Purpose: We unravel the effect of anthocyanin-containing purple sweet potato synbiotic yogurt (PSPY) on 3T3-L1 adipocyte differentiation and its fundamental molecular mechanisms. Methods: Molecular docking simulation was performed to observe and identify the affinity and interaction between bioactive compounds and targeted proteins. MDI (isobutylmethylxanthine, dexamethasone, and insulin)-containing medium, a cocktail that stimulates adipogenesis, was used in this study. The toxic effect possibility of the yogurt product was evaluated using 3-[4, 5-dimethylthiazol-2-yl]-2.5 diphenyl tetrazolium bromide (MTT) assay. A 0.25%, 0.5%, 1%, and 5% (v/v) plain or purple sweet potato yogurt supernatant was given to 3T3-L1 preadipocyte culture medium from 24 h after seeding until day 11 of MDI-induced differentiation. The mRNA expression and lipid accumulation were analyzed using RT-qPCR and Oil red O staining, respectively, on day 11 after differentiation induction. Results: In silico study suggested that anthocyanin-derived compounds have the potential to inhibit peroxisome proliferator activated receptor gamma (PPAR-γ), a master regulator for white adipogenesis. Anthocyanin-containing PSPY significantly suppressed the expression of Pparg, Adipoq, Slc2a4, and Pgc1a. PSPY significantly suppressed Pparg with 1% and 5% concentrations, while with a concentration of 0.25%, PSPY significantly suppressed Adipoq expression as compared to control. Significant inhibition of Slc2a4 and Pgc1a was observed starting from a 0.25% concentration of PSPY. The suppression of adipogenic genes was also observed with the treatment of plain yogurt; however, the effects were relatively lower than the PSPY. The group treated with 1% and 5% of PSPY also showed inhibition effects on lipid accumulation. Conclusion: This study demonstrated PSPY inhibition effect on white adipocyte differentiation through suppression of Pparg and its downstream genes, Adipoq and Slc2a4, indicating the potential of this yogurt as a functional food for obesity management and prevention.

Background: Adipokines are dysregulated in obesity and exacerbate proinflammatory conditions. Although several studies have investigated adipokine levels in obesity, their findings have been inconsistent, leaving the precise nature of these alterations uncertain. This systematic review and meta‐analysis aimed to provide an updated overview of circulating adipokines, particularly adiponectin, leptin, fibroblast growth factor 21 (FGF21), growth differentiation factor 15 (GDF15), interleukin‐6 (IL‐6), and tumor necrosis factor‐α (TNF‐α) in the context of obesity. Methods: This study adhered to the Preferred Reporting Items for Systematic Reviews and Meta‐Analyses guidelines and PROSPERO registration (CRD42024525103). PubMed/MEDLINE, Scopus, and Journal of Clinical Investigation databases were searched from inception to August 25, 2025. Eligible observational studies were assessed using the ROBINS‐I and GRADE frameworks. Standardized mean differences (SMDs) were calculated using a random‐effects model. Results: From 2378 records, 30 and 16 studies were included in the review and meta‐analysis, respectively. Adiponectin levels were significantly lower in persons with obesity than in those with normal weight ( p = 0.007). Conversely, leptin, TNF‐α, and FGF21 levels were significantly higher in persons with obesity ( p < 0.01). No significant differences were found for GDF15 ( p = 0.62) and IL‐6 ( p = 0.17). Conclusions: Adiponectin, leptin, TNF‐α, and FGF21 show consistent directionality and may serve as robust biomarkers in obesity‐related risk profiling. Conversely, GDF15 and IL‐6 exhibit context‐dependent variability. Further prospective cohort studies are warranted to better understand these adipokines, as persons with normal weight may still be at a high risk of cardiometabolic diseases.

Background. Leprosy is a chronic infectious disease for which effective therapy has been long since invented. Thus, the morbidity has been decreased as technology has advanced, but the permanent disability has continuously generated stigma for centuries. The stigma causes the emergence of a poor psychological impact on people with leprosy (PwL). These impacts make new PwL reluctant to get appropriate therapy for their initial symptoms and are, thus, troublesome in accomplishing the goals of the leprosy elimination program. The aim of this review is to provide the history of psychological impact amongst PwL in countries across the globe. Methods. This is a literature review study. A keyword‐based search was conducted in digital libraries. Articles reporting on PwL’s psychology and related issues, such as quality of life, opportunity of building a marriage, and getting hired, were included. The data were presented based on a leprosy history timeline with cutoff points, namely, the invention of promin (1941) and multidrug treatment (1970). Results. In total, 38 studies were included in this review. These studies showed that PwL’s knowledge towards leprosy has been increasing; nevertheless, their attitude is still lacking. The emotional response was described by various negative feelings that had persistently occurred. These poor psychological impacts were followed by poor treatment‐seeking behavior and resulted in low quality of life. Conclusions. From year to year, the PwL’s knowledge about leprosy has been getting better; nevertheless, their attitude towards the disease is still poor. The emotional response, social participation, and quality of life of PwL are persistently poor due to the persistent stigma.

Background: Metabolic syndrome (MetS) is a risk factor for cardiovascular disease and is linked to obesity. Subjects with MetS who have normo-weight potentially show higher mortality and morbidity. Purpose: This study aims to reveal the critical essential metabolic parameters associated with endothelial dysfunction in MetS subjects with normo-weight compared to obese. Patients and Methods: The study was designed using a case–control approach. Ninety-nine MetS subjects (34 Normo-weight and 65 obese) from the urban population were enrolled in this study. The components of MetS are based on NCEP/ATP III criteria. Asymmetric dimethylarginine (ADMA) and vascular cell adhesion molecule 1 (VCAM-1) as markers for endothelial dysfunction were measured in both groups. Results: Fasting blood glucose (FBG) levels were higher in the normo-weight group (143.38 ± 79.8 mg/dL) compared to the obese group (120.89 ± 46.5 mg/dL). High-density lipoprotein cholesterol (HDL-c) levels in the normo-weight group were lower (42.82 ± 10.1 mg/dL) compared to obesity (45.74 ± 9.3 mg/dL), while triacylglycerol (TAG) levels were higher in the obese (197.25 ± 110.5 mg/dL) compared to the normo-weight group (167.03 ± 98.4 mg/dL), although the differences were statistically not significant (all p > 0.05). The difference between ADMA and VCAM-1 levels was statistically not significant in both groups. Correlation between MetS components with endothelial dysfunction parameters shows that metabolic parameters correlate strongly. Interestingly, a stronger correlation between FBG and ADMA was observed in normo-weight (r = 0.519) compared to obese groups (r = 0.445). In addition, TAG consistently shows a significant correlation with ADMA and VCAM-1 in normo-weight groups. Conclusion: Metabolic parameters, especially FBG and TAG, correlate strongly with endothelial dysfunction parameters in normo-weight subjects with metabolic syndrome.

Atherosclerosis is one of the most dominant pathological processes responsible in cardiovascular diseases (CVD) caused by cholesterol accumulation accompanied by inflammation in the arteries which will subsequently lead to further complications, including myocardial infarction and stroke. Although the incidence of atherosclerosis is decreasing in some countries, it is still considered the leading cause of death worldwide. Atherosclerosis is a vascular pathological process that is chronically inflammatory and is characterized by the invasion of inflammatory cells and cytokines. Many reports have unraveled the pivotal roles of epigenetics such as DNA methylation, post-translational histone modifications, and non-coding RNAs (ncRNAs) in atherogenesis, which regulate the expression of numerous genes related to various responsible pathways. Many studies have been conducted to develop new therapeutical approaches based on epigenetic changes for combating atherosclerosis. This review elaborates on recent updates on the development of new atherosclerosis drugs whose mechanism of action is associated with the modulation of DNA methylation, posttranslational histone modifications, and ncRNA-based gene regulation.