International Journal for Vitamin and Nutrition Research最新文献

Background: This cross-sectional study aimed to investigate the relationships between gut microbiota compositional alterations and chronic metabolic disorders by analyzing taxonomic diversity, community structure, and species-level differences in individuals with hyperuricemia (HUA) and a history of being overweight. Our findings offer novel insights into microbiota-targeted therapeutic strategies for managing metabolic diseases. A total of 144 participants were recruited and divided into three diagnostic categories: healthy controls (HL, n = 29), hyperuricemia group (HU, n = 24), and overweight (OW, n = 91).

Methods: Comprehensive phenotypic profiles and metagenomes were analyzed for fecal samples from the three groups.

Results: Significant differences were observed in psychological states and microbial ecology between the metabolic disorder groups (HU and OW) and the control group (HL) (p < 0.05). Both the overweight individuals and those with HUA presented significant changes in gut microbial composition, with reduced α-diversity indices (Shannon index: HU vs HL Mann-Whitney U = 306; p = 0.462; OW vs HL Mann-Whitney U = 1008; p = 0.040; richness index: HU vs HL Mann-Whitney U = 307; p = 0.469; OW vs HL Mann-Whitney U = 1072; p = 0.092) compared to healthy individuals. Moreover, analysis of the linear discriminant analysis effect size (LEfSe) identified four discriminatory species in the HU group (Alistipes putredinis, Mediterraneibacter faecis, Streptococcus oralis, and Gemella sanguinis), and five in the OW group (Pantoea endophytica, Pantoea vagans, Phocaeicola coprophilus, Ruminococcus SGB4421, and Klebsiella oxytoca), representing potential biomarkers for the progression of chronic metabolic diseases.

Conclusion: This study elucidates the characteristics of overweight individuals and those with HUA in terms of phenotypic features and gut microbiota, providing a theoretical reference for gut microbiota-targeted therapies and lifestyle interventions in chronic metabolic diseases.

The prevalence of liver disease is steadily increasing worldwide. Meanwhile, metabolic dysfunction-associated steatotic liver disease (MASLD) has become the most prevalent chronic liver disease globally, characterized by the extensive involvement of multiple organs. Currently, the recommended treatment for MASLD is adopting a healthy lifestyle, which includes regular exercise and a balanced diet that incorporates plenty of vegetables. In this context, black radish is a cruciferous vegetable rich in glucosinolates, which represent the most beneficial active components. Glucosinolates act by preventing the induction of reactive oxygen species (ROS) and factors related to lipid metabolism, such as fibroblast growth factor 21 (FGF21) and nuclear factor erythroid 2-related factor 2 (Nrf2). There are several other components, such as precursors for glutathione (GSH) synthesis, which regulate liver enzymes and lipid peroxidation, as well as flavonoids, which help ameliorate lipid accumulation and possess antioxidant properties. These preventive health effects contribute to lipid metabolism and cellular energy balance, which, in turn, aid in liver detoxification and preventing diseases. This review aims to assess the biological detoxification mechanisms and effects of black radish in MASLD and related chronic diseases.

Gluten-free diets (GFDs) are gaining popularity worldwide. Originally, GFDs were designed for individuals with gluten intolerance, including conditions such as celiac disease, non-celiac gluten sensitivity, gluten ataxia, or dermatitis herpetiformis. However, many individuals without gluten sensitivity have subsequently adopted this diet, leading to a growing demand for gluten-free food products. Meanwhile, the health risks associated with a long-term gluten-free diet (LTGFD) and the inherent related issues, such as nutrient imbalances, remain uncertain. Scientific studies have indicated that obesity, non-alcoholic fatty liver disease (NAFLD), dysbiosis, and poor mental health represent the most probable health risks associated with a LTGFD. Moreover, high fat and simple carbohydrate content, increased calorie content, and vitamin deficiencies, including vitamin B derivatives (B1, B2, B3, B5, B6, B7, B9, and B12), vitamin D, and minerals (Fe, Mg, Se, and Zn), are key components in a GFD that are at the helm of health issues due to a LTGFD. Anthocyanins, a class of flavonoids found predominantly in red, purple, and blue fruits and vegetables, may provide a promising solution to alleviate health risks associated with a LTGFD due to their inherent antioxidant, anti-inflammatory, neuroprotective, anti-diabetic, and anti-obesity properties. Therefore, this review critically examines in vivo, in vitro, clinical, and mechanistic studies to explore the potential of anthocyanin-enriched GFDs in alleviating the health risks associated with a LTGFD, highlighting their significant advantages over regular GFDs.

Background: Phosphorus is an essential component of bone and energy metabolism; however, the mechanism involved in the regulation of phosphorus under postmenopausal conditions remains insufficiently understood. Interestingly, the disruption of estrogen status can alter mineral homeostasis. Meanwhile, phytoestrogens and probiotics may offer a non-pharmacological strategy to support mineral homeostasis; nonetheless, evidence of their impact on phosphorus distribution remains limited. Thus, this study aimed to evaluate the effect of daidzein, tempeh, and Lactobacillus acidophilus on phosphorus distribution in ovariectomized (OVX) rats.

Methods: A total of 64 female Wistar rats were allocated to sham-operated (n = 8) or OVX (n = 56) groups. Following a three-week calcium-deficient diet, the OVX rats were randomized to seven dietary interventions for six weeks: control (O), alendronate (OB), daidzein (10 mg/kg diet/day; OD), tempeh (250 g/kg diet/day; OT), probiotic L. acidophilus (1 × 10¹⁰ CFU/day; OL), daidzein + probiotic (ODL), or tempeh + probiotic (OTL). Food intake, body mass, and phosphorus concentrations in feces, the femur, kidney, pancreas, spleen, heart, and liver were analyzed.

Results: OVX groups (O, 366 ± 14 g; p = 0.01; OD, 361 ± 18 g; p = 0.02; OL, 358 ± 29 g; p = 0.04) gained significantly more body mass than sham controls (311 ± 30 g). Dietary interventions with daidzein, tempeh, and L. acidophilus enhanced phosphorus deposition in the femur, kidney, and pancreas compared with the OVX controls. The OT group showed the highest femoral phosphorus levels (178,111 ± 32,628 mg/kg d.w., p = 0.02), while the ODL group revealed elevated phosphorus levels in the kidney (12,966 ± 462 mg/kg d.w.; p = 0.01). The OD (914 ± 115 mg/kg d.w.; p < 0.001), ODL (913 ± 39 mg/kg d.w.; p < 0.001), and OTL (926 ± 70 mg/kg d.w.; p < 0.001) groups showed significantly increased levels of pancreatic phosphorus. A positive correlation was noted between the pancreatic and femoral phosphorus levels (r = 0.33; p = 0.02). Alendronate treatment had no significant effect.

Conclusions: Dietary daidzein, tempeh, and probiotics modulate phosphorus distribution in postmenopausal rats. These results support the translational potential of dietary bioactives to improve phosphorus metabolism in postmenopausal women.

Magnesium is an essential mineral required for energy metabolism, glucose regulation, cardiovascular function, bone integrity, and neural activity. Despite the vital physiological roles of magnesium, , dietary magnesium deficiency remains a widespread and underrecognized global public health concern. The recommended dietary allowance (RDA) for adults in the United States is approximately 420 mg/day for men and 320 mg/day for women, yet large proportions of the population fail to meet these levels with national nutrition surveys consistently documenting inadequate intake. For instance, 64.4% of Chinese adults consume less than the estimated average requirement (EAR) of 270 mg/day for both males and females. Globally, an estimated 2.4 billion people, or roughly 31% of the global population, fail to meet the recommended magnesium intake levels. This deficiency reflects multiple converging factors, including modern dietary patterns low in whole grains and vegetables, soil nutrient depletion from intensive agriculture, food processing losses, aged populations, chronic diseases, and socioeconomic disparities. The health implications are substantial, as magnesium deficiency is associated with elevated risks of cardiovascular disease, metabolic disorders, bone loss, and neuropsychiatric conditions. This review synthesizes current evidence on the biological importance of magnesium, global intake patterns, and determinants of deficiency, and discusses strategic interventions (such as dietary diversification, food fortification, biofortification, supplementation, and public health policies) to enhance magnesium nutrition and reduce the burden of noncommunicable diseases worldwide.

Background: Hypertension increases cardiovascular risk in type 2 diabetes mellitus (T2DM) patients. Magnesium is an important nutrient that promotes vascular function and insulin sensitivity, yet its potential role in managing blood pressure (BP) in patients with T2DM remains unclear. This study evaluates the impact of a magnesium-focused nutrition education intervention on dietary magnesium intake and BP control in patients with T2DM.

Methods: Thirty patients with T2DM (25 women; mean age, 55.7 ± 9.8 years; body mass index, 33.44 ± 7.17 kg/m²) participated in two clinical visits for data collection and BP measurement and received 12 weeks of magnesium-focused nutrition education to promote dietary magnesium intake.

Results: The education intervention significantly increased dietary magnesium intake by 81.81 mg (p < 0.001). However, there were no significant changes in systolic or diastolic BP. Analysis showed no significant correlation between dietary magnesium intake and systolic or diastolic BP (p ≥ 0.56).

Conclusion: While the intervention successfully increased dietary magnesium intake, it did not affect BP. These findings suggest that increasing dietary magnesium intake through nutrition education may not significantly impact BP in individuals with T2DM. However, further research is needed to confirm these results and explore other factors that may influence BP management in this population.

Background: Diabetic peripheral neuropathy (DPN), a prevalent microvascular complication of diabetes mellitus, poses a substantial clinical burden and has a detrimental impact on quality of life. This triple-blind, randomized, placebo-controlled trial investigated the effects of an 8-week supplementation with selenium-enriched yeast on DPN symptoms, neuropathy severity, pro-oxidant-antioxidant balance (PAB), and sexual satisfaction in individuals aged 40-70 years with DPN.

Methods: Fifty participants were randomized in a 1:1 ratio to receive either a daily 200 μg dose of Saccharomyces cerevisiae yeast-derived selenium (in a 500 mg capsule) or a placebo. Outcomes were assessed using validated tools: The Michigan Neuropathy Screening Instrument (MNSI) for symptoms, the Toronto Clinical Scoring System (TCSS) for severity, the Larson Sexual Satisfaction Questionnaire (LSSQ), and serum PAB levels via a specialized assay. Analyses followed a modified intention-to-treat approach, with ANCOVA and logistic regression used to adjust for confounders.

Results: Post-intervention, both groups exhibited significant reductions in neuropathy symptoms (selenium: p < 0.001; placebo: p = 0.001), though intergroup differences were non-significant [adjusted mean difference (aMD): -0.92; 95% CI: -1.9 to 0.10]. Neuropathy severity decreased significantly in the selenium group (p = 0.002) but not in the placebo group. While PAB levels declined markedly with selenium (p = 0.001), the between-group difference was non-significant (aMD: -32.1; 95% CI: -66.02 to 1.87). Sexual satisfaction scores improved significantly in the selenium group versus the placebo group (aMD: 8.51; 95% CI: 0.74 to 16.28).

Conclusion: These findings suggest that selenium-enriched yeast supplementation may enhance biochemical markers (PAB) and quality-of-life parameters (sexual satisfaction) in DPN. However, its limited efficacy in improving neuropathy-specific outcomes underscores the need for larger trials to clarify its therapeutic potential.

Clinical trial registration: This trial was registered at the Iranian Registry of Clinical Trials (IRCT20131009014957N10, https://trialsearch.who.int/Trial2.aspx?TrialID=IRCT20131009014957N10).

Background: Icariin (ICA) is a flavonoid, that has been shown to exert antioxidant and anti-inflammatory effects. We aimed to explore the effects of acute exhaustive exercise on skeletal muscle injury and inflammatory factor levels, and investigate the anti-injury and anti-inflammatory effects of ICA through gut microbiota modulation.

Methods: Thirty C57BL/6J mice were administered ICA by gavage for 8 consecutive weeks, which were randomly divided into 3 groups as follows: solvent gavage control group (CON), 25 mg/kg ICA gavage group (ICA-L), and 50 mg/kg ICA gavage group (ICA-H). Serum biochemical and skeletal muscle antioxidant indicators were measured. Antioxidant enzyme activities and anti-inflammatory factor levels were determined. Additionally, gut microbiota were sequenced and analyzed by 16S rDNA and the correlations between metabolic indices and microbial species were assessed using Spearman correlation analysis.

Results: ICA alleviated oxidative stress in skeletal muscle by reducing malondialdehyde (MDA) levels and upregulating the activities and mRNA expression of antioxidant enzymes (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-PX)). In addition, ICA suppressed inflammation through downregulation of tumor necrosis factor (TNF-α), nuclear factor-κB (NF-κB), and inflammatory cytokines (interleukin-6 (IL-6) and interleukin-1β (IL-1β)). Gut microbiota analysis revealed ICA enriched short-chain fatty acid (SCFA)-producing bacteria while inhibiting pathogens, with microbial shifts significantly correlated with muscle injury and antioxidant parameters, including Lachnospiraceae_NK4A136_group, Mucispirillum, and Harryflintia.

Conclusions: Our study demonstrated that ICA ameliorated exercise-induced acute muscle injury and inflammation in mice by modulating gut microbiota composition and regulating NF-κB signaling pathway along with related antioxidant enzyme gene expression.

Background: Taste disorders are associated with various health conditions, including COVID-19. However, the prevalence and correlation of taste disorders are not comprehensively described at the population level. This study aimed to (i) estimate the prevalence of taste disorders, (ii) identify modifiable and non-modifiable correlates, and (iii) investigate the association between taste disorders and diet quality and macronutrient intake.

Methods: This cross-sectional study analyzed data from 7408 adults aged ≥40 years in the 2011-2014 National Health and Nutrition Examination Survey (NHANES). Taste disorders and sociodemographic factors were identified through self-reported questionnaires and interviews. Dietary quality was assessed using the Healthy Eating Index (HEI)-2015. Weighted logistic regression models were used to identify correlates of taste disorders, while Wilcoxon rank-sum tests and linear regression models were used to analyze dietary quality and macronutrient intake. Multivariable-adjusted models were adjusted for age, sex, race/ethnicity, socioeconomic status (as measured by educational attainment and family income level), smoking status, physical activity, body mass index (BMI), and a history of chronic diseases (hypertension, high cholesterol, cardiovascular disease, diabetes, and cancer).

Results: Taste disorders had a prevalence of 5.1% (95% confidence interval (CI): 4.5-5.6). Higher rates were observed in individuals with lower educational attainment, lower income, and a history of diabetes (7.3%; 95% CI: 5.8-8.7), cardiovascular disease (9.7%; 95% CI: 7.7-12.0), and cancer (7.0%; 95% CI: 4.1-10.0). Those with taste disorders had poorer diet quality, lower energy intake, lower protein intake, and higher sugar consumption compared with those without (all p < 0.01).

Conclusions: US adults exhibited a high prevalence of taste disorders, particularly among individuals with lower socioeconomic status, chronic conditions, and those who are non-Hispanic White, non-Hispanic Black, and Hispanic. An increased prevalence is associated with poorer diet quality, highlighting the need for targeted interventions to address the nutritional impacts. Due to the limitations of the cross-sectional design, this study could not establish causality between taste disorders and dietary intake or patterns, underscoring the need for longitudinal studies to confirm the observed relationships.

Calcium plays a central role in gastrointestinal (GI) physiology through regulating smooth muscle contractility, acid secretion, epithelial barrier integrity, and immune signaling. The dysregulation of calcium homeostasis has been increasingly implicated in the pathogenesis of GI disorders, including colorectal cancer, inflammatory bowel disease, peptic ulcer, and pancreatitis. Specifically, aberrant calcium-sensing receptor (CaSR) signaling has emerged as a critical molecular mechanism in colorectal tumorigenesis; meanwhile, calcium-mediated pathways influence gastric acid production and intestinal motility. This review critically evaluated recent advances in calcium signaling within the GI tract, highlighting the crosstalk involved with the gut microbiota and the roles of downstream effectors, including transient receptor potential vanilloid type 6 and store-operated calcium entry. This review also examined the therapeutic implications of calcium supplementation across various GI conditions, including bioavailability challenges under different disease states and nutrient interactions involving vitamin D and phosphate. Our review further addresses the role of calcium in mucosal immunity, the clinical relevance of hypocalcemia in GI diseases, and the potential of microbiome-guided nutritional interventions. However, despite growing mechanistic insights, considerable gaps remain in understanding host-microbiota-calcium interactions, genotype-specific responses to calcium, and long-term clinical outcomes. Thus, future research should clarify the dose-response relationships, stratify patient populations by CaSR polymorphisms and microbiome profiles, and establish precision strategies for calcium-based interventions in digestive health.