Nutrients最新文献

The journal retracts the article "Hesperetin, a Citrus Flavonoid, Attenuates LPS-Induced Neuroinflammation, Apoptosis and Memory Impairments by Modulating TLR4/NF-κB Signaling" [...].

The journal retracts the article "Natural Dietary Supplementation of Curcumin Protects Mice Brains against Ethanol-Induced Oxidative Stress-Mediated Neurodegeneration and Memory Impairment via Nrf2/TLR4/RAGE Signaling" [...].

Background/Objectives: The hepcidin-ferroportin (Fpn1) axis is central to intestinal iron absorption, and dysregulation of this axis underlies all known forms of iron disorders. Hemochromatosis, the most common iron overload disorder in humans, results from systemic iron accumulation due to decades of uncontrolled intestinal absorption. Despite major advances in medicine in recent years, strategies for iron overload management are still lagging as they primarily rely on iron chelation and repeated phlebotomies. Fpn1, the cellular iron exporter, is ubiquitously expressed and plays a critical role in maintaining systemic iron homeostasis. Methods: To investigate the specific contribution of intestinal Fpn1 to systemic iron overload, we employed a CRISPR-based adenoviral hepcidin knockout mediated mouse iron overload model, combined with intestine-specific deletion of Fpn1. Results: An initial time-dependent experiment establishes the efficiency of hepcidin knockout (KO) by as early as 1 week of adenovirus injection. At 2 weeks of injection, a perfect reciprocal relationship between hepcidin gene suppression and liver iron levels (5-7-fold induction from the baseline) was established. Finally, intestine-specific Fpn1 deletion effectively prevented iron accumulation in hepcidin KO mice, as evidenced by nearly 4-fold lower liver iron levels compared to hepcidin KO animals with intact intestinal Fpn1. Conclusions: In summary, our results demonstrate that ablation of intestinal Fpn1 is sufficient to attenuate systemic iron accumulation in this mouse model of hemochromatosis. These findings suggest that selective targeting of intestinal Fpn1 may represent a promising strategy for the management of iron overload.

Background/Objectives: Up-to-date, relevant and detailed food composition databases (FCDs) are a central component of mHealth apps. Thus, the expansion and/or update of such FCDs though the aggregation of branded food data (BFCDs) could prove as a cost-efficient methodology. However, a framework for data aggregation from BFCDs has yet to be documented. Methods: Products (n = 3988) available in the HelTH BFCD were grouped following a three-step process. Firstly, foods were grouped based on their name, and then the aggregated nutritional composition was tested for heterogeneity using a coefficient of variation cut-off of 20% followed by a search of the ingredient list and other product characteristics to identify descriptors that reduced heterogeneity. Results: Following a three-step process, n = 347 new generic food names were proposed, each derived from at least three branded products, of which n = 235 were populated with aggregated nutritional content values. We found that 95.3%, 88.6%, 86% and 82.6% of aggregated energy, protein, carbohydrate and sodium values, respectively, had a coefficient of variation <40%. Aggregated saturated fatty acid and total sugar values were less likely to fall in the homogeneity level (76.3% and 65.3%, respectively). The heterogeneity was concentrated in specific subcategories like baked goods, milk products and milk imitation products, primarily. Conclusions: BFCDs can be used as a resource to expand existing databases with relatively homogeneous and up-to-date nutritional composition data. The application of this framework on larger datasets could improve the generic food name yield and homogeneity and support mHealth apps and other uses.

Background/Objectives: Ischemic stroke is a leading cause of death and disability, and neuroprotection therapies, or those that increase recovery, are not available. While the garlic-derived bioactive compound S-allyl cysteine (SAC) has shown neuroprotective properties, its subacute long-term effects remain underexplored, particularly in females. Methods: We evaluated whether SAC supports functional recovery after ischemia/reperfusion (IR), focusing on neurotrophin signaling, tropomyosin receptor kinase B (TrkB), protein kinase B (AKT), and extracellular signal-regulated kinase (ERK). Adult female Wistar rats underwent 1 h of ischemia and 15 days of reperfusion. SAC (100 mg/kg, i.p.) was administered at the onset of reperfusion and daily for 15 days. Motor and cognitive deficit tests were performed. Infarct area, Ki67, brain-derived neurotrophic factor (BDNF), vascular endothelial growth factor (VEGF), nerve growth factor (NGF), pTrkB, pAKT, and pERK levels were quantified in the cortex, striatum, and hippocampus. Results: MicroPET analysis revealed comparable glucose uptake between the IR and IR + SAC groups, indicating similar ischemic severity. SAC reduced infarct area (54.7%) and significantly improved motor deficits (53.9%), circling behavior (38.9%), and long-term memory compared with ischemia/reperfusion (IR) animals. SAC increased the proportion of Ki67-positive cells (4.3-fold in the cortex and 1.8-fold in the striatum) and enhanced neurotrophin levels, NGF (cortex), BDNF (cortex and striatum), VEGF (striatum), pTrkB, pAKT, and pERK (cortex and striatum). Conclusions: SAC supports post-ischemic recovery, improving motor performance and preserving long-term recognition memory, effects that could be associated with increased cell proliferation, neurotrophin levels, and activation of the TrkB, AKT, and ERK pathways.

Background: Obesity-related cardiometabolic disorders have been linked to alterations in selected gut microbiome components, yet clinically relevant microbial signatures remain incompletely defined. Objectives: This study investigated associations between selected gut bacterial taxa and cardiometabolic risk phenotypes in individuals with obesity. Methods: In this cross-sectional study, 100 adults with obesity were stratified according to metabolic syndrome status. Gut microbiome composition was assessed using targeted multiplex real-time PCR of functionally relevant bacterial taxa. Associations with anthropometric and cardiometabolic parameters were examined using correlation analysis, ROC curves, and multivariable logistic regression models. Results: Reduced relative abundance of Lachnospiraceae was associated with metabolic syndrome, lower Faecalibacterium abundance with arterial hypertension, and increased Prevotella abundance with dyslipidemia. ROC analyses identified cohort-specific discriminative thresholds with moderate accuracy. Conclusions: Selected taxon-specific gut microbiome signatures are associated with cardiometabolic risk phenotypes in obesity. These findings are exploratory and require validation in longitudinal and independent cohorts.

Background/objectives: Oats and oat bran are rich in polyphenols and soluble fiber, which are metabolized by gut microbiota into bioactive compounds. Previous studies identified ursodeoxycholic acid (UDCA), 3-(3-hydroxyphenyl)propionic acid (3-HPP), and avenanthramide C (AVC) as key microbial metabolites with protective effects against colitis.

Methods: This study aimed to elucidate their antioxidant and anti-inflammatory activities and underlying mechanisms using LPS-induced RAW 264.7 macrophages and AAPH-induced oxidative stress in zebrafish embryos. All three metabolites significantly reduced intracellular reactive oxygen species (ROS), nitric oxide (NO), malondialdehyde (MDA), and pro-inflammatory cytokines (IL-6, TNF-α). They also restored mitochondrial membrane potential and enhanced superoxide dismutase (SOD) activity.

Results: In vivo, treatment improved zebrafish survival, normalized SOD activity to 76-89% of control levels, and decreased ROS and MDA by 2.4 to 3.8 fold, with UDCA showing the greatest efficacy. Molecular docking revealed strong binding affinities to Keap1, particularly UDCA, which interacted with residues Met577, Ala440, Val532, and Val486. qRT-PCR further demonstrated downregulation of Keap1 and upregulation of Nrf2 and SOD, indicating activation of the Keap1-Nrf2 pathway.

Conclusions: Collectively, these findings show that oats and bran-derived microbial metabolites exert potent antioxidant and anti-inflammatory effects via modulation of the Keap1-Nrf2 axis. Among the metabolites, UDCA exhibited the strongest biological activity at equivalent concentrations. This study provides mechanistic insight into how microbiota-derived oat metabolites contribute to redox balance and immune regulation, supporting their potential as functional components in dietary strategies for managing oxidative stress-related inflammatory diseases.

Objective: This randomized, double-blind, placebo-controlled clinical trial assessed the efficacy and safety of steamed ginger extract (GGE03), standardized to high levels of 1-dehydro-6-gingerdione (GD), in reducing body fat and weight among overweight individuals.

Methods: Eighty adults aged 18 to 60 years, with a body mass index (BMI) of 25.0 to 29.9 kg/m², were randomly assigned to receive either GGE03 (n = 40; 480 mg/day) or a placebo (n = 40) for 12 weeks. Efficacy and safety parameters were evaluated at baseline and after the intervention period.

Results: After 12 weeks, the GGE03 group showed statistically significant reductions in body fat percentage and body fat mass compared to the placebo group, as measured by dual-energy X-ray absorptiometry (DEXA). Additionally, significant decreases in body weight, BMI, waist circumference, and hip circumference were observed following GGE03 supplementation. Serum triglyceride (TG) and total cholesterol (TC) levels were also significantly lower in the GGE03 group compared to the placebo group. No product-related adverse events or clinically significant laboratory abnormalities were noted, indicating that GGE03 was well tolerated.

Conclusions: Twelve weeks of GGE03 supplementation were associated with statistically significant improvements in body composition and lipid parameters without safety concerns. These findings support the potential of GD-standardized GGE03 as a well-tolerated functional dietary ingredient for body fat management and metabolic health.

Background: Food insecurity may adversely affect cognitive function through pathways involving nutritional deficiencies, chronic stress, and comorbid health conditions, with potentially different effects across cognitive domains. Longitudinal evidence remains limited by time-varying confounding, and it is unclear whether Supplemental Food Assistance Program (SNAP) participation modifies these associations. Objectives: To examine the longitudinal association between food insecurity and cognitive function using marginal structural models (MSMs), and whether SNAP participation buffers these associations for overall cognition, episodic memory, and attention/mental processing. Methods: 30,641 adults aged ≥50 in the 1998-2020 Health and Retirement Study (HRS) contributed 156,066 person-year observations. MSMs with stabilized inverse probability of treatment weights were used to account for time-varying socioeconomic, health, and cognitive confounding affected by prior exposure. Weighted pooled linear regression models estimated marginal associations and interaction effects. Results: Moderate and high food insecurity were associated with lower overall cognition (b = -0.36 and -0.71, respectively; p < 0.001). Similar graded associations were observed for episodic memory (b = -0.22; -0.43) and attention/mental processing (b = -0.15; -0.28; all p < 0.001). SNAP participation significantly attenuated these associations across cognitive domains, with stronger buffering effects among non-Hispanic Black and Hispanic respondents. Effect sizes corresponded to differences equivalent to several years of cognitive aging. Conclusions: Food insecurity is associated with poorer cognitive function across multiple domains, while SNAP participation mitigates these associations. Despite limitations of observational data, these findings highlight the methodological value of MSMs and the potential role of food assistance programs in reducing cognitive health disparities in later life.