Nutrition & Metabolism最新文献

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).

Background: Cognitive dysfunction in diabetes significantly impairs quality of life, yet effective therapies remain limited. Our previous work showed that α-methyltryptophan (α-MT), an inhibitor of the amino acid transporter SLC6A14 and indoleamine 2,3-dioxygenase 1 (IDO1), ameliorates diabetic nephropathy by modulating renal metabolism. Given its role in metabolic regulation, we hypothesized that α-MT may also protect against cognitive decline in diabetes by influencing gut-brain metabolic crosstalk.

Methods: Db/db mice were used as an in vivo model of type 2 diabetes, complemented by high-glucose-treated Caco-2 cells in vitro. Cognitive function was assessed using the Morris water maze. Gene expression related to synaptic plasticity (c-FOS, ARC, BDNF, EGR1) was measured by RT-qPCR. Colon morphology and SLC6A14 expression were evaluated by H&E, AB-PAS, immunohistochemistry, and Western blotting. ¹H NMR-based metabolomics was applied to profile metabolic changes in the colon and hippocampus.

Results: α-MT treatment significantly reduced hyperglycemia, restored intestinal barrier integrity, and improved cognitive performance in db/db mice. It also downregulated SLC6A14 overexpression under hyperglycemic conditions in both models. Metabolomic analysis revealed that α-MT induced significant metabolic reprogramming in the colon, with amino acid metabolism as the most affected pathway. Notably, metabolite alterations in the colon were positively correlated with those in the hippocampus, and both were negatively associated with increased expression of c-FOS, ARC, BDNF, and EGR1, suggesting coordinated gut-brain metabolic responses.

Conclusions: These findings indicate that α-MT alleviates diabetes-associated cognitive impairment by promoting gut-brain metabolic remodeling. Targeting intestinal amino acid transport may represent a promising nutritional and therapeutic strategy for neuroprotection in diabetic encephalopathy (DE).

Background: The Planetary Health Diet proposed by the EAT-Lancet Commission aims to promote global health and environmental sustainability through a predominantly plant-based, carbohydrate-rich nutritional model. Despite its appeal, its universal application raises concerns regarding human metabolic compatibility, nutrient sufficiency, and evolutionary coherence.

Objectives: This article critically evaluates the Planetary diet through the lenses of evolutionary biology, clinical nutrition, cancer metabolism, and anthropological diversity. An alternative framework is proposed: The autogenous diet, which aligns more with human physiological and ecological heritage.

Methods: A narrative synthesis was conducted of peer-reviewed literature from evolutionary nutrition, clinical trials, oncology, and chronobiology. Comparative analysis highlights the metabolic divergence between high-carbohydrate, standardized diets and fat-adapted, ancestral nutritional models.

Results: The planetary diet fails to meet several human biological requirements. It neglects nutrient-dense animal foods rich in DHA, vitamin B12, and bioavailable iron; promotes chronic glycemic load and insulin signaling; and ignores interindividual genetic and epigenetic variability. By contrast, the autogenous diet contains a species-appropriate macronutrient distribution (moderate protein, high fat, low carbohydrate), prioritizes local and minimally processed foods, aligns with circadian biology and fasting cycles, and elicits tumor-suppressive mechanisms.

Conclusion: The universalization of the planetary diet represents a biological and cultural oversimplification. Nutritional strategies must account for evolutionary metabolism, regional diversity, and clinical outcomes. Ancestral, autogenous diets may offer a more effective and ecological solution that can meet nutritional requirements based on fundamental physiology.

Background: The complex interaction of food habits, stress levels, and gut microbiota is instrumental in shaping global human well-being. Lifestyle indicators like diet, stress, and exercise have immense potential to drive gut health but are usually plagued by the divide between knowledge and action.

Methodlogy: This research compared lifestyle variables and awareness of gut health in 51 participants on a standardized questionnaire. It analyzed variables such as frequency of meals, intake of processed foods, intake of dietary fiber and probiotics, history of digestive diseases, perceived influence of stress, and knowledge of the gut-brain axis.

Results: Results indicated that 69.05% of the participants ate only 1-2 meals a day, and 71.43% had moderate consumption (1-2 times per week) of fast or processed foods. A concerning fact is that only 7.14% ate probiotic foods daily, and only 28.57% had high-fiber foods in their daily diet. Gastrointestinal problems were prevalent, with 56.41% having issues and 51.28% having occasional problems (1-2 times per week). In addition, 66.67% thought that stress influences their digestion, and 74.36% experienced changes in diet influencing their gut. Just 13.16% were physically active daily, and 44.74% slept for less than six hours daily, both are known to influence the gut microbiome. While 76.32% understood the diet-stress-microbiota connection, just 57.89% were of the view that dietary modifications can help manage stress.

Conclusion: The research points to an important gap between knowledge and practical behaviors concerning gut health and stress management. There is a need for public health programs to enhance sustainable lifestyle and dietary changes to improve microbial diversity, digestive well-being, and mental health.