Keyword: leptin

Exploratory results of circulating chemerin testing in humans

Objective: Currently, the global epidemiologic impact of obesity requires continuous seeking of practical biomarkers; hence, this current study aimed to address the gap of chemerin assays in obese versus non-obese females and to analyze its circulating levels in relationship with the glucose profile and other circulating adipokines. Methods: This is an exploratory, prospective, cross-sectional analysis in females aged between 50 and 80 years. We excluded individuals with diabetes, cancers, endocrine, kidney, cardiovascular, and bone conditions. Enzyme-linked immunosorbent assay-based circulating adipokines testing was performed. The final analysis was focused on circulating chemerin (ng/mL) in the obese [body mass index (BMI) ≥ 30 kg/sqm] versus non-obese (BMI < 30 kg/sqm) group. Results: The obesity (N=12) versus the non-obesity (N=12) group showed a statistically significantly higher HOMA-IR (p=0.04), fasting insulin (p=0.01), but similar circulating chemerin. Chemerin positively correlated with BMI only in the obesity group (r=0.881, p=0.0039), but not with patients’ age and glucose profile-based features in any group. Chemerin showed a statistically significant positive, strong correlation with VEGF-A level (r=0.857, p=0.0065) and an inverse statistically significant strong association with circulating leptin (r= -0.713, p=0.0092) and circulating IL-12 p40 (r= -0.829, p=0.0416) in the obesity group. Conclusion: As a potential hypothesis-generating analysis, this pilot study showed different statistical results in BMI-based groups, despite the fact that direct comparison of circulating chemerin and even leptin, VEGF-A, and IL-12 p40 did not reach between-group statistical significance. A larger sample size and a multimodal integration of the adipokines panel might serve for practical points in addressing obesity. Citation: Schipor SV, Manda D, Ciobica ML, Sima OC, Preda EM, Ciuche A, et al. Exploratory results of circulating chemerin testing in humans. R. J. Mil. Med. 2026, CXXIX(4): 404-412 https://doi.org/10.55453/rjmm.2026.129.4.6 Academic Editor: Raluca Mititelu

Salivary Investigation of the Complex Relationship between NLRP3 Inflammasome, Leptin and Total Antioxidant Capacity in the Context of Periodontal Disease

Periodontal disease is a chronic pathology, resulting from the action of microbial communities that become dysbiotic, accompanied by immune response impairment in periodontal tissues, leading to an inflammatory process that promotes progressive tissue destruction. Abnormal activation of nucleotide-binding oligomerization domain (NOD-), leucine-rich repeat (LRR-), and pyrin domain (PYD)-containing protein 3 (NLRP3) promotes chronic inflammation. Research shows that leptin and oxidative stress (OS) are involved in the activation of the inflammatory pathways, including the activation of the NLRP3 inflammasome. In this context, the main objective of our study was to determine the levels of the NLRP3, leptin, and total antioxidant capacity (TAC) in the saliva of patients with periodontal disease. The present cross-sectional study included 44 patients with periodontitis, while the control group was represented by 19 clinically and biologically healthy adults. Saliva samples were collected from all participants in the study, and salivary levels of NLRP3, leptin, and TAC were determined using the Enzyme-linked immunosorbent assay (ELISA) and commercial kits. The results show that NLRP3 had statistically significantly increased levels in the study group versus the control group (p< 0.00001). Although TAC was also increased in the patients compared to the healthy subjects (p=0.491), no statistically significant differences were found. On the other hand, leptin levels were significantly lower in periodontitis patients compared to the control group (p< 0.00001). The results obtained in the present study are promising, but further studies are needed to obtain a more comprehensive understanding of the complex molecular mechanisms underlying periodontal disease.