Universal Scientific Education and Research Network

The aim of this systematic review and meta-analysis was to evaluate comprehensively the therapeutic potential of Abelmoschus esculentus (okra) supplementation across the diabetes spectrum of key metabolic risk factors. A search was conducted in PubMed, Scopus, Web of Science, EMBASE and the Cochrane Library, up to 23 July 2025, to identify randomized controlled trials evaluating the effects of okra supplementation on metabolic risk factors in diabetes. Fourteen randomized controlled trials published between 2020 and 2025, including a total of 836 participants, were analysed. Okra supplementation led to significant reductions in 2h postprandial glucose [weighted mean difference (WMD)=-22.39mg/dL, 95% confidence interval (CI): -41.39 to -3.38; P=0.021], fasting blood sugar (WMD=-23.66mg/dL, 95% CI: -34.20 to -13.12; P<0.001), glycosylated haemoglobin (WMD=-0.30%, 95% CI: -0.59 to -0.02; P=0.034), homeostatic model assessment for insulin resistance (WMD=-0.59 units, 95% CI: -1.01 to -0.18; P=0.005), low-density lipoprotein cholesterol (WMD=-8.55mg/dL, 95% CI: -14.42 to -2.68; P=0.004) and total cholesterol (WMD=-12.58mg/dL, 95% CI: -22.78 to -2.37; P=0.016) levels. The certainty of evidence was very low for most outcomes, except for diastolic blood pressure and glycosylated haemoglobin, which were rated as low. Regarding methodological quality, six trials were rated as good, two as fair and six as poor. Okra supplementation might improve glycaemic control and lipid profiles, indicating its potential as a complementary approach in diabetes management. Despite limitations from small and heterogeneous trials, these findings support future research on optimal dosing, safety and personalized applications in metabolic disease management.

GSK-3β is an important therapeutic target in Alzheimer's disease due to its central role in tau hyperphosphorylation, and synaptic dysfunction. In this study, a κ-casein-derived peptide (LALTLPFLGA) was identified via HADDOCK and introduced to MD simulations for MM/PBSA per-residue analysis, revealing four unfavorable mutation sites (L12, L14, T15, F18). Using MCSM and ΔΔG-based substitution, a 48-peptide library was generated; 22 candidates satisfied toxicity/allergenicity filters. Docking and MD simulations prioritized four leads-PEP8, PEP36, PEP40, and PEP44-with PEP8 (- 89.1kcal·mol⁻¹) and PEP44 (- 88.4kcal·mol⁻¹) as top binders. These mutants, all carrying L12H/L14H substitutions, demonstrated stronger HADDOCK scores (- 89.1 to - 84.6kcal/mol) compared with the template. Additionally, PEP8 carried F18→Asp, and T15→Leu/Ile developed affinity in other mutants. PEP8 established 21 contacts, followed by PEP44 (19), PEP40 (17), and PEP36 (15), indicating that larger interaction networks are vital for binding. PEP8 contacted with the ATP-binding pocket (Val135, Thr138, and Tyr134), whereas PEP44 contacted catalytic Asp200. MD results also showed reduced RMSD, slightly lower Rg/SASA, and tighter PCA clustering, exhibiting that PEP8 and PEP44 induced compaction and restricted conformational freedom, and possibly, hindering substrate binding. MMPBSA confirmed PEP44 and PEP8 as strongest complexes (- 188.482 and - 184.404kJ/mol), governed by van der Waals and electrostatic contacts, while PEP36 suffered solvation penalties and PEP40 remained hydrophobic-driven. Together, our computational pipeline highlights PEP8 and PEP44 as promising κ-casein-derived inhibitors of GSK-3β, illustrating a rational design of food-derived peptides as potential multifunctional candidates for Alzheimer's disease.

Colorectal cancer (CRC) is a genetically varied malignancy noted for its metabolic flexibility, which enables cancer cells to adapt to different energy sources. Beta-hydroxybutyrate (BHB), a significant ketone body that is elevated during ketogenic diets, has attracted considerable attention for its potential therapeutic benefits. ​However, recent evidence indicates that BHB may paradoxically facilitate the advancement of CRC by acting as an alternative energy source, especially in cancer cells with mutations in critical genes such as APC, KRAS, and TP53. This review investigates the mechanisms through which CRC cells utilize BHB for their survival, focusing on enhanced metabolic plasticity, resistance to apoptosis, and modified responses to chemotherapy and immunotherapy. It also explores the interaction between BHB and the tumor microenvironment (TME), emphasizing how BHB can influence immune responses and tumor progression. Given the complexity of BHB’s role in CRC, the review underscores the necessity for personalized approaches that consider the tumor’s genetic and metabolic characteristics. Understanding the dual role of BHB in CRC is essential for devising more effective therapeutic strategies that can either harness or counteract its effects, thereby guiding the application of ketogenic diets and other metabolic interventions in the treatment of CRC.

The evidence considering the potential protective impact of statins on the mortality rate caused by colorectal cancer (CRC) is controversial. This study aimed to systematically assess the effect of statins on the survival rate of CRC patients. A comprehensive search was conducted in Scopus, PubMed, and Web of Science to assess the relationship between statin consumption and cancer-specific mortality (CSM), all-cause mortality (ACM), disease-free survival (DFS), and recurrence-free survival (RFS). Subgroup analyses were performed to assess data stratified by country, study design, disease stage, time to use, CRC, and treatment type due to high heterogeneity. Thirty-two studies were included; the data of 24 articles composed the meta-analysis. Statins improved prognosis of CRC, particularly in lower ACM (HR: 0.80; 95% CI: 0.74-0.87) with I²=90%, P-value < 0.01, and lower CSM (HR: 0.74; 95% CI: 0.67-0.82) with I²=88%, P-value < 0.01 when compared to non-users. Both pre- and post-diagnostic statin use were linked to lower ACM and CSM, though high heterogeneity was observed across studies. However, the results for statin use on RFS indicated an HR of 1.01 with 95% CI of 0.94 to 1.09 (I² = 0% and P-value = 0.93). Additionally, for DFS, the HR was 0.93 (95% CI: 0.85-1.01) with I² = 47%, suggesting no meaningful effect of statin use on DFS. No significant publication bias was found. Statin use was associated with a reduction in ACM and CSM in CRC patients. However, the variances in RFS and DFS were not statistically significant. However, these findings should be interpreted cautiously due to substantial heterogeneity among some included studies.

To assess the diagnostic performance of different quantitative ultrasound elastography (USE) parameters in differentiating five stages of diabetic kidney disease (DKD) from each other as well as from healthy participants and type 2 diabetic patients without nephropathy. The protocol was pre-registered at https://osf.io/dfu8b/ . Using PubMed, Web of Science, Embase, and Cochrane Library, we found studies up to October 10, 2023. Risk of bias was assessed using Quality Assessment of Diagnostic Accuracy Studies-2 (QUADAS-2). The USE parameter of cortical stiffness was compared in an inter-stage manner based on mean differences, standardized mean differences, and ratios of means. In addition, cortical stiffness was evaluated for its diagnostic accuracy in staging DKD. Sensitivity and publication bias analyses were also conducted. Certainty of evidence was assessed using Grading of Recommendations, Assessment, Development, and Evaluation (GRADE). Eighteen studies were included with 2814 participants. The mean stiffness value consistently increased with the progression of the disease. Differentiation of five stages of DKD from two non-DKD groups, respectively, showed sensitivity, specificity, positive likelihood ratio, negative likelihood ratio, diagnostic odds ratio, and area under curve of 79%, 83%, 4.70, 0.25, 18.68, and 0.88. These values for differentiation of stages 3 to 5 of DKD from the other four milder groups were 80%, 79%, 3.85, 0.25, 15.53, and 0.87, respectively. USE shows promise as a noninvasive, simple, and quantitative diagnostic tool for staging DKD, especially in its early stages. With standardized protocols, its application could benefit patient management by enhancing the accuracy of DKD staging.

BackgroundAerobic exercise improves fitness but can induce oxidative stress, muscle damage, and inflammation. Sesame (Sesamum indicum L.), rich in lignans and antioxidants, may help reduce these effects and support immune function.AimThis systematic review examines the synergistic effects of sesame supplementation and aerobic exercise on oxidative stress, muscle damage, immune response, and inflammatory markers in athletes.MethodsFollowing PRISMA guidelines, a systematic search of PubMed, Scopus, Web of Science, CENTRAL, and EMBASE was conducted up to September 2024. Eligible randomized controlled trials included semiprofessional athletes receiving sesame supplementation (oil, extract, capsule, or whole seed) for ≥4 weeks, with placebo or no-supplement comparators under identical training protocols. Primary outcomes assessed oxidative stress biomarkers, muscle damage markers, inflammatory cytokines, and immune response parameters.ResultsA total of 290 studies were initially identified, with four randomized controlled trials meeting the inclusion criteria after screening. These trials, spanning 4-10 weeks with a total of 140 participants, revealed that sesame supplementation significantly enhanced antioxidant defenses, as indicated by increased levels of glutathione peroxidase (GPx), superoxide dismutase (SOD), and vitamins A, C, and E, while reducing oxidative stress markers such as malondialdehyde (MDA). Additionally, the combination of aerobic exercise and sesame improved anti-inflammatory markers, including a reduction in interleukin-6 (IL-6) and interleukin-1β (IL-1β), though cytokine modulation appeared to be primarily attributable to exercise alone.ConclusionThese findings highlight the potential of sesame supplementation as a natural adjunct to exercise regimens in mitigating oxidative and inflammatory stress, with implications for enhancing athletic performance and recovery.

Childhood obesity and dental caries are among the most prevalent chronic conditions, but their biological interplay remains poorly understood. This study aimed to investigate the associations between childhood obesity, salivary adiponectin levels, and dental caries. In this comparative cross-sectional study, 120 children aged 7–12 years were recruited and classified into two groups: Group 1 (body mass index (BMI) percentile < 85; underweight or normal-weight, n = 60) and Group 2 (BMI percentile ≥ 85; overweight or obese, n = 60). The dental caries experience was recorded using WHO criteria for primary (dmft) and permanent (DMFT) scores. Unstimulated whole saliva samples were collected, processed, and analyzed for adiponectin concentrations using an ELISA assay. Dietary behaviors (sugar intake, consumption of acidic or pickled foods, and dairy intake) and oral hygiene practices were assessed. Student t-test, Mann-Whitney test, Spearman’s correlations, and multivariable linear regression were conducted. Overweight/obese children exhibited significantly lower salivary adiponectin levels (2.49 ± 0.39 vs. 2.84 ± 0.43 ng/mL; P < 0.001) compared to their normal-weight peers and significantly lower total dental caries scores compared with normal-weight peers (5.05 ± 2.46 vs. 7.37 ± 3.25; P < 0.001). Salivary adiponectin was inversely correlated with BMI (Spearman’s correlation coefficient (ρ) = −0.39) and dental caries (ρ = 0.14). Obese children showed lower salivary adiponectin levels but unexpectedly had lower dental caries scores than their normal-weight peers. These findings reinforce the multifactorial nature of pediatric oral health and highlight the need to integrate metabolic, behavioral, and environmental factors into preventive strategies.Supplementary InformationThe online version contains supplementary material available at 10.1038/s41598-025-33579-2.