Circulating Myonectin and Oxytocin Levels in Pediatric Obesity: A Comparative Study
Muammer Buyukinan1, Ummugulsum Can2, Zafer Bagci3
1Department of Pediatric Endocrinology, Medical Faculty, Selcuk University, Konya 42130, Turkey.
None:
Background/Objectives: The development of obesity is not only related to excessive adipose tissue accumulation but also involves complex inter-organ signaling pathways linking skeletal muscle and neuroendocrine systems. The present study aimed to evaluate circulating levels of myonectin (CTRP15), a skeletal muscle-derived metabolic regulator, and oxytocin, a neuropeptide with anorexigenic properties, in children with obesity. In addition, we examined the potential associations of these biomarkers with insulin resistance and metabolic risk indicators. Methods: This cross-sectional study included 53 children with obesity (body mass index standard deviation score [BMI-SDS] > 2) and 37 healthy children with normal body weight serving as controls. Anthropometric parameters, fasting glucose, insulin, lipid profile, and the Homeostasis Model Assessment of Insulin Resistance (HOMA-IR) index were assessed in all participants. Circulating concentrations of myonectin and oxytocin were measured and compared between groups, and correlations with metabolic variables were explored. Results: Children with obesity exhibited a less favorable metabolic profile characterized by higher HOMA-IR values, hyperinsulinemia, and elevated triglyceride levels. Serum myonectin concentrations were significantly lower in the obesity group compared with controls (4.01 ± 3.66 vs. 8.35 ± 12.00 ng/mL; p = 0.019). In contrast, circulating oxytocin levels were significantly higher among children with obesity (median [IQR] 156.2 [83.9-754.9] vs. 141.7 [47.7-221.5] pg/mL; p = 0.044). Neither hormone demonstrated a significant linear relationship with age, BMI-SDS, or HOMA-IR. Conclusions: Our findings indicate that childhood obesity is associated with reduced circulating myonectin levels and increased oxytocin concentrations. These observations suggest potential alterations in both muscle-derived metabolic signaling and neuroendocrine regulation in pediatric obesity. However, due to the cross-sectional design of the present study, causal relationships cannot be established.
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