The Naples Prognostic Score (NPS), a comprehensive indicator of inflammation and nutrition, remains unstudied in relation to cataract prevalence. We analyzed 8612 adults (≥20 years) from the National Health and Nutrition Examination Survey (NHANES) 1999-2008 in this cross-sectional study. Each 1-point increase in NPS was associated with 25% higher odds of cataract, and high NPS participants had 80% higher odds than low NPS. Restricted cubic spline (RCS) analysis indicated a significant linear association. Subgroup analysis strengthens the positive correlation between NPS and cataracts. Exploratory mediation analysis suggested that the triglyceride-glucose index-based A Body Shape Index (TyG-ABSI) may partially explain this association, particularly among nondiabetic individuals. These findings indicate that high NPS is independently and linearly associated with increased cataract prevalence in US adults, and exploratory analyses suggest that TyG-ABSI may partially mediate this association. These results support the potential benefit of maintaining optimal NPS values in mitigating cataract development.

Type 2 diabetes mellitus (T2DM) is a major risk factor for atherosclerotic cardiovascular disease (CVD), and hyperlipidemia (HLD) frequently coexists. Shear wave elastography (SWE) quantifies carotid stiffness and may improve CVD risk stratification. To evaluate the impact of HLD on carotid stiffness in T2DM using SWE. We conducted a cross-sectional study of 112 adults with T2DM: simple diabetes (Group B, n = 52) and T2DM with HLD (Group C, n = 60): and 55 healthy controls (Group A). Demographic, clinical, and biochemical data were collected. Conventional ultrasound measured carotid intima-media thickness, diastolic diameter, systolic diameter, and peak systolic velocity. Arterial distensibility and the stiffness coefficient were calculated. SWE provided maximum, mean, and minimum elastic moduli. Pearson correlation tested associations between SWE parameters and risk factors; multivariable linear regression identified independent determinants of SWE values. Compared with controls, Groups B and C had higher fasting glucose, glycated hemoglobin, total cholesterol (TC), triglycerides (TG), and LDL-C (all P < .05); TC, TG, and LDL-C were higher in Group C than Group B (all P < .05). high-density lipoprotein cholesterol (HDL-C) were lower in both Group B and Group C compared to Group A (both P < .05), and were also lower in Group C than in Group B (P < .05). Mean elastic modulus, maximum elastic modulus, and minimum elastic modulus were greater in Groups B and C than in controls and were highest in Group C (all P < .05). SWE parameters correlated positively with carotid intima-media thickness, TC, TG, and LDL-C, and negatively correlated with HDL-C (all P < .05). In multivariable models, hyperlipidemia: driven primarily by elevated TC, TG, and LDL-C and reduced HDL-C: was independently associated with increased SWE values in T2DM (all P < .05). HLD exacerbates carotid atherosclerosis in T2DM. SWE is a noninvasive, quantitative, and efficient method for assessing carotid stiffness and cardiovascular risk in T2DM, particularly among patients with concurrent HLD.

Coronary artery disease (CAD) remains a major cause of morbidity and mortality worldwide. Although guideline-directed Western medical therapy improves cardiovascular outcomes, residual symptoms remain common. Integrated traditional Chinese and Western medicine is frequently used as an adjunctive strategy in China, but its real-world, short-term clinical associations require further characterization. This retrospective observational study included 215 patients with CAD treated between January 2022 and December 2024, including 106 patients receiving conventional Western medical therapy alone and 109 receiving adjunctive traditional Chinese medicine based on syndrome differentiation. Symptom status, laboratory parameters, overall clinical response, and documented adverse events were compared between groups. Because treatment allocation was nonrandom and the analyses were unadjusted for potential confounders, all between-group findings were interpreted as associations. No statistically significant differences were observed in the measured baseline demographic, clinical, or laboratory characteristics between the 2 groups. After treatment, the integrated-treatment group had lower rates of residual chest pain, chest tightness, and fatigue and greater changes in total cholesterol, triglycerides, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, fibrinogen, and D-dimer. The observed overall clinical response rate was higher in the integrated-treatment group (90.8% vs 76.4%, P = .004). Documented adverse-event incidence did not differ significantly between groups. In this retrospective real-world cohort, adjunctive traditional Chinese medicine was associated with greater short-term improvement in selected symptoms and laboratory parameters and a higher observed clinical response rate, without a detectable increase in documented short-term adverse events. These unadjusted observational findings are exploratory, do not establish causal superiority or improved cardiovascular prognosis, and are insufficient by themselves to modify current guideline-directed CAD practice.

Organophosphorus pesticides (OPPs) are widely used and have recently been linked to metabolic syndrome (MS). This study aimed to investigate the probable association between chronic OPP exposure and MS among farm workers in Sharkia Governorate, Egypt, and to assess the potential role of peroxisome proliferator-activated receptor gamma (PPARγ). This comparative cross-sectional study included 140 participants, equally divided into OPP-exposed farm workers and non-exposed subjects. OPP exposure was confirmed by detecting plasma residues and cholinesterase activity. MS was diagnosed by assessing body mass index (BMI), waist circumference (WC), blood pressure, plasma glucose, serum insulin, and lipid parameters. Oxidative and inflammatory markers, including malondialdehyde (MDA), gamma-glutamyl transferase (GGT), ferritin, superoxide dismutase (SOD), tumor necrosis factor-alpha (TNF-α), and high-sensitivity C-reactive protein (hs-CRP), were measured. The mRNA expression of the PPARγ and paraoxonase 1 (PON1) genes was also investigated. In total, 60% of farm workers demonstrated MS, compared with 10% of non-exposed participants. Workers exhibited elevated oxidative and inflammatory indices and reduced PPARγ and PON1 expression. PPARγ positively correlated with high-density lipoprotein (HDL), SOD, and PON1, while negatively correlating with glucose, insulin resistance (IR), low-density lipoprotein (LDL), triglycerides (TGs), MDA, GGT, ferritin, TNF-α, and hs-CRP. The study concluded that chronic OPP exposure was associated with increased oxidative stress and inflammation, reduced PPARγ and PON1 expression, disturbed glucose and lipid metabolism, and increased IR. The observed associations between PPARγ downregulation, metabolic disturbances, and oxidative and inflammatory markers suggest that PPARγ dysregulation may represent a potential mechanistic link between chronic OPP exposure and MS. However, this proposed mechanism requires further validation.

To investigate the associations between single and mixed exposure to air pollutants in underground coal mine environments and the risk of metabolic syndrome (MetS) among workers, we conducted a cross-sectional study. Multivariable logistic regression, Bayesian kernel machine regression (BKMR), and quantile-based g-computation (Qgcomp) were used to evaluate the joint effects of mixed pollutant exposures and to identify the major contributing components. In addition, untargeted urinary metabolomics analysis was performed to explore the potential biological mechanisms. After adjusting for confounding factors, logistic regression analysis revealed that exposure to coal dust (CD), carbon monoxide (CO), carbon dioxide (CO2), and nitrogen dioxide (NO2) was associated with an increased risk of MetS. Furthermore, BKMR and Qgcomp models consistently indicated a significant positive association between mixed pollutant exposure and MetS risk, with CD and NO2 identified as the primary components with the strongest statistical contribution. CD exposure was mainly associated with central obesity and hypertension, whereas NO2 exposure was primarily linked to elevated blood glucose and triglyceride levels. MetS patients exhibited significant alterations in urinary metabolic profiles, with more than 113 differentially abundant metabolites identified. Notably, leukotrienes were positively correlated with NO2 exposure, while acylcarnitines were associated with CD exposure. Pathway enrichment analysis indicated significant disturbances in pyrimidine and arachidonic acid metabolism. These findings provide important evidence for developing comprehensive occupational health strategies in mining environments.

Background: Type 2 diabetes mellitus (T2DM) and hyperlipidemia are interrelated metabolic disorders that significantly increase cardiovascular risk. Thiazolidinediones are known insulin sensitizers, whereas quinoline derivatives possess diverse pharmacological activities. To explore their complementary activity, we designed a novel hybrid compound integrating a thiazolidinedione core with a quinoline moiety via a carbon spacer. Materials and Methods: The hybrid molecule was synthesized through a straightforward route and structurally confirmed by spectroscopic analyses. Zebrafish (Danio rerio) were employed as an in vivo model, with hyperglycemia induced by immersion in 100 mM glucose monohydrate for 12 days. Fish were divided into treatment groups receiving 20 or 80 mg/kg of the compound, alongside the controls. Biochemical parameters (glucose, triglycerides, insulin) and gene expression levels (NF-κB, ACOX1, ACCα) were assessed. In silico docking was conducted to predict molecular interactions. Results: Treatment with the hybrid compound significantly restored glucose, triglyceride, and insulin levels. High-dose administration suppressed NF-κB expression and normalized ACOX1 levels, while both low- and high-dose treatments downregulated ACCα compared with untreated hyperglycemic controls. Computational studies supported multitarget activity through predicted binding to PPAR-α and ACOX1. Conclusions: Quinoline-Thiazolidine-2,4-Dione demonstrated strong antihyperglycemic and antihypertriglyceridemic activities in zebrafish models, supported by in silico validation.

Dietary factors may influence cognitive aging and Alzheimer's disease (AD), but observational associations, mechanistic findings, and intervention effects should not be considered equivalent evidence. This critical narrative review examines how dietary patterns, micronutrient adequacy, and metabolic health may modify AD-related vulnerability. A targeted search of PubMed/MEDLINE, Scopus, and Web of Science through April 2026 prioritized systematic reviews, meta-analyses, randomized trials, and prospective cohorts. Mediterranean, Mediterranean-DASH Intervention for Neurodegenerative Delay (MIND), and healthful plant-based dietary patterns have been associated with better cognitive outcomes and lower dementia risk. However, evidence remains predominantly observational, and randomized trials have not consistently demonstrated prevention of cognitive decline. Strict vegan diets have not shown additional protection beyond high-quality plant-based diets and require careful attention to vitamin B12 and overall nutritional adequacy. Ketogenic diets and medium-chain triglycerides may increase cerebral ketone availability, but their cognitive benefits remain inconsistent, and disease modification has not been established. Although vitamin B12, folate, and vitamin D support neural and metabolic functions, correcting deficiency should not be equated with treating AD. Overall, nutrition should be viewed as a contributor to cardiometabolic and neurological resilience and as part of person-centered dementia care, rather than as a stand-alone disease-modifying therapy. Future studies should integrate accurate dietary assessment, objective adherence measures, metabolic phenotyping, AD biomarkers, and clinically meaningful outcomes.

The bioactive flavonoid compound anthocyanin that is present in berries and other pigmented fruits has received interest for effects on substrate oxidation during exercise. The databases MEDLINE (via PubMed) and SPORTDiscus (via EBSCOhost) were searched from 4 March to 5 August 2026 for trials examining the exercise-induced metabolic effects of anthocyanin-rich foods and supplements. Twenty-three studies were included in this narrative review with observations from blackcurrant, blueberry, tart cherry, blackberry and elderberry. After short-term supplementation (up to 14 days), extract from New Zealand grown blackcurrants provided the strongest evidence, with many studies reporting up to 30% increases in fat oxidation and typically ~5-12% decreases in carbohydrate oxidation during continuous moderate-intensity exercise (cycling, walking and running). The exercise-induced metabolic responses appear to be influenced by the baseline respiratory exchange ratio, body composition, duration of dosing, and environmental exercise conditions. The findings for effects from other anthocyanin-rich sources were few and less clear. New Zealand blackcurrant extract increases moderate-intensity exercise-induced fat oxidation without alteration of the total energy expenditure. Mechanistic evidence for blackcurrant-induced effects suggests altered intramuscular triglyceride use and glycogen availability. Information from other anthocyanin-rich sources is limited for now. It cannot be excluded, however, that the changes in exercise-induced substrate oxidation may be anthocyanin-type (and thus berry) dependent, but more studies are needed on other anthocyanin-rich non-blackcurrant sources. Future studies are required to confirm mechanisms. And studies with experimental design and methodology are needed to examine responsiveness and the factors that may play a role, such as training status, exercise modality, age, and habitual diet, to advance our understanding for the implications of anthocyanin-rich supplementation for sport and exercise nutrition.

Background and Objectives: Gestational diabetes mellitus (GDM) is usually diagnosed at 24-28 gestational weeks, although metabolic and placental alterations may emerge considerably earlier. This study evaluated whether routinely available first-trimester placental biomarkers, metabolic indices, and insulin-like growth factor (IGF)-axis components are associated with GDM diagnosed later in pregnancy and whether these markers provide complementary information across distinct biological domains. Materials and Methods: Of 200 women completing the 75-g OGTT (34 with GDM and 166 normoglycemic), deferred IGF-1 and IGFBP-5 assays were performed in a complete-biomarker analytic cohort of 90 participants with complete clinical follow-up and available stored specimens (30 GDM and 60 controls). At 11+0-13+6 weeks, pregnancy-associated plasma protein-A (PAPP-A), free β-human chorionic gonadotropin (free β-hCG), IGF-1, IGF-binding protein-5 (IGFBP-5), fasting glucose, insulin, and lipid parameters were assessed. HOMA-IR, the triglyceride-glucose (TyG) index, TG/HDL-C, and LDL/HDL-C were calculated. GDM was diagnosed using a 75-g oral glucose tolerance test at 24-28 weeks. Group comparisons, correlation analyses, and logistic regression were performed. Results: Compared with controls, women who later developed GDM had higher first-trimester insulin, HOMA-IR, triglycerides, VLDL-C, TyG, and TG/HDL-C and lower HDL-C, free β-hCG, PAPP-A, PAPP-A MoM, and IGF-1 (all p < 0.05). Birth weight was also higher in the GDM group. Correlation patterns differed between groups, suggesting distinct relationships among placental, metabolic, and IGF-related markers. In the four-variable adjusted model, higher HOMA-IR (OR 2.123, 95% CI 1.089-4.137; p = 0.027) and TyG (OR 3.747, 95% CI 1.010-13.894; p = 0.048) were associated with increased GDM odds, whereas free β-hCG MoM (OR 0.325, 95% CI 0.115-0.920; p = 0.034) and IGF-1 (OR 0.856, 95% CI 0.748-0.980; p = 0.024) showed inverse associations. Conclusions: Pregnancies that subsequently developed GDM showed detectable first-trimester differences across metabolic, placental, and IGF-related pathways. The combined pattern supports further evaluation of multidomain early-risk assessment, although clinical predictive utility requires validation in larger independent cohorts.

Background/Objectives: Overlapping clinical and imaging features complicate the early differentiation between spontaneous spinal cord infarction (SCI) and seronegative acute myelitis (SAM). We aimed to compare the clinical and laboratory characteristics of SCI and SAM and, as an exploratory analysis, to develop and internally validate multivariable diagnostic models evaluating whether routinely available laboratory parameters provide additional discriminatory information beyond selected clinical features. Methods: We retrospectively analyzed 75 patients (34 SCI, 41 SAM) treated between January 2017 and June 2025. Between-group laboratory comparisons were adjusted for multiple testing using the Benjamini-Hochberg false-discovery-rate procedure. Penalized logistic regression analyses were performed using clinical variables, laboratory variables, and their combination, with candidate variables defined on clinical and data-quality grounds rather than by univariate statistical significance. Model discrimination was evaluated using repeated nested cross-validation. Bootstrap optimism correction was additionally performed for the full-data combined model, and decision curve analysis was conducted as an exploratory secondary analysis. Results: SCI patients were older, more often male, and had higher prevalence of hypertension and diabetes. Radicular pain was markedly more common in SCI. After Benjamini-Hochberg correction, five laboratory parameters remained significantly different between groups: CRP, triglycerides, monocyte percentage, and absolute monocyte count were higher in SCI, whereas HDL cholesterol was lower. In the combined penalized analysis, age, hypertension, radicular pain, CRP, triglycerides, absolute monocyte count, and absolute eosinophil count were retained. The clinical, laboratory, and combined models yielded AUCs of 0.821 (95% CI 0.718-0.910), 0.756 (95% CI 0.633-0.865), and 0.871 (95% CI 0.776-0.947), respectively. Compared with the clinical model, the combined model showed a modest increase in discrimination (ΔAUC 0.050, 95% CI 0.005-0.101, p = 0.030). Bootstrap internal validation of the full-data combined model yielded an optimism-corrected AUC of 0.902, compared with an apparent AUC of 0.937, with a mean optimism of 0.035. Exploratory decision curve analysis showed a potential net benefit of the combined model across a range of threshold probabilities. Conclusions: Spontaneous SCI and SAM showed distinct clinical and laboratory profiles in this retrospective cohort. Routine laboratory parameters provided modest additional discriminatory information beyond clinical features, and the combined model maintained discrimination during internal validation. These findings are exploratory and require validation in larger, independent cohorts before clinical application.

This study aimed to elucidate the role of Lactococcus G423 in regulating the AMPK (AMP-activated protein kinase) signaling pathway and gut microbiota, and to investigate the mechanisms underlying its potential to improve lipid metabolism in broilers. In this trial, 960 one-day-old Arbor Acres (AA) broilers were randomly assigned to one of three groups: a control group (CON), a low-dose Lactococcus G423 group (Lac-L), and a high-dose Lactococcus G423 group (Lac-H). Each group consisted of eight replicates, with 40 individuals per replicate. Compared with the CON group, the Lac-L and Lac-H groups showed no significant differences in ADFI (Average Daily Feed Intake), ADG (Average Daily Gain), FCR (Feed Conversion Ratio), breast muscle yield, leg muscle yield, or abdominal fat yield (p > 0.05). Compared with the control group, neither Lac-L nor Lac-H affected serum TG (Triglyceride) or LDL (Low-Density Lipoprotein) levels (p > 0.05). However, both Lac-L and Lac-H significantly decreased serum CHO (Cholesterol) and increased serum HDL (High-Density Lipoprotein) (p < 0.05). Regarding the AMPK signaling pathway, both the Lac-L and Lac-H groups significantly downregulated the hepatic mRNA expression of Acetyl-CoA carboxylase (ACC) (p < 0.05). The Lac-L groups significantly increased the mRNA expression of AMP-activated protein kinase (AMPK) and Sterol Regulatory Element-Binding Protein 1 (SREBP1) (p < 0.05), and the Lac-H groups significantly increased the mRNA expression of Apolipoprotein A1 (APOA1) and Protein kinase B (PKB) (p < 0.05) and significantly reduced the mRNA expression of Fatty acid-binding protein 1 (FABP1) (p < 0.05), compared to the CON group. Gut microbiota analysis indicated that both treatment groups exhibited significantly increased α-diversity indices (p < 0.05) and altered microbial composition at an order level comparable with that of the CON group. Specifically, the abundances of beneficial families such as Lachnospirales and Lactobacillales were elevated, while significant changes were observed in other taxa including Ruminococcaceae and Akkermansiaceae (p < 0.05). These changes corresponded with significant differences in the MDI and GMHI (p < 0.05). In conclusion, Lactococcus G423 may regulate lipid metabolism in broilers through the combined modulation of the AMPK signaling pathway and the gut microbiota. Specifically, Lactococcus G423 appears to regulate broiler lipid metabolism by modulating the gut microbiota-hepatic lipid metabolism axis.

Mycobacterium tuberculosis (M. tb) possesses a unique, lipid-rich cell envelope that is critical for virulence, drug resistance, and persistence. Here, we identify the PPE family protein PPE57 as a key regulator of mycolic acid transport and host lipid exploitation. PPE57 physically interacts with the essential lipid transporter MmpL3, promoting trehalose monomycolate (TMM) translocation, enhancing trehalose dimycolate (TDM) synthesis, and increasing cell wall lipid content. Site-directed mutagenesis identified G175 as a critical residue for PPE57-MmpL3 binding. Deletion of PPE57 reduces cell wall thickness, alters lipid composition, and impairs biofilm formation. Mechanistically, PPE57 facilitates bacterial cholesterol acquisition, and during infection, activates the host PPAR-γ pathway in macrophages, leading to enhanced cholesterol uptake, lipid droplet accumulation, and increased intracellular triglyceride and cholesteryl ester levels. These changes provide a nutrient-rich niche that promotes bacterial survival and persistence. In a mouse model of infection, PPE57 deficiency results in reduced bacterial burden, milder lung pathology, and diminished lipid droplet-positive cell accumulation in lung tissues. These findings establish PPE57 as an essential accessory component of the MmpL3 lipid transport system, bridging mycobacterial cell wall assembly with host nutrient exploitation during persistent infection.

Extreme ultramarathon running provides a unique human model for examining physiological responses under sustained metabolic stress. This study compared acute endocrine and lipid responses across 100, 308, and 622 km ultramarathon events, with particular attention to whether these responses were uniformly amplified with increasing race distance or differed according to event characteristics. Forty-four experienced male ultramarathon runners participated in the study (100 km group: n = 17; 308 km group: n = 18; 622 km group: n = 9). Venous blood samples were collected within 2 h before race start and generally within 5 min after race completion, and post-race biochemical concentrations were corrected for participant-specific plasma volume changes. Insulin and triglycerides decreased significantly across all three events, whereas T3 and HDL-C increased across all events. FSH and C-peptide decreased significantly in the 100 and 308 km groups, and FT4 increased significantly in these two groups. LH showed a significant time × event group interaction, with a significant reduction in the 100 km group and no significant within-group change in the 308 or 622 km groups. Because LH secretion is pulsatile and only one venous sample was obtained at each pre- and post-race time point, these findings should be interpreted as acute differences in circulating LH concentrations rather than evidence of altered gonadotropin regulation or hypothalamic-pituitary-gonadal axis suppression. Total cholesterol decreased significantly only after the 622 km event, whereas LDL-C decreased after the 308 and 622 km events. The observed endocrine and lipid response patterns differed across ultramarathon events characterized by distinct cumulative durations, pacing characteristics, nutritional exposure, hydration conditions, and recovery opportunities. Extreme ultramarathon running may therefore serve as a useful physiological model for investigating context-dependent endocrine and lipid responses to prolonged endurance stress.