The incidence of papillary thyroid cancer (PTC) has increased in recent years. To improve the diagnostic management of PTC, we propose the use of microRNAs (miRNAs) as a biomarker. Our aim in this study was to evaluate the miRNA expression pattern in PTC using NanoString technology. We identified ten miRNAs deregulated in PTC compared with reference tissue: miR-146b-5p, miR-221-3p, miR-221-5p, miR-34-5p, miR-551b-3p, miR-152-3p, miR-15a-5p, miR-31-5p, and miR-7-5p (FDR < 0.05; |fold change (FC)| ≥ 1.5). The gene ontology (GO) analysis of differentially expressed miRNA (DEM) target genes identified the predominant involvement of epidermal growth factor receptor (EGFR), tyrosine kinase inhibitor resistance, and pathways in cancer in PTC. The highest area under the receiver operating characteristic (ROC) curve (AUC) for DEMs was found for miR-146-5p (AUC = 0.770) expression, indicating possible clinical applicability in PTC diagnosis. The combination of four miRNAs (miR-152-3p, miR-221-3p, miR-551b-3p, and miR-7-5p) showed an AUC of 0.841. Validation by real-time quantitative polymerase chain reactions (qRT-PCRs) confirmed our findings. The introduction of an miRNA diagnostic panel based on the results of our study may help to improve therapeutic decision making for questionable cases. The use of miRNAs as biomarkers of PTC may become an aspect of personalized medicine.

The global increase in obesity is strongly associated with insulin resistance (IR) and related metabolic impairments. Asprosin (ASP), a glucogenic adipokine induced by fasting, has recently emerged as a potential biomarker of IR and abnormal body composition. However, its physiological role in obesity remains incompletely understood. To evaluate the associations between serum ASP levels, IR indices, oxidative stress markers (OS), liver function and inflammation parameters, and body composition in overweight and obese adults during a standardized 4-hour oral glucose tolerance test (OGTT). This cross-sectional study included 150 adults categorized by BMI into three groups: control (CG; BMI < 25 kg/m²), overweight (O1; BMI > 25 kg/m²), and obese (O2; BMI > 30 kg/m²). Participants underwent dual-energy X-ray absorptiometry (DXA), including visceral adipose tissue quantification, bioelectrical impedance analysis (BIA), and biochemical assessment. Measurements included serum ASP, C-peptide, HbA1c, lipid profile, total oxidative capacity (TOC), total antioxidative capacity (TAC), liver transaminases (ALT, AST) and C-reactive protein (CRP). IR was assessed using HOMA-IR, QUICKI, Matsuda Index, TyG, and the composite TyG-WHR index as a proxy for hepatic IR. ASP levels were significantly higher in O1 and O2 compared with CG (p < 0.001), and in O2 compared with O1 (p < 0.01). ASP positively correlated with fat mass, TOC, HOMA-IR, TyG, TyG-WHR, ALT, and CRP, and negatively with muscle mass, total body water, resting metabolic rate, QUICKI, and Matsuda Index (p < 0.05). ASP is strongly associated with IR and adverse metabolic profiles in obesity. Its preferential correlation with hepatic IR markers (TyG-WHR, ALT, CRP) and fat mass suggests that ASP may primarily reflect liver-specific metabolic dysfunction rather than peripheral IR. These findings highlight ASP as a promising biomarker and potential therapeutic target in obesity-related metabolic disease.

It is hypothesized that growth hormone deficiency (GHD) is associated with increased oxidative stress (OS), contributing to elevated cardiovascular risk. This preliminary study evaluates changes in OS markers and cardiovascular biomarkers in 15 adult patients with severe GHD undergoing 12 months of recombinant human growth hormone (rhGH) therapy. IGF-1 concentrations increased significantly following 6 and 12 months of therapy (p = 0.0003 and p = 0.0001, respectively). These changes were accompanied by a significant decrease in endothelin-1 (ET-1) levels at 12 months (p = 0.007), as well as reductions in asymmetric dimethylarginine (ADMA) levels at both 6 and 12 months (p = 0.01 for each timepoint). Total oxidative capacity (TOC) decreased significantly after 6 months of therapy (p = 0.02), followed by a significant increase at 12 months (p = 0.04), whereas total antioxidant capacity (TAC) showed a significant increase at 12 months (p = 0.02). Tissue fat % showed significant reductions at 6 months (p = 0.006), suggesting early improvements in body composition. Correlation analyses indicated negative associations between IGF-1 and TOC (p < 0.006; R = −0.73), and positive associations with TAC (p < 0.001; R = 0.83). These findings suggest that rhGH therapy in adult patients with severe GHD reduces OS and cardiovascular risk through the modulation of biomarkers and improved body composition. This study explores the role of rhGH therapy in reducing cardiovascular risks in GHD, emphasizing the importance of individualized treatment approaches.

Genetic predisposition, inflammation, and oxidative stress are known contributors to the development of Hashimoto's thyroiditis (HT). While genetic factors are non-modifiable, lifestyle, nutritional factors and oxidative stress may represent areas for intervention. This study aimed to assess biochemical markers of oxidative stress and evaluate dietary intake in women with newly diagnosed HT, identified through population-based screening. A cross-sectional analysis was conducted on 600 women aged 18-45 years, where 92 were diagnosed with euthyroid HT. Nutrients, based on a seven-day food diary, and biochemical evaluation, including thyroid autoantibodies (anti-thyroid peroxidase (ATPO) and anti-thyroglobulin (ATG)), metabolic parameters, and oxidative stress markers (total oxidative capacity (TOC), total antioxidant capacity (TAC), TOC/TAC ratio), were performed. Results revealed elevated TOC and TOC/TAC ratios in the HT group, suggesting oxidative stress despite preserved TAC. Dietary analysis showed significantly lower intake of cholesterol (p = 0.017) and retinol (p = 0.014) in the HT group. Additionally, negative correlations were observed between ATPO levels and dietary intake of vitamin E (r = -0.33; p < 0.01), vitamin C (r = -0.22; p = 0.05), and retinol (r = -0.23; p = 0.04). While ATG levels correlated negatively with HDL (r = -0.30; p = 0.01) and retinol (r = -0.23; p = 0.04). Additionally, TOC levels showed positive correlations with fasting insulin (r = 0.30; p = 0.01), triglycerides (r = 0.25; p = 0.04), and free triiodothyronine (FT3) (r = 0.28; p = 0.01) concentrations, suggesting potential links between oxidative stress, metabolic activity, and thyroid function. In conclusion, maintaining an adequate intake of antioxidant nutrients with limiting potentially pro-oxidative dietary factors, may represent a reasonable adjunctive approach in the dietary management of HT. Further research is needed to clarify the role of diet in modulating oxidative stress and immune activity in HT and to explore its potential as a supportive strategy in disease management.

Background: Adult growth hormone deficiency (GHD) is linked to increased cardio-vascular and metabolic risk due to oxidative stress (OS), endothelial dysfunction, and adverse body composition. Long-term systemic effects of recombinant human growth hormone (rhGH) therapy remain insufficiently defined. This study assessed the impact of 24-month rhGH replacement on OS, vascular markers, body composition, and bone mineral density (BMD) in adults with severe GHD. Methods: Fifteen adults with confirmed GHD received rhGH for 24 months. Serum insulin-like growth factor -1 (IGF-1), oxidized LDL (Ox-LDL), thioredoxin (Trx), 8-oxoguanine DNA glycosylase (OGG1), E-selectin, ICAM-1, and VCAM-1 were meas-ured at baseline, 12, and 24 months. Body composition and BMD were evaluated by DXA. Results: IGF-1 increased significantly at 12 and 24 months (p < 0.001). Ox-LDL decreased markedly (p < 0.00001), while Trx and OGG1 increased (p < 0.05). Levels of E-selectin, ICAM-1, and VCAM-1 declined, indicating improved endothelial function. Lean body mass and BMD (lumbar spine and femoral neck) increased, whereas body fat percentage decreased. Lipid profiles were unchanged. Significant correlations were observed be-tween vascular markers and adiposity, and between BMD, triglycerides, and IGF-1. Conclusion: A 24-month rhGH therapy improves redox balance, vascular function, and body composition in adults with severe GHD, supporting the use of redox and vascular biomarkers to monitor treatment efficacy.

Adult growth hormone deficiency (GHD) is linked to increased cardiovascular and metabolic risk due to oxidative stress (OS), endothelial dysfunction, and unhealthy body composition. Long-term systemic effects of recombinant human growth hormone (rhGH) therapy remain insufficiently defined. This study assessed the impact of 24-month rhGH replacement on OS, vascular markers, body composition, and bone mineral density (BMD) in adults with severe GHD. Fifteen adults with confirmed GHD received rhGH for 24 months. Serum insulin-like growth factor 1 (IGF-1), oxidized LDL (Ox-LDL), thioredoxin (Trx), 8-oxoguanine DNA glycosylase 1 (OGG1), E-selectin, intercellular adhesion molecule 1 (ICAM-1), and vascular cell adhesion molecule 1 (VCAM-1) were measured at baseline and 12 and 24 months. Body composition and BMD were evaluated by DXA. IGF-1 increased significantly at 12 and 24 months (p < 0.001). Ox-LDL markedly decreased (p < 0.00001), while Trx and OGG1 increased (p < 0.05). Levels of E-selectin, ICAM-1, and VCAM-1 declined, indicating improved endothelial function. Lean body mass and BMD increased, while body fat parameters showed heterogeneous changes. Lipid profiles were unchanged. Significant correlations were observed between vascular markers and adiposity, and between BMD, triglycerides, and IGF-1. A 24-month course of rhGH therapy improves redox balance, vascular function, and body composition in adults with severe GHD, supporting the use of redox and vascular biomarkers to monitor treatment efficacy.