Key result
Primary hypertension is linked to higher serum asprosin, but levels do not track subclinical atherosclerosis.
Why the study?
Hypertension and subclinical atherosclerosis drive cardiovascular morbidity, and the relationship between serum levels of the novel metabolic biomarker asprosin and subclinical atherosclerosis in primary hypertension needed investigation.
Are serum asprosin levels elevated in primary hypertension and associated with subclinical atherosclerosis?
Cross-Sectional (n=176)
No
Are serum asprosin levels elevated in primary hypertension and associated with subclinical atherosclerosis?
Absolute Event Rate: 3% vs 2.6%
p-value: p=0.012
Elevated serum asprosin in primary hypertension reflects metabolic-inflammatory dysregulation rather than acting as a direct biomarker for coronary artery calcification.
Elevated asprosin in primary hypertension may signal metabolic dysregulation but should not guide atherosclerosis assessment; leaves open its biomarker role pending prospective studies.
Hypertension and subclinical atherosclerosis are major contributors to cardiovascular morbidity. Asprosin, a fasting-induced adipokine involved in glucose homeostasis and inflammation, has been proposed as a novel metabolic biomarker. This study investigated the relationship between serum asprosin levels and subclinical atherosclerosis in patients with primary hypertension. A total of 114 patients with primary hypertension and 62 age- and sex-matched healthy controls were enrolled between July 2022 and June 2023. Coronary artery calcium (Agatston) score was used to assess subclinical atherosclerosis. Serum asprosin concentrations were measured using the ELISA method. Correlation, regression, and ROC analyses were performed to identify determinants and discriminatory performance. Serum asprosin levels were significantly higher in hypertensive patients than in controls (3.0 ± 0.9 ng/mL vs. 2.6 ± 0.8 ng/mL, p = 0.012). In hypertensive individuals, increasing age, blood pressure, and ASCVD risk score were independently associated with higher atherosclerotic burden, whereas the neutrophil-to-lymphocyte ratio (NLR) was inversely related (p < 0.05). ROC analysis showed that serum asprosin could discriminate hypertensive patients with subclinical atherosclerosis (AUC = 0.710 [95% CI: 0.62-0.80, p = 0.001]) at a cut-off > 3.05 ng/mL, with 69% sensitivity and 72% specificity. Serum asprosin levels were elevated in patients with primary hypertension and may reflect metabolic-inflammatory alterations rather than directly indicate subclinical atherosclerosis. Given its modest discriminatory performance, serum asprosin should be considered an exploratory and complementary biomarker, not a standalone clinical tool. Larger longitudinal studies are required to validate its clinical relevance.Clinical trial numberNot applicable.
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Özet et al. (2026) conducted a cross-sectional in Primary hypertension (n=176). Primary hypertension vs. Healthy controls was evaluated on Serum asprosin levels (p=0.012). Serum asprosin levels were significantly elevated in patients with primary hypertension compared to controls (3.0 vs 2.6 ng/mL, p=0.012), but showed no independent correlation with subclinical coronary atherosclerotic burden.
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