Key result
Metabolic and pre-metabolic syndrome are linked to ~47% lower HDL cholesterol efflux capacity.
Why the study?
The study aimed to evaluate HDL functionality using cholesterol efflux capacity across control, pre-metabolic syndrome, and metabolic syndrome groups in a South Indian cohort and determine its association with metabolic parameters and disease severity.
Does pre-metabolic syndrome and metabolic syndrome impair HDL cholesterol efflux capacity compared to healthy controls in a South Indian adult cohort?
Cross-Sectional (n=88)
No
Does pre-metabolic syndrome and metabolic syndrome impair HDL cholesterol efflux capacity compared to healthy controls in a South Indian adult cohort?
Answers are grounded in this paper and cite their sources.
HDL cholesterol efflux capacity is markedly impaired as early as the pre-metabolic syndrome stage in South Indian adults, independent of HDL-C and ApoA1 levels, highlighting its potential as an early functional biomarker for cardiometabolic risk.
Background:To evaluate high density lipoprotein(HDL) functionality using cholesterol efflux capacity(CEC) across control, pre-metabolic syndrome(PreMetS) and metabolic syndrome(MetS) groups in a South Indian cohort and determine its association with metabolic parameters and disease severity. Methods:This cross-sectional study included 88 adults [Control (n = 38; age 32.9 ± 6.20 years; M:F 19:19), Pre-MetS (n = 24; age 36.5 ± 3.50 years; M:F 15:9), MetS (n = 26; age 46.6 ± 5.68 years; M:F 17:9)] classified using modified NCEP ATP III criteria. Anthropometric (BMI, waist circumference, blood pressure) and biochemical parameters (fasting glucose, triglycerides, HDL-C, LDL-C, ApoA1, insulin, HOMA-IR) were assessed using standardised protocols. HDL functionality was measured via BODIPY-cholesterol efflux in PMA-differentiated THP-1 macrophages. Multiple linear regression and Spearman correlations were performed (p < 0.05). Results:Progressive intergroup differences were observed in waist circumference, BMI, fasting glucose, insulin, triglycerides, and HOMA-IR (p < 0.001). ApoA1 declined proportionally across groups (231 vs 206 vs 187 ng/mL; ε 2 = 0.839, p < 0.001), representing the largest effect size in the dataset. Notably, CEC considerably reduced at the Pre-MetS stage and remained diminished with progressive metabolic deterioration, emphasizing early detection and intervention. CEC differed significantly across the metabolic spectrum (p < 0.001). Multiple linear regression identified triglycerides and insulin resistance as independent negative predictors of CEC, adjusting for HDL-C and ApoA1 (adjusted R 2 = 0.769). Conclusion:CEC is significantly diminished at the Pre-MetS stage and remains reduced with progressive metabolic deterioration. Triglyceride enrichment and insulin-mediated suppression of ApoA1 synthesis likely impair HDL remodelling and efflux capacity. These findings highlight CEC as an indicator of HDL dysfunction with implications for earlier cardiometabolic risk assessment in South Indian populations.
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A et al. (2026) conducted a cross-sectional in Metabolic syndrome and pre-metabolic syndrome (n=88). Metabolic syndrome and pre-metabolic syndrome status vs. Healthy controls (0 NCEP ATP III criteria) was evaluated on Macrophage-specific HDL cholesterol efflux capacity (CEC) in arbitrary units (A.U.) (ε² = 0.723 (Pre-MetS median 0.869 A.U., MetS median 0.930 A.U. vs Control 1.761 A.U.), p=<0.001). Pre-metabolic syndrome and metabolic syndrome were associated with reduced HDL cholesterol efflux capacity compared to controls.
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