Serum levels of adipokines in women with cervical cancer

Cervical cancer remains one of the most common malignancies among women worldwide and represents a major public health problem. Adipose tissue functions as an active endocrine organ that secretes biologically active molecules known as adipokines, including leptin and adiponectin. These mediators regulate important physiological processes such as inflammation, immune response, angiogenesis, and cell proliferation. Dysregulation of adipokine secretion has been associated with tumor development and progression in several malignancies. Therefore, evaluation of adipokine levels in women with cervical cancer may provide insight into the metabolic mechanisms involved in tumor progression.

Aim: The aim of this study was to evaluate serum levels of leptin and adiponectin in women with cervical cancer and to determine their association with disease stage.

Materials and Methods. The study included women diagnosed with cervical cancer and a control group of healthy individuals. Venous blood samples were collected from all participants, and serum adipokine levels were measured using enzyme-linked immunosorbent assay (ELISA).

Results. Significant differences in adipokine levels were observed between patients with cervical cancer and healthy controls. Serum leptin levels were significantly higher in patients than in the control group (32.8 ± 6.4 ng/mL vs 18.5 ± 4.2 ng/mL, p < 0.001). In contrast, adiponectin concentrations were significantly lower in patients (5.9 ± 1.3 μg/mL vs 9.8 ± 2.1 μg/mL, p < 0.001). Stage-based analysis showed that leptin levels increased with disease progression, reaching 38.6 ± 5.8 ng/mL in stage III compared with 27.4 ± 4.9 ng/mL in stage I (p = 0.009). Conversely, adiponectin levels decreased as the disease advanced (4.8 ± 1.1 μg/mL in stage III vs 6.7 ± 1.4 μg/mL in stage I, p = 0.043).

Conclusion. Cervical cancer is associated with significant alterations in adipokine balance. Increased leptin and decreased adiponectin levels may reflect metabolic and inflammatory mechanisms contributing to tumor progression.