Key result
Central obesity in PCOS is linked to ~75% higher sE-selectin levels, driven by fasting insulin.
Why the study?
PCOS is commonly linked with insulin resistance and early cardiovascular dysfunction, but immune and endothelial responses reflected by markers like sCD40L and sE-selectin require evaluation.
Do biomarkers of immune activation (sCD40L) and endothelial activation (sE-selectin) exhibit differential associations with insulin resistance in women with PCOS stratified by central obesity?
Cross-Sectional (n=80)
No
Do biomarkers of immune activation (sCD40L) and endothelial activation (sE-selectin) exhibit differential associations with insulin resistance in women with PCOS stratified by central obesity?
Absolute Event Rate: 72.93% vs 41.7%
p-value: p=0.001
In women with PCOS, insulin resistance is strongly associated with endothelial activation (sE-selectin), while immune activation (sCD40L) shows an inverse relationship with fasting glucose, highlighting divergent cardiometabolic pathways.
Captured external expert commentary on this paper, strongest first. Original sources are linked where available.
“The manuscript written by Daniela Koleva-Tyutyundzhieva et al describes the role of two biomarkers, i.e. sCD40L as a surrogate for immune activation and soluble E-selectin as a surrogate for endothelial cell activation, in the context of polycystic ovary syndrome and compares the effect between non-obese and obese women. This cross-sectional study is interesting whereas some issues need to be addressed prior accepatance.”
“The manuscript is typically well-written, and the study shows promise. However, before the text can be considered for publication, a few minor issues must be resolved and clarified. Add more recent research (2024–2026) on immunological activation, cardiovascular biomarkers, and endothelial dysfunction in PCOS to the introduction section.”
“A discussion of clinical relevance should clarify how sCD40L and sE-selectin are measured. We have now expanded the Discussion to clarify their potential clinical relevance. Specifically, we emphasize that circulating sE-selectin may serve as a marker of endothelial activation, whereas sCD40L reflects immune- and platelet-related activation.”
Central obesity may amplify endothelial/immune activation in PCOS; hypothesis-generating and should not yet change practice.
Polycystic ovary syndrome (PCOS) is a heterogeneous endocrine–metabolic disorder commonly associated with insulin resistance and early cardiovascular dysfunction. Soluble CD40 ligand (sCD40L) and soluble E-selectin (sE-selectin) are circulating markers reflecting immune activation and endothelial stress, respectively. This cross-sectional study investigated 80 women with PCOS, stratified by central obesity (waist-to-height ratio, WHtR > 0.50 vs ≤ 0.50). While age and systemic inflammatory markers (TNF-α, IL-6) did not differ significantly between groups, centrally obese women exhibited higher fasting insulin, HOMA-IR, triglycerides, non-HDL cholesterol, systolic blood pressure, and sE-selectin, together with reduced HDL cholesterol. In multivariable models adjusted for age, body mass index (BMI) and waist circumference, fasting glucose independently predicted sCD40L (β = 0.27, p = 0.02), whereas fasting insulin was the strongest determinant of sE-selectin (β = 0.41, p < 0.001). These findings reveal divergent immune and endothelial responses to insulin resistance in PCOS, underscoring the potential utility of sCD40L and sE-selectin as complementary biomarkers for early cardiometabolic risk stratification and personalised management in affected women.
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Koleva-Tyutyundzhieva et al. (2026) conducted a cross-sectional in Polycystic Ovary Syndrome (n=80). Central obesity (WHtR > 0.50) vs. No central obesity (WHtR <= 0.50) was evaluated on sE-selectin levels (ng/mL) (p=0.001). Central obesity in women with polycystic ovary syndrome was associated with significantly higher sE-selectin levels (72.93 vs 41.70 ng/mL), with fasting insulin as its strongest independent predictor.
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