Search Results (2,019)

Background: Plasma branched-chain amino acid (BCAA) concentrations are positively associated with low-density lipoprotein cholesterol (LDL-C) levels. However, the relationship between dietary branched-chain amino acids and hyper-LDL-cholesterolemia is unclear in children and adolescents. Methods: This study explored the correlation between BCAAs and hyper-LDL-cholesterolemia risk through propensity score matching and conditional logistic regression. Machine learning based on LightGBM indicated the important role of BCAAs in the prediction of hyper-LDL-cholesterolemia. To examine the dose–response relationship, Restricted Cubic Splines (RCS) and receiver operating characteristic curves (ROC) were employed. The causal link between BCAA and cardiovascular disease (CVD) was explored via mediation Mendelian randomization. Results: For every 1 g/day increment in the intake of isoleucine, leucine, and valine, there was a corresponding 30%, 11%, and 16% rise in the risk of hyper-LDL-cholesterolemia, respectively. The optimal cut-off values stood at 5.53, 6.40, and 4.18 g/day, respectively. Utilizing the inverse variance weighted method for estimation revealed that the total effect of BCAA on CVD was OR = 1.06 (95% CI: 1.02~1.11), with p = 0.005. The indirect effect, mediated by LDL-C, was OR = 1.02 (95% CI: 1.00~1.02), with p = 0.026. The direct effect was noted at OR = 1.05 (95% CI: 1.01~1.09), with p = 0.017. Conclusions: Dietary BCAAs are positively correlated with hyper-LDL-cholesterolemia in children and adolescents. LDL-C serve as a mediator of CVD caused by BCAAs. Full article

Background: Metabolic syndrome (MetS) is a set of cardiometabolic abnormalities, including central obesity, dyslipidemia, hypertension, and hyperglycemia, that substantially increases the risk of cardiovascular disease and type 2 diabetes. Marine-derived omega-3 polyunsaturated fatty acids (n-3 PUFAs), especially eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), may improve MetS components through triglyceride-lowering, anti-inflammatory, and insulin-sensitizing effects; however, randomized controlled trial (RCT) results remain inconsistent, and the influence of dose and intervention duration is unclear. Methods: Following PRISMA guidelines, PubMed, Embase, Scopus, and Web of Science were searched to June 2024 for RCTs in adults with MetS or its components. Eligible trials assessed marine-derived omega-3 supplementation (EPA/DHA) versus placebo or control and reported at least one MetS diagnostic criterion (triglycerides, HDL cholesterol, fasting plasma glucose, blood pressure, or waist circumference) or related parameter (LDL cholesterol, HOMA-IR, or HbA1c). Data were extracted in duplicate and quality assessed using the Cochrane Risk-of-Bias Tool. Trials were categorized by dose—low (<1000 mg/day), medium (1000–2000 mg/day), and high (>2000 mg/day)—and duration: short-term (ST; ≤8 weeks), medium-term (MT; >8–12 weeks), and long-term (LT; >12 weeks). Meta-regression using ordinary least squares estimated dose–duration effects. Publication bias was assessed with funnel plots and Egger’s test for outcomes with ≥3 studies. Results: Twenty-one RCTs (n ≈ 1950) were included. For triglycerides, the largest reductions occurred in the high-dose LT (−56.78 mg/dL ± 3.44) and ST (−50.873 mg/dL ± 3.04) groups, and MT duration (−41.536 mg/dL ± 4.12), showing that in high doses of omega-3, the beneficial effect of reducing TGs was more prominent in long-term and short-term treatment other than with medium-term duration of treatment. In comparison, the result for medium-dose with MT duration was (−24.93 mg/dL ± 0.464) and for LT duration was (−31.843 mg/dL ± 0.46), all p < 0.001. In LDL cholesterol, an increase in the low-dose ST group (+7.04 mg/dL ± 4, p < 0.001) and low-dose LT group (+35.525 mg/dL ± 4.33, p < 0.001) was observed. In other subgroups, either there were no data available or the number of studies was limited and could not be considered as statistically significant in meta-analysis due to low power. As for HDL cholesterol, FBS, SBP, DBP, waist circumference, BMI, and HOMA-IR, the data extracted from the included studies were not sufficient to be eligible for the meta-analysis. Conclusions: Marine-derived omega-3 supplementation produces substantial triglyceride reductions, especially at doses >2000 mg/day for ≥8 weeks. HDL cholesterol and blood pressure benefits are not consistent, fasting glycemia is largely unaffected, and LDL cholesterol may increase, especially in low doses. High-dose marine omega-3s can be considered as part of dietary strategies for MetS management, with monitoring for LDL changes. Standardized intervention protocols and long-term RCTs are needed to clarify dose and duration–response relationships. Full article

Background: Dyslipidaemia promotes atherosclerotic plaque formation. Plaques that are vulnerable to rupture have a higher proportion of inflammatory (M1:CD86) macrophages in their cap. Many plaque macrophages are derived from blood monocytes which have been exposed to elevated blood lipid levels. Here, we explored whether the inflammatory state of monocyte-derived macrophages is associated with blood lipid levels and assessed whether oxidised low-density lipoprotein (oxLDL) directly induces some of the observed changes. Method: Blood was collected from 20 individuals. Lipid profiles were measured, and monocytes differentiated into macrophages. Macrophage inflammatory state was assessed by flow cytometry for phenotypic markers (e.g., CD86 and CD163) and cytokine production: TNF, IL-1β, and IL-6. Furthermore, monocytes were isolated from 6 normo-lipidaemic individuals and cultured with oxLDL, followed by stimulation with LPS/IFNγ and assessment of the cytokine response. Results: The inflammatory phenotype acquired by macrophages (ex vivo) was related to levels of in vivo circulating lipids. Correlations for CD86/CD163 were found with CVD risk markers; most strongly with triglycerides (TG) and TG/HDL-C, but also with cholesterol/HDL-C and ApoB/ApoA1 and inversely with LDL particle size. Functionally, macrophage production of inflammatory cytokines (TNF and IL-1β) correlated with oxLDL levels and inversely with ApoA1. Macrophages differentiated from monocytes cultured with oxLDL produced significantly higher IL-1β but lower IL-10 (in response to LPS/IFNγ), compared to control cells. Conclusions: Monocyte-derived macrophages adopt an inflammatory phenotype relative to the levels of circulating lipid factors that are characteristic of atherogenic dyslipidaemia (such as high TG, TG/HDL-C and low LDL particle size), but not LDL-C. Full article

Neurotransmitters play a pivotal role not only in central nervous system signaling but also in the regulation of systemic energy metabolism, insulin sensitivity, and cardiovascular function. The contribution of neuroendocrine dysregulation to the development of type 2 diabetes mellitus (T2DM) is increasingly being recognized; however, the interplay between neurotransmitter levels and lipid/insulin resistance profiles in T2DM and prediabetes (PreDM) remains poorly characterized. We evaluated serum dopamine (DA), norepinephrine (NE), epinephrine (EPI), and serotonin (ST) in 110 individuals with PreDM (n = 40) or newly diagnosed T2DM (n = 70). Extended metabolic profiling included HbA1c, lipid panels, and insulin resistance indices (triglyceride-to-glucose index (TyG), TyG-derived indices). Neurotransmitter levels were compared across body mass index (BMI) categories, gender, and glycosylated hemoglobin A1c (HbA1c) quartiles. We applied multivariable linear regression (MLR) adjusted for body mass index (BMI), age, sex, lipids, penalized logistic regression (predicting T2DM status), and exploratory Spearman correlations with False Discovery Rate (FDR) correction. All four neurotransmitters were significantly higher in T2DM versus PreDM (p < 0.001). In T2DM patients, DA and NE levels increased across HbA1c quartiles, and NE levels were significantly higher in quartile 3 compared to quartile 2 (p = 0.045). In multivariable models, T2DM status was the only consistent predictor of neurotransmitter elevations. Logistic regression identified ST (OR = 8.70) and NE (OR = 3.76) as key discriminators of T2DM status, in addition to HbA1c. Exploratory correlation analyses in T2DM showed trends between EPI and insulin resistance indices (TyG adjusted for waist circumference (TyG-WC), TyG adjusted for waist-to-height ratio (TyG-WHtR)) and between DA and low-density lipoprotein cholesterol (LDL-C), although these did not survive to FDR correction. Neurotransmitter levels are elevated in T2DM and correlate with glycemic and metabolic profiles, suggesting early neuroendocrine involvement in the pathogenesis of diabetes. Serotonin and norepinephrine may serve as adjunctive biomarkers for disease stratification, meriting further prospective and mechanistic investigation. Full article

Background and Objectives: The comprehensive control of diabetes and its related comorbidities is essential to avoid diabetes complications and reduce diabetes care expenses. Nevertheless, several reports have uncovered a gap in diabetes management and confirmed suboptimal glycemic control globally. This study aims to assess metabolic control among patients with diabetes attending primary care clinics (PCCs) in Madinah, Saudi Arabia. Materials and Methods: This cross-sectional descriptive study took place in Madinah city, Saudi Arabia, in 15 primary care centers. A consecutive series of 692 adult diabetic patients who attended the clinics in one year were included. The primary outcome measures were achieving blood glucose, blood pressure, and lipids goals. The achievement of adequate metabolic control followed the American diabetes association (ADA) guidelines. Results: The majority (98%) of the patients had type 2 diabetes (T2DM) with a mean age of 55.1 ± 11.6 years and a mean diabetes duration of 11.02 ± 7.8 years. The mean HbA1c was 8.39 ± 1.7, and glycemic goals (HbA1C < 7%) were achieved in 15.7%. The achievement of LDL, triglyceride, and HDL goals were as follows; 46.4%. 53.3%, and 70.8%, respectively. In total 66.3% of subjects achieved systolic blood pressure goals, and 88.7% achieved diastolic blood pressure goals. Younger age, longer diabetes duration, and higher LDL levels were associated with poor glycemic control. Conclusions: Glycemic control is inadequate among patients with diabetes at PCCs in Madinah, Saudi Arabia. A patient-centered approach and individualized management plan considering all risk factors are required. Full article

This study investigates the protective effects and underlying mechanisms of Mao Jian Black tea ethanol extract (MJBT_EE) on a mouse model of acute alcohol-induced liver injury (ALI). The animal model was established using the NIAAA method, and C57BL/6 mice were divided into the following groups: negative control group (NC), model control group (MG), silibinin positive control group (SL, 54 mg/kg), and MJBT_EE high- and low-dose groups (40 mg/mL, 20 mg/mL). The results showed that, compared to the MG, MJBT_EE significantly reduced serum levels of ALT, AST, TC, TG, LDL-C, TBIL, ALP and inflammatory cytokines IL-6, TNF-α, and IL-1β (p < 0.01), while upregulating HDL-C (p < 0.01). It also enhanced the activity of hepatic antioxidant enzymes SOD and GSH (p < 0.01) and reduced MDA content (p < 0.01). Further histopathological examination of liver tissue revealed that MJBT_EE_H markedly alleviated hepatocellular hydropic degeneration, swelling, and steatosis. The mechanism of action of MJBT_EE_H primarily involved activation of the PI3K/Akt pathway and suppression of excessive p-NF-κB activation. These findings indicate that Maojian black tea ethanol extract exerts significant protective effects against alcohol-induced liver injury, potentially through improving lipid metabolism, reducing oxidative stress and inflammatory responses, and modulating the PI3K/Akt/NF-κB signaling pathway. Full article

Background: Coronary artery disease (CAD) and left-ventricular (LV) diastolic dysfunction are leading drivers of morbidity and mortality. Clarifying how anatomical CAD burden relates to diastolic impairment may refine diagnosis and risk stratification. Methods: We conducted a cross-sectional analytical study of 200 adults with intermediate pretest probability of CAD who underwent both coronary CT angiography (CCTA) and transthoracic echocardiography (TTE) within ≤1 year. Coronary burden was quantified by Segment Involvement Score (SIS). Diastolic function was graded by contemporary echocardiographic guidelines. Patients were classified as obstructive (≥50% LM or ≥70% in other major epicardial arteries) or non-obstructive CAD. Results: Obstructive CAD was present in 73/200 (36.5%). Diastolic dysfunction occurred in 161/200 (80.5%) and was markedly more prevalent/severe in obstructive vs. non-obstructive CAD (p < 0.001). SIS rose stepwise with higher diastolic dysfunction grades; SIS correlated strongly with diastolic grade (r = 0.809, p < 0.001). Compared with non-obstructive CAD, obstructive CAD showed worse diastolic indices (higher E/e′, larger LAVI, shorter DT and IVRT; all p < 0.001) and a shift toward Grades II–III. Obstructive CAD was also associated with higher total cholesterol, triglycerides, LDL, HbA1c, lower HDL (all p ≤ 0.002), and a greater prevalence of hypertension and diabetes. Discussion: Increasing coronary atherosclerotic burden—captured by SIS, parallels progressive impairment of LV relaxation and elevated filling pressures, supporting a pathophysiologic link between epicardial disease extent and diastolic dysfunction. Conclusions: In symptomatic intermediate-risk patients, greater CAD extent on CCTA is strongly associated with higher grades of LV diastolic dysfunction on echocardiography. Integrating anatomic (SIS) and functional (TTE) metrics may enhance risk assessment and guide management in CAD. Full article

Residual cardiovascular risk remains substantial despite widespread adoption of intensive lipid-lowering strategies—statins, PCSK9 inhibitors, and RNA-based agents—that achieve very low LDL-C and apoB levels. Over the past three years, converging epidemiologic and mechanistic evidence has highlighted emotional stress—including anger, grief, anxiety, and chronic psychosocial strain—as a biologically active determinant of atherosclerotic disease and a frequent trigger of acute events. We propose the Emotion–Lipid Synergy Model, in which lipid burden establishes the atherothrombotic substrate while emotion-driven autonomic and vascular perturbations amplify endothelial dysfunction, microvascular constriction, inflammation, and thrombogenicity—thereby widening the residual-risk gap even when lipid targets are met. From this perspective, prevention should evolve toward precision psychocardiology: systematically screening for distress and stress reactivity; leveraging wearables to detect high-risk emotional states; and delivering timely, scalable, just-in-time behavioral interventions alongside guideline-directed lipid management. Particular attention is warranted for women and patients with angina and no obstructive coronary disease, who appear disproportionately susceptible to mental-stress ischemia. We outline a research agenda—flagship outcomes trials, mechanistic studies, and multimodal phenotyping—and discuss implementation pathways that integrate emotion metrics into cardiac rehabilitation and routine care. Integrating emotion assessment and modulation with lipid control offers a pragmatic route to reduce residual risk and advance equitable, personalized cardiovascular prevention. Full article

Background: Cardiovascular disease (CVD) is the leading global cause of death and is shaped by interacting biological, environmental, lifestyle, and social factors. Traditional models often treat risk factors in isolation and may miss dependencies among exposures and biomarkers. Objective: To map interdependencies among environmental, social, behavioral, and biological predictors of CVD risk using Bayesian network models. Methods: A cross-sectional analysis was conducted using NHANES 2017–2018 data. After complete-case procedures, the analytic sample included 601 adults and 22 variables: outcomes (systolic/diastolic blood pressure, total/LDL/HDL cholesterol, triglycerides) and predictors (BMI, C-reactive protein (CRP), allostatic load, Dietary Inflammatory Index, income, education, age, gender, race, smoking, alcohol, and serum lead, cadmium, mercury, and PFOA). Spearman’s correlations summarized pairwise associations. Bayesian networks were learned with two approaches: Grow–Shrink (constraint-based) and Hill-Climbing (score-based, Bayesian Gaussian equivalent score). Network size metrics included number of nodes, directed edges, average neighborhood size, and Markov blanket size. Results: Correlation screening reproduced expected patterns, including very high systolic–diastolic concordance (p ≈ 1.00), strong LDL–total cholesterol correlation (p = 0.90), inverse HDL–triglycerides association, and positive BMI–CRP association. The final Hill-Climbing network contained 22 nodes and 44 directed edges, with an average neighborhood size of ~4 and an average Markov blanket size of ~6.1, indicating multiple indirect dependencies. Across both learning algorithms, BMI, CRP, and allostatic load emerged as central nodes. Environmental toxicants (lead, cadmium, mercury, PFOS, PFOA) showed connections to sociodemographic variables (income, education, race) and to inflammatory and lipid markers, suggesting patterned exposure linked to socioeconomic position. Diet and stress measures were positioned upstream of blood pressure and triglycerides in the score-based model, consistent with stress-inflammation–metabolic pathways. Agreement across algorithms on key hubs (BMI, CRP, allostatic load) supported network robustness for central structures. Conclusions: Bayesian network modeling identified interconnected pathways linking obesity, systemic inflammation, chronic stress, and environmental toxicant burden with cardiovascular risk indicators. Findings are consistent with the view that biological dysregulation is linked with CVD and environmental or social stresses. Full article

Background: Isorhamnetin (ISO), a dietary O-methylated flavonol, was evaluated for hypoglycemic activity and mechanism in a streptozotocin (STZ) model of type 1 diabetes. Methods: We conducted untargeted plasma metabolomics (ESI±), network integration and docking, and measured pancreatic PI3K, phosphorylated AKT, and COX-2; INS-1 β cells challenged with the PI3K inhibitor LY294002 were used to assess viability, intracellular ROS, and PI3K phosphorylation. Results: ISO lowered fasting glycemia, increased circulating insulin, improved dyslipidemia by reducing low-density lipoprotein cholesterol (LDL-C), and preserved islet architecture. Untargeted plasma metabolomics (ESI±) indicated broad remodeling with enrichment of arachidonic-, linoleic-, starch/sucrose- and glycerophospholipid pathways. Network integration and docking prioritized targets converging on PI3K/AKT and COX-2/eicosanoid signaling. Consistently, in pancreatic tissue, ISO increased PI3K, phosphorylated AKT, and reduced COX-2. In INS-1 beta cells challenged with the PI3K inhibitor LY294002, ISO improved viability, decreased intracellular ROS, and partially restored PI3K phosphorylation at 4 µM. Conclusions: Together, these data indicate that ISO exerts hypoglycemic effects while supporting β-cell integrity through activation of PI3K/AKT and tempering of COX-2–linked lipid-mediator pathways. ISO therefore emerges as a food-derived adjunct candidate for autoimmune diabetes, and the work motivates targeted lipidomics and in vivo pathway interrogation in future studies. Full article

Metabolic syndrome (MetS) is a complex condition characterized by a group of interconnected metabolic abnormalities. Due to its increasing prevalence, better predictive markers are needed. Therefore, this study aims to develop predictive models for MetS by integrating adipokines, metabolic and cardiovascular risk factors, and anthropometric indices. Data were collected from 381 subjects aged 20 to 59 years (242 women and 139 men) from Guadalajara, Jalisco, Mexico, who were classified as having MetS or non-MetS based on the ATP-III criteria. Four supervised machine learning models were developed—Logistic Regression (LR), Support Vector Machine (SVM), Random Forest (RF), and eXtreme Gradient Boosting (XGBoost)—and their performance was evaluated using the Area under the Curve (AUC), calibration curves, Decision Curve Analysis (DCA), and local interpretability analysis. The RF and XGBoost models achieved the highest AUCs (0.940 and 0.954). The RF and LR models were the best calibrated and showed the highest net benefit in DCA. Key variables included age, anthropometric indices (BRI and DAI), insulin resistance measures (HOMA-IR), lipid profiles (sdLDL-C and LDL-C), and high-molecular-weight adiponectin, used to classify the presence of MetS. The results highlight the usefulness of specific models and the importance of anthropometric variables, cardiovascular risk factors, metabolic profiles, and adiponectin as indicators of MetS. Full article

This study investigated the effects of asparagus powder supplementation on blood glucose regulation, insulin, lipid profile, and oxidative stress in overweight and obese individuals. Forty-four adults aged 18–59 years participated in a 12-week randomized controlled trial and were randomly assigned to receive either asparagus powder (40 mg/kg/day) or a placebo (maltodextrin, 40 mg/kg/day). Assessments included an oral glucose tolerance test (OGTT), fasting blood glucose (FBG), insulin, homeostasis model assessment of insulin resistance (HOMA-IR) and β-cell function (HOMA-B), lipid profile, and oxidative stress markers (malondialdehyde [MDA], protein carbonyl, and superoxide dismutase [SOD]). In the asparagus group, OGTT at 30 min and low-density lipoprotein cholesterol (LDL-C) significantly decreased, while SOD activity significantly increased (all p < 0.05). In contrast, the placebo group showed significant increases in OGTT at 30 min, insulin, HOMA-IR, HOMA-B, triglycerides (TG), the TG/high-density lipoprotein cholesterol (HDL-C) ratio, and the total cholesterol (TC)/HDL-C ratio (all p < 0.05). Between-group comparisons indicated that FBG, area under the BG curve at 30–120 min, TG, TG/HDL-C, and MDA levels were significantly lower in the asparagus group than in the placebo group (all p < 0.05), whereas OGTT, LDL-C, SOD activity, insulin, HOMA-IR, HOMA-B, and TC/HDL-C did not differ significantly. Other indices, including TC, HDL-C, and protein carbonyl, showed no significant within- or between-group differences. In conclusion, 12 weeks of asparagus powder supplementation partially improved glycemic control, lipid profile, and oxidative stress in overweight and obese individuals. These findings suggest a potential role of asparagus as a complementary nutritional strategy to reduce the risk of diabetes and cardiovascular disease in this population. Full article

Background/Objectives: The search for new bioactive molecules increasingly extends beyond conventional medicinal plants, highlighting the importance of exploring alternative botanical sources. Parasitic plants represent a promising but underexploited reservoir of pharmacologically relevant compounds. Cuscuta australis (CA), a parasitic species with a history of traditional use, remains poorly characterized. This study aimed to investigate its phytochemical composition and evaluate its antioxidant, anti-inflammatory, and hepatoprotective properties. Methods: The phytochemical profile of CA extract was characterized by LC-MS. Antioxidant capacity was assessed using DPPH and ABTS assays. In vivo hepatoprotection was evaluated in male rats subjected to CCl₄-induced hepatotoxicity and treated orally with CA (30 or 60 mg/kg body weight). Biochemical, lipid, oxidative stress, and histological parameters were determined. Molecular docking was conducted to predict the binding of major identified compounds against selected protein targets. Results: CA significantly and dose-dependently improved biochemical and histological markers. At 60 mg/kg, ALT, AST, ALP, and bilirubin were reduced by 32%, 33%, 63%, and 51%, respectively. Lipid metabolism was improved by decreased TC, TG, and LDL-C with increased HDL-C. Antioxidant defense was enhanced through elevated CAT, SOD, and GPx activities, accompanied by reduced MDA levels. TNF-α and IL-6 decreased by 48% and 53%, respectively. Histopathology confirmed hepatoprotection and reduced fibrosis. Docking studies revealed strong binding affinities (−7.07 to −19.20 kcal/mol) for several metabolites, notably quercetin glucoside, diosmetin glucoside, caffeic acid glucoside, feruloylquinic acid, and isorhamnetin glucoside, against CYP450, IL-2, TNF-α, and IL-6. Conclusions: These findings demonstrate that C. australis is a promising source of bioactive compounds with hepatoprotective, antioxidant, antihyperlipidemic, and anti-inflammatory effects, supporting its potential as a natural therapeutic agent. Full article

Cholesterol blood levels in low-density lipoproteins (LDLs) are a key parameter for assessing the risk of cardiovascular diseases. Direct quantification of LDL cholesterol at the point of care would be possible if all other lipoproteins, particularly the high-density lipoproteins (HDLs), could be removed prior to measurement. Here, we investigated whether a molecularly imprinted membrane (MIM) could be used for the solid-phase affinity extraction (SPAE) of HDL in a paper-based lateral flow test. Samples traveled by capillarity through the MIM before reaching a detection zone where LDL cholesterol was quantified enzymatically. MIMs were produced by impregnation of the membrane with a dispersion of molecularly imprinted polymers (MIPs) selective for HDL. MIPs were synthesized using precipitation polymerization and exhibited good selectivity for HDL compared with LDL and an uptake capacity of 5.0–7.0 µg of HDL-C/mg of MIP. The MIM enabled the removal of HDL with an efficiency of typically 68%. However, quantification of LDL cholesterol suffered from strong non-specific binding of LDL, likely due to its inherent colloidal instability. Overall, our results highlight the challenges associated with SPAE of colloidal particles. Furthermore, our study demonstrates a novel, efficient, and potentially generic modality to integrate SPAE into paper-based POC diagnostic tests. Full article

Background/Objectives: Ustekinumab (UST) and upadacitinib (UPA) are molecules that have been used in patients with ulcerative colitis (UC) since 2019 and 2022, respectively. Both agents are generally preferred for biologically experienced UC patients. However, the number of head-to-head studies comparing the efficacy and adverse events of UST and UPA in this patient group is limited. Methods: This was a retrospective cohort study evaluating the efficacy and safety of UST (n = 57) and UPA (n = 32) in biologically experienced UC patients during the induction and 24-week maintenance treatment periods. Most patients in both groups had received prior anti-TNF treatment (98.2% and 96.9%, respectively). Clinical response and remission rates were determined based on the partial Mayo score (PMS). Additionally, patients’ pre-treatment laboratory parameters were compared with their results at week 24. Results: During the induction phase, clinical response and remission were achieved in 84.2% and 43.9% of the UST group and 93.8% and 50% of the UPA group, respectively (OR [95% CI] = 2.81 [0.57–6.87] and 1.28 [0.54–3.05]). At week 24, the clinical response and remission rates in the UST and UPA groups were similar (77.1% vs. 80% and 58.3% vs. 63.3%, respectively). No statistically significant difference was found between the groups (p > 0.05). Both UST and UPA provided a marked reduction in fecal calprotectin and CRP levels. Regarding safety, UPA treatment led to increased total, LDL, and HDL cholesterol levels, whereas UST did not. In both groups, glucose; HbA1c; and thyroid, renal, and liver functions remained stable. No serious adverse events were observed in either group. At week 24, treatment continuation rates were 68.4% (n = 39) for UST and 78.2% (n = 25) for UPA (OR = 0.61 [0.22–1.66]). Conclusions: In biologically experienced ulcerative colitis, both UST and UPA are effective and safe treatment options. This study did not statistically demonstrate the superiority of UPA over UST. Given the preliminary nature and limited patient numbers of this investigation, our findings require confirmation through future multicenter, large-scale, and long-term prospective studies. Full article