Adipokine, endocrine, and fibrinolysis-related alterations across abdominal obesity and metabolic syndrome phenotypes in young adults.

Background Abdominal obesity in young adults may reflect a biologically active metabolic phenotype, even before full metabolic syndrome develops. However, how endocrine, adipokine, insulin-resistance, and fibrinolysis-related biomarkers vary across early metabolic phenotypes remains incompletely understood. This study examined whether selected circulating biomarkers differ among normal-weight controls, young adults with abdominal obesity, and those with metabolic syndrome. Methods This cross-sectional secondary biomarker analysis included 175 young adults aged 19-21 years who were classified according to International Diabetes Federation criteria as controls (n = 106), abdominal obesity (n = 37), or metabolic syndrome (n = 32). Fasting insulin, HOMA-IR, cortisol, 25-hydroxyvitamin D, leptin, adiponectin, the adiponectin/leptin ratio (A/L ratio), ghrelin, and plasminogen activator inhibitor-1 (PAI-1) were analyzed. Between-group differences were assessed using nonparametric tests, ordered trends were evaluated across the phenotype gradient, sensitivity analyses were adjusted for sex, smoking status, and physical activity, and penalized logistic regression was used to explore biomarker associations with abdominal obesity and metabolic syndrome. Results Insulin, HOMA-IR, cortisol, leptin, and PAI-1 showed positive ordered phenotype-related patterns, whereas ghrelin, adiponectin, and the A/L ratio showed negative ordered patterns. Vitamin D concentrations were lower in the abdominal obesity and metabolic syndrome groups than in controls. The strongest between-group effects were observed for PAI-1, cortisol, ghrelin, adiponectin, and the A/L ratio. Overall group effects remained significant after adjustment and false discovery rate correction. In mutually adjusted penalized models, the A/L ratio remained associated with abdominal obesity, whereas PAI-1 remained associated with metabolic syndrome. Conclusion Young adults with abdominal obesity showed measurable endocrine, adipokine, insulin-resistance, and fibrinolysis-related alterations, including those who did not meet criteria for metabolic syndrome. The A/L ratio and PAI-1 may provide complementary information, with the A/L ratio more closely associated with abdominal obesity and PAI-1 more closely associated with metabolic syndrome in exploratory models. These findings support further evaluation of phenotype-based biomarker profiling for characterizing early cardiometabolic dysregulation in young adults and should be confirmed in larger, sex-balanced cohorts.