Search Results (1,877)

Traditional treatment strategies for Type 2 diabetes (T2D) adopt a “one-size-fits-all” approach, limiting individual effectiveness. This study presents an explainable, data-driven framework for multi-treatment and single-treatment selection of SGLT2 inhibitors (SGLT2-i) and DPP-4 inhibitors (DPP4-i) based on patient-specific health characteristics. Our approach evaluates treatment effectiveness across four outcomes—glycosylated hemoglobin (HbA1c), low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, and body mass index (BMI)—to enable individualized treatment recommendations. The multi-treatment model, based on multi-output regression, achieved an R² score of 0.44 and an RMSE of 5.58, identifying benefit subgroups for SGLT2-i and DPP4-i across all outcomes. Integrated with SHapley Additive exPlanations (SHAP) analysis, the model offers insights into the factors influencing treatment effects. The single-treatment selection algorithm achieved an accuracy of 0.47 and an F1 score of 0.46, showing a higher average treatment effect with SGLT2-i on all outcomes, notably in the reduction in HbA1c, LDL, and BMI and a modest increase in HDL. While DPP4-i demonstrated beneficial effects on HbA1c, LDL, and HDL, it was associated with an increase in BMI. These findings highlight the benefits of a multi-faceted, patient-centered precision medicine approach for T2D management, enabling treatment strategies that address individual health needs beyond HbA1c. Full article

Intensive aquaculture of rice field eel (Monopterus albus) is constrained by oxidative stress induced by high-density culture resulting in growth inhibition, while prophylactic antibiotics pose escalating risks of drug resistance and food safety hazards. This study addresses the critical need for developing efficient, environmentally friendly functional feed additives as sustainable growth promoters in intensive aquaculture. To investigate the dietary berberine (BBR) effect on promoting growth performance, hepatic antioxidant capacity and metabolism in M. albus, four experimental groups were established: control (CON, 0 mg/kg) and berberine-supplemented groups (BBR25, 25 mg/kg; BBR50, 50 mg/kg; BBR100, 100 mg/kg). Growth performance, serum biochemical parameters, hepatic antioxidant capacity, and liver metabolomics (LC-MS) were evaluated after the 8-week feeding trial. BBR50 and BBR100 had significantly increased final weight, weight gain rate (WG), and survival rate (SR), while reducing feed conversion ratio (FCR) (p < 0.05). Serum glucose (Glc), total cholesterol (TC), triglycerides (TG), and low-density lipoprotein cholesterol (LDL-C) were decreased (p < 0.05), while high-density lipoprotein cholesterol (HDL-C) and phosphofructokinase (PFK) activity were increased (p < 0.05). Alanine aminotransferase (ALT), aspartate aminotransferase (AST) and alkaline phosphatase (ALP) were significantly reduced (p < 0.05). Superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) were upregulated (p < 0.05), whereas malondialdehyde (MDA) was downregulated (p < 0.05). Metabolomics identified 98 differential metabolites, with significant enrichment of metabolites associated with arachidonic acid metabolism, histidine metabolism, arginine/proline metabolism, tryptophan metabolism, and pathways related to mTOR signaling. Overall, dietary supplementation with 50 mg/kg BBR emerged as a practically favorable dose among the tested concentrations for promoting growth performance and feed utilization efficiency, whereas 100 mg/kg BBR was associated with lipid and amino acid metabolic alterations suggestive of metabolic reprogramming and antioxidant-related shifts, without conferring additional growth benefits. Full article

Background and Aims: Atherosclerotic cardiovascular disease (ASCVD) remains a leading cause of mortality worldwide, with lipid abnormalities playing a central role in disease development. While the causal role of low-density lipoprotein cholesterol (LDL-C) in ASCVD is well-established, the long-term population impact of combined lipid profiles, particularly the HDL-C/LDL-C ratio, remains less clearly quantified. This study aimed to estimate the lifetime burden of cardiovascular outcomes associated with different lipid risk profiles using a patient-level simulation framework. Methods: The authors analyzed projected lifetime ASCVD events across four HDL-C/LDL-C risk strata, ranging from low (≥0.45) to very high (<0.25), using the National Health Model Database of Projected and Estimated Outcomes (NHM-DPEO)—a digital twin of national healthcare systems built from multiple data sources, including national health and demographic statistics and estimates from the relevant literature. The framework is structured as a patient-level simulation model that projects individual health trajectories over a lifetime horizon. Model outputs were assessed for plausibility by comparison with published epidemiological estimates. Results: The NHM simulation revealed a strong, graded relationship between lipid profiles and cardiovascular survival. Life expectancy declined from 80.2 years in the lowest risk group (HDL-C/LDL-C ≥ 0.45) to 63.0 years in the very-high-risk group (HDL-C/LDL-C < 0.25), a reduction of 17.2 years, with 13.7 fewer QALYs. Similarly, participants with LDL-C > 5.0 mmol/L had a life expectancy 13.4 years shorter than those with LDL-C < 3.1 mmol/L. The burden of ASCVD increased exponentially with worsening lipid ratios: MI events rose from 5000 to 73,090 per 100,000 births, with onset in the highest risk group occurring as early as age 20. Ischaemic heart disease followed a similar pattern, showing up to 92% of events attributable to elevated lipid risk. While ischaemic stroke risk displayed a more complex pattern due to earlier MI mortality in high-risk groups, overall cardiovascular mortality and lifetime event burden were dominated by LDL-driven disease. These findings demonstrate that sustained LDL-C reduction and balanced HDL-C/LDL-C ratios confer substantial survival benefits across both sexes and all age groups. Conclusions: This study shows that lipid balance has a decisive influence on cardiovascular survival. Sustained LDL-C reduction and favourable HDL-C/LDL-C ratios markedly extend life expectancy and delay the onset of MI and IHD. The magnitude of this survival benefit highlights the need for early and continuous lipid control as a cornerstone of ASCVD prevention. The NHM quantifies these lifetime effects, offering valuable insights for targeted strategies that improve both longevity and quality of life. Full article

Previous studies have demonstrated that phloretic acid (PA), a phenolic compound, exerts beneficial effects on inflammation, oxidative stress, and aging. However, its effects on obesity and associated metabolic abnormalities, including dyslipidemia and metabolic dysfunction-associated steatotic liver disease (MASLD), remain unclear. To evaluate the effects of PA on these obesity-related metabolic alterations and explore the underlying mechanisms, male C57BL/6J mice were divided into three groups and fed for 10 weeks with a low-fat diet (10 kcal% fat), a high-fat diet (HFD, 60 kcal% fat), or an HFD containing 0.02% (w/w) PA. PA-supplemented mice showed no significant weight loss and fat loss. However, PA supplementation significantly reduced circulating levels of free fatty acid, triglyceride, and non-high-density lipoprotein cholesterol (HDL-C) while increasing HDL-C levels in HFD-fed mice. It also reduced hepatic lipid deposition and alleviated hepatocellular injury. These effects were accompanied by the coordinated modulation of hepatic lipid metabolism, including reduced lipogenesis and cholesterol esterification, enhanced fatty acid oxidation, and increased bile acid synthesis and excretion. Furthermore, PA attenuated hepatic oxidative stress and suppressed systemic and hepatic inflammation. These observations suggest that PA may counteract HFD-induced MASLD by modulating hepatic lipid metabolism, and that its anti-inflammatory and antioxidant effects may also contribute to these metabolic improvements. Full article

Objective: In this study, Dehydroepiandrosterone (DHEA-induced Polycystic Ovary Syndrome (PCOS) mice were used as models to evaluate the improvement effect of Vitexin (Vit) on ovarian fibrosis and explore the mechanism of action of the NR4A1/NLRP3 signaling pathway. Method: Sixty 4-week-old female ICR mice of the same batch number were selected and their systems were divided into 6 groups (n = 10): normal (Control, Ctrl) group, model (Polycystic Ovary Syndrome, PCOS) group, treatment (Vitexin, The Vit group, normal NR4A1 gene silencing group (Ctrl NR4A1^-/-), NR4A1 gene silencing model group (PCOS NR4A1^-/-), and NR4A1 gene silencing treatment group (Vit NR4A1^-/-). Silencing gene modeling was performed by tail vein injection of adeno-associated virus (serotype AAV-8), and the mouse genotypes were detected by qRT-PCR technology 14 days after injection. After the genotype was determined, the PCOS group and the PCOS NR4A1^-/- group were administered dehydroepandrosterone (6 mg/100 g/d) by gavage for 28 consecutive days for modeling, while the Vit group and the Vit NR4A1^-/- group were treated with dehydroepandrosterone + vitexin (10 mg/kg/d) by gavage for 28 consecutive days. All mice were raised with pure water and regular maintenance food. After 4 weeks of drug intervention, the mice were euthanized and samples were collected. The pathological changes in ovarian tissue were observed by H&E staining, and the degree of ovarian tissue fibrosis was observed by Masson staining. The levels of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), malondialdehyde (MDA), total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) in mouse serum were detected by biochemical kits. The levels of inflammatory factors (IL-1β, IL-6, IL-18, TNF-α) in mouse serum were determined by enzyme-linked immunosorbent assay. Real-time fluorescence quantitative PCR (qRT-PCR) was used to detect oxidative kinase (Gsta4, Prdx3, Mgst1, Gpx3, Gsr), inflammatory factors (Nlrp3, Caspase-1, Asc, Il-1β, Il-18, Tnf-α) and fibrotic pathway-related genes (Tgf-β1, Smad3, Collagen1, CTGF, α-SMA, Mmp-13, and β-catenin) in ovarian tissues. The levels of inflammatory factors (NLRP3, Caspase-1, ASC, IL-1β, IL-18, TNF-α, IκBα) and fibrosis in mice were determined by Western blot method, and statistical description and analysis were performed using SPSS software. Result: In the wild-type genotype group, compared with the PCOS group, Vit treatment could effectively regulate the metabolic abnormalities of PCOS mice, including inhibiting excessive weight gain, restoring normal glucose tolerance, and reducing body fat content. After Vit treatment, the levels of MDA, TC, TG, LDL, IL-1β, IL-6, IL-18 and TNF-α in the serum of PCOS mice were significantly reduced, while the levels of SOD and HDL in the serum of PCOS mice were increased. The staining results indicated that Vit treatment could significantly inhibit the process of ovarian fibrosis in PCOS mice. The results of WB and PCR demonstrated that after Vit gavage treatment in mice, inflammatory and fibrotic factors such as Nlrp3, Caspase-1, Asc, Il-1β, Il-18, Tgf-β1, Smad3, Collagen1, CTGF, and α-SMA in ovarian tissues could be significantly down-regulated, and the fibrotic level of ovarian tissues could be reduced. Among the same measurement indicators, the silenced NR4A1 group showed a certain degree of increase compared with the wild genotype group, but there was no significant difference. Conclusions: Vit intervention can restore the sex hormone levels and follicular development in ovarian tissues of PCOS mice, regulate reproductive endocrine disorders and abnormal lipid metabolism levels, and regulate the expression of Collagen I, a-SMA and CTGF in the ovaries by inhibiting the NR4A1/NLRP3 signaling pathway, thereby improving the ovarian fibrosis level of PCOS mice. It is suggested that it may play a key role in the treatment of PCOS and the prevention and delay of its long-term complications. Full article

Low levels of high-density lipoprotein cholesterol (HDL-C) are strongly associated with increased cardiovascular risk. However, under various pathological conditions, high-density lipoprotein (HDL) particles may undergo structural and functional modifications, leading to a progressive loss of antioxidant capacity and a shift from a cardioprotective to a proatherogenic phenotype. In this cross-sectional study, we investigated differences in HDL particle distribution and antioxidant function between individuals with elevated lipoprotein(a) [Lp(a)] levels (≥30 mg/dL) and those with low Lp(a) levels (<10 mg/dL). Serum low-density lipoprotein (LDL) and HDL subfractions were analyzed in twenty subjects with high Lp(a) and ten low-Lp(a) controls using non-denaturing polyacrylamide gel electrophoresis (PAGE, Lipoprint system). Enzymatic activities of paraoxonase-1 (PON1) and HDL-associated lipoprotein-associated phospholipase A₂ (HDL-Lp-PLA₂) were measured. Electrophoretic analysis revealed a significant increase in small HDL (S-HDL) in the high-Lp(a) group compared to the controls (34.1 ± 13.2% vs. 21.5 ± 2.7%, p = 0.01), alongside a reduction in large HDL (L-HDL) (19.6 ± 9.9% vs. 33.4 ± 3.8%, p < 0.001). Furthermore, the high Lp(a) group exhibited significantly lower HDL-PON1 activity (55 ± 12 vs. 67 ± 7 U/mL, p < 0.001) and HDL-Lp-PLA₂ activity (2.6 ± 1.0 vs. 3.6 ± 1.2 nmol/min/mL, p < 0.02) compared with the controls. These findings suggest that markedly elevated Lp(a) levels are associated with a shift toward a more proatherogenic HDL subfraction profile and impaired antioxidant functionality, which may reflect mechanisms linked to increased atherosclerotic cardiovascular disease (ASCVD) risk. Full article

Glycation of biomolecules leads to the formation of advanced glycation end products (AGEs) and is implicated in molecular mechanisms of human chronic diseases. We compared the glycation properties of D-ribose and methylglyoxal on human high-density lipoprotein (HDL). The increase in fluorescent AGEs in HDL samples treated with methylglyoxal confirms that HDLs are sensitive to glycation treatment. Our results demonstrated that even D-ribose glycates HDL as shown by changes induced by D-ribose on HDL apoprotein. Biochemical markers of lipid and protein oxidative damage were also evaluated. The increase in protein carbonyl contents and thiobarbituric acid reactive substances (TBARS) demonstrates a glyco-oxidative stress occurs in D-ribose treated HDL. In addition, HDL treated with D-ribose showed a significant decrease in the activity of the enzyme paraoxonase 1 and an increased HDL redox activity. These data demonstrate that D-ribose-induced glycation of HDL may impair lipoprotein functionality and may contribute to molecular mechanisms of dysmetabolic diseases. Full article

Background/Objectives: Using a well-established model of streptozotocin-induced diabetic retinopathy (DR), this study sought to evaluate the neuroprotective effect of intravitreal Forskolin (FSK) on retinal ganglion cell survival and glial activation and explore the association of circulating miR-200b with metabolic and oxidative stress in DR. Methods: A total of 18 male Wistar rats were divided into a control group (n = 6) and a streptozotocin-induced diabetic group (n = 12), which were further divided into diabetic control and FSK-treated groups (n = 6 each). Total antioxidant capacity (TAC), total peroxide (TP), triglycerides (TGs), total cholesterol, and high-density lipoprotein cholesterol (HDL-C) were measured. qRT-PCR analysis for miRNA-200b and immunohistochemistry were performed. Results: Diabetic rats showed oxidative stress and hyperlipidemia associated with increased circulating miR-200b levels. The retina showed reduced neuron numbers (Caspase-3), altered glial and astrocyte staining (IBA1, GFAP), and changes in microglia/macrophage morphology and distribution. Intravitreal FSK improved retinal ganglion cell survival and reduced glial activation, while systemic lipid profile and oxidative stress markers remained largely unchanged. Circulating miR-200b levels showed a positive correlation with oxidative stress markers across groups. Conclusions: Intravitreal FSK was able to limit the disease exacerbation via improved neuronal survival through inhibition of apoptosis. FSK did not produce observable qualitative changes in GFAP expression or IBA1+ cell morphology under the conditions tested. Full article

Objective: The aim of this study was to examine the association between dietary copper intake and incident metabolic syndrome (MetS) in Chinese adults. Methods: Data were obtained from the China Health and Nutrition Survey (CHNS) in 2009, 2015, and 2018. A total of 2418 adults aged 18–64 years who were free of MetS at baseline in 2009 were included. Person-period data were constructed, and discrete-time hazard models with a complementary log-log link were used to evaluate the associations of dietary copper intake with incident MetS and its components. Restricted cubic spline analysis (RCS) was used to assess the dose–response relationship. Results: After multivariable adjustment, compared with the lowest quartile (Q1) of dietary copper intake, the Q4 groups had a higher risks of incident MetS, with HR (95% CI) of 1.32 (1.06–1.65) (p = 0.014). When analyzed as a continuous variable, each 1 mg/1000 kcal increase in energy-adjusted dietary copper intake was associated with an approximately 27% higher risk of incident MetS (HR = 1.27, 95% CI: 1.03–1.53) (p = 0.023). RCS indicated a significant overall association without evidence of nonlinearity. Component analyses suggested that higher dietary copper intake might be associated with increased risks of reduced high-density lipoprotein cholesterol (HDL-C) and abdominal obesity. Sensitivity analyses were generally consistent with the main findings. Conclusions: Higher dietary copper intake was associated with an increased risk of incident MetS in Chinese adults. Component analyses suggested a more consistent association for reduced HDL-C, while an additional possible association was observed for abdominal obesity. Full article

Background: While reducing LDL cholesterol (LDL-C) remains central focuses of conventional preventive cardiology, substantial heterogeneity exists in the cardiovascular risk associated with even extreme LDL-C elevations, likely depending heavily on the broader metabolic context. Specifically, the lean mass hyper-responder (LMHR) phenotype—characterized by markedly elevated LDL-C with elevated high-density lipoprotein cholesterol (HDL-C) and low triglycerides in the setting of a ketogenic diet—has recently been described, though its long-term risk profile remains poorly defined. Case Presentation: We describe a male in his 30s without any congenital dyslipidemia who adopted a ketogenic diet for the management of ulcerative colitis and who subsequently exhibited a sixfold increase in LDL-C from a baseline of 95 mg/dL to 574 mg/dL, with total cholesterol of up to 705 mg/dL, HDL-C at 124 mg/dL, and triglycerides at 34 mg/dL. Despite maintaining these extreme lipid levels for nearly seven years, he demonstrated no coronary plaque or stenosis on coronary computed tomography angiography (CCTA; CAD-RADS = 0). Additionally, quantification of coronary plaque as assessed by AI-guided quantified analysis by Heartflow^® identified 0 mm³ plaque in any vessels, placing him in the lowest percentile for atherosclerotic plaque. Conclusions: This case represents an extreme and extensively characterized example of the LMHR phenotype and highlights the limitations of extrapolating cardiovascular risk from LDL-C levels alone without consideration of broader patient context and the etiology of hypercholesterolemia. While a single case cannot redefine clinical practice, this well-characterized case is consistent with emergent literature on LMHR, and careful study of such individuals may provide valuable insights into lipid metabolism, atherosclerosis biology, and precision cardiovascular risk assessment. Full article

Three medium-chain fatty acids (MCFAs), namely decanoic acid, octanoic acid, and hexanoic acid, were identified in ozonated sunflower oil (OSO) using high-performance liquid chromatography (HPLC) and liquid chromatography-mass spectrometry (LC/MS). All three MCFAs exhibited strong in vitro antioxidant activity to enhance high-density lipoprotein (HDL)-associated paraoxonase and protected low-density lipoproteins (LDL) from oxidative damage caused by Cu²⁺ ions. Consistently, MCFAs displayed substantial cellular antioxidant activity and minimized carboxymethyllysine (CML)-induced reactive oxygen species (ROS) generation and apoptotic cell death in zebrafish embryos. In adult zebrafish, MCFAs treatment mitigated CML-induced acute death and swimming abnormalities, and substantially augmented plasma sulfhydryl content, ferric ion reduction ability (FRA), and paraoxonase (PON)-like activity. Also, MCFA-treated zebrafish showed lower blood glucose, total cholesterol (TC) and triglycerides (TG) with raising HDL cholesterol levels. The MCFAs showed substantial inhibition of hepatic ROS generation, neutrophil efflux, interleukin (IL)-6 production, and steatosis, leading to hepatoprotection against CML-triggered adversity. Consistent with hepatic histology results, reduced plasma hepatic function biomarkers aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels were observed in MCFA-treated groups than in the CML-treated group. In the kidney, MCFA treatment effectively reduced oxidative stress and cellular senescence and protected against kidney damage induced by exposure to CML. The study concludes the presence of three MCFAs in the OSO, which serve as functional antioxidants and anti-inflammatory agents, accounting for its diverse pharmacological properties. Full article

Background/Objectives: For hyperlipidemic patients with statin resistance, a fixed-dose combination of a non-statin drug such as ezetimibe (EZT) and bempedoic acid (BA) provides a significant benefit. Although both drugs exhibit poor aqueous solubility, the oral bioavailability of EZT is more critically limited by dissolution, whereas BA maintains adequate absorption due to its high intestinal permeability. With regard to the reference product, Nexlizet^® (180/10 mg), our study focused on developing a novel tablet with superior in vitro performance without incorporating sodium lauryl sulfate (SLS), as it may potentially alter BA absorption. Methods: The solid dispersion technique (co-precipitation) was applied using the Kollidon^® VA64 polymer, and the solid state was characterized through differential scanning colorimetry (DSC), X-ray powder diffraction (XRPD), and Fourier transform infrared spectroscopy (FTIR). The prepared solid dispersions (SDs) were formulated into film-coated tablets (FCTs) and were characterized physically and for drug performance, and an animal model study was also conducted. Results: The solid-state analysis of the optimized SD formula (S30) revealed reduced drug crystallinity with no drug–carrier chemical interaction. The optimized formula (F30), a film-coated tablet, successfully achieved comparative in vitro dissolution versus Nexlizet^® and passed the accelerated stability study. Furthermore, in vivo evaluation revealed that F30 significantly reduced serum total cholesterol (TC), triglycerides (TG), and low-density lipoprotein (LDL), with an increase in high-density lipoprotein (HDL), in an animal model. Conclusions: These findings confirm that the SD technique is an effective one-step approach to co-formulating both APIs, simplifying manufacturing processes and optimizing the batch size. Full article

Coronary microvascular dysfunction (CMD) has emerged as a crucial contributor to cardiovascular morbidity and mortality, particularly in patients with ischemia and non-obstructive coronary arteries (INOCA). The condition arises from a complex interplay of structural and functional abnormalities within the small coronary vessels, driven by underlying molecular mechanisms including endothelial nitric oxide synthase (eNOS) uncoupling, oxidative stress, and chronic inflammation. Lipid metabolism plays a central role in this pathology, especially in the setting of elevated low-density lipoprotein cholesterol (LDL-C). Furthermore, the protective capacity of high-density lipoprotein (HDL) is increasingly understood to depend on its functionality rather than absolute levels, as it can become dysfunctional and pro-inflammatory in pathological states. Emerging evidence has identified lipoprotein(a) [Lp(a)] and triglyceride-rich lipoproteins as significant, independent contributors to microvascular injury. Comprehensive clinical assessment of microvascular dysfunction therefore requires integration of advanced lipid profiling, including apolipoprotein B (ApoB), [Lp(a)], and the triglyceride-glucose (TyG) index with invasive and non-invasive measures of coronary flow reserve to more precisely stratify risk. In this narrative review, we synthesize current observational, mechanistic, and early interventional data linking diverse lipid phenotypes to coronary microvascular dysfunction. We propose a concept of lipid-driven CMD endotypes, such as ApoB-/particle overload, dysfunctional HDL, Lp(a)-mediated risk, and metabolic/TyG-high states, and map these to a practical, mechanism-informed management framework. While intensive LDL-C lowering with high-intensity statins and combination therapy remains guideline-directed care for high-risk patients, evidence for dedicated microvascular benefit from newer lipid and cardiometabolic agents is still largely hypothesis-generating. A personalized approach that aligns lipid phenotyping, CMD endotyping, and existing guideline-based therapies may help refine risk assessment and inform future trials. Full article

Background/Objectives: There is growing interest among researchers in improved biological risk factor indices or combinations of indices, which have emerged as a major focus in evaluating the risk of cardiovascular disease (CVD). This study aimed to identify latent profiles based on the clustering of biological factors and to explore associations between lifestyle factors and CVD outcomes across the identified latent profiles. Methods: This epidemiological health survey was performed during 2023–2024. A random sample of Kaunas inhabitants aged 25–69 years, stratified by sex and age, was randomly selected from the Lithuanian population register. The 3426 individuals were screened. Latent profile analysis was performed using Latent Gold 6.1 and IBM SPSS Statistics 30. Multinomial logistic regression and multivariable binary logistic regression were used to evaluate the associations between biological risk factor profiles, lifestyle factors, and CVD outcome. Results: Three biological risk factor profiles were identified: low-risk profile (42.6%) was considered the healthiest, having the lowest levels of body mass index (BMI), fasting glucose, systolic blood pressure (SBP), and the highest level of high-density lipoprotein (HDL) cholesterol. Medium-risk profile (50.4%), having intermediate indicators of those factors. The high-risk profile (7.0%) was characterized by the lowest HDL cholesterol and the highest values of triglycerides, fasting glucose, SBP, and BMI. Conclusions: Compared to the low-risk profile, medium- and high-risk biological profiles were independently associated with higher odds of CVD, according to sociodemographic and lifestyle factors. The study suggests that integrating multiple biological risk factors rather than a single risk factor in clinical practice may enhance diagnostic accuracy. Full article

This study evaluated the protective effects of green coffee (Coffea arabica L.) extract (GCE) against metabolic and endocrine disturbances induced by fipronil (FIP) in male rats. Animals were randomly allocated into four groups (n = 6): control, GCE (100 mg/kg), FIP (4.85 mg/kg), and combined FIP + GCE, and treated orally for 90 days. FIP exposure significantly impaired glucose homeostasis, as indicated by a 14.8% increase in the oral glucose tolerance test (OGTT) response and a 2.4-fold increase in the homeostatic model assessment of insulin resistance (HOMA-IR). It also disrupted lipid metabolism, with marked elevations in triglycerides (74.10%) and total cholesterol (57.55%). Endocrine imbalance was evident, including increased resistin levels (113.86%) and reduced triiodothyronine (T3; −37.5%), adiponectin (−42.73%), and high-density lipoprotein (HDL; −9.31%). Oxidative stress and inflammation were significantly enhanced, as demonstrated by elevated malondialdehyde (MDA; +93.56%) and pro-inflammatory cytokines (IL-1β: +246.56%; IL-6: +275%), alongside a reduction in total antioxidant capacity (TAC; −45.24%). Additionally, serum albumin levels decreased markedly (−54%). Co-administration of GCE significantly improved metabolic, hormonal, and inflammatory parameters, including insulin resistance (HOMA-IR). Histopathological analysis further confirmed its protective effects on hepatic and renal tissues. Overall, GCE mitigates FIP-induced metabolic and endocrine dysfunction, likely through its antioxidant and anti-inflammatory properties. Full article