fecal neutral sterol excretion (114.5%). In addition, curcumin significantly reduced the gene expression of NPC1L1, SREBP-2, and HNF1α and the nuclear abundance of SREBP-2 and HNF1α in the small intestine and liver of HFD-fed hamsters. Furthermore, the dual luciferase assay showed that the promoter activity of NPC1L1 and the transcriptional activity of SREBP-2 and HNF1α in Caco-2 and HepG2 cells were dose-dependently inhibited after 24 h curcumin treatment, and maximally inhibited by 50 µmol/L curcumin. Additionally, the gene expression of NPC1L1, SREBP-2, and HNF1α and the nuclear abundance of SREBP-2 and HNF1α in Caco-2 and HepG2 cells were consistently suppressed by curcumin. Curcumin also significantly reduced the cholesterol uptake in both Caco-2 and HepG2 cells.

Conclusions: Our findings indicate that curcumin prevents HFD-induced hypercholesterolemia by transcriptionally suppressing intestinal and hepatic NPC1L1 expression and cholesterol absorption via inhibition of SREBP-2 and HNF1α transcriptional activity. Our research provides evidence for curcumin as a potential nutraceutical for hypercholesterolemia treatment by regulating NPC1L1 and enterohepatic circulation metabolism of cholesterol.

Background: Postmenopausal women are subject to hormonal fluctuations, a rapid decline in bone mineral density (BMD) and a significant increase in fracture risk, and both exercise and nutritional interventions have a positive impact on BMD. The aim of this study was to evaluate the effects of combined exercise and nutrition interventions compared to single nutrition or exercise interventions on BMD in postmenopausal women and specific combined strategies to improve BMD.

Methods: A systematic search on PubMed, Embase, Cochrane Library, Web of Science, Google Scholar databases and studies identified until April 4, 2025 were performed following strictly the PRISMA evaluation guidelines.The risk of bias was assessed using the Cochrane Risk of Bias Tool, the quality of evidence was evaluated using the GRADE approach, and data analysis was performed using Stata 17.0.

Results: A total of 24 RCTs involving 2,236 postmenopausal women were included. Meta-analysis results showed that EN vs. N demonstrated a positive effect on BMD at the femoral neck (SMD = 0.17, 95% CI: 0.07-0.27, p = 0.0006), lumbar spine (SMD = 0.20, 95% CI: 0.07-0.33, p = 0.003), and total hip (SMD = 0.16, 95% CI: 0.03-0.28, p = 0.014). However, no statistically significant difference in BMD at the same anatomical site was observed EN vs. N. The robustness of the results of subgroup analysis is limited due to differences in intervention regimens, study populations, and sample sizes across different studies.

Conclusions: Based on current evidence, there is insufficient support for universal evidence-based recommendations regarding specific combined intervention strategies.

Trial registration/protocol registration: PROSPERO (CRD420251053527).