Journal
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR AND CELL BIOLOGY OF LIPIDS
Volume 1867, Issue 2, Pages -Publisher
ELSEVIER
DOI: 10.1016/j.bbalip.2021.159087
Keywords
Reverse cholesterol transport; HDL; LCAT; Inflammation; Abdominal obesity; Oxidative stress
Funding
- MIUR [PRIN 2017J3E2W2_002]
- JPI-EU FATMAL
- Interreg V-A Greece-Italy 2014-2020 [MIS 5003627]
- NR-NET FP7 Marie Curie ITN
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This study aimed to investigate the impact of cardiometabolic risk factors on the anti-atherogenic function of HDL particles, revealing associations between cardiometabolic risk and HDL function and maturation, with abdominal obesity identified as a significant contributor to alterations in key metrics of RCT.
Cardiometabolic risk factors increase the risk of atherosclerotic cardiovascular disease (ASCVD), but whether these metabolic anomalies affect the anti-atherogenic function of reverse cholesterol transport (RCT) is not yet clearly known. The present study aimed to delineate if the function and maturation of high density lipoprotein (HDL) particles cross-sectionally associate with surrogate markers of ASCVD in a population comprising of different degree of cardiometabolic risk. We enrolled 131 subjects and characterized cardiometabolic risk based on the IDF criteria's for metabolic syndrome (MS). In this population, cholesterol efflux capacity (CEC), Lecithin-cholesterol acyltransferase (LCAT) and ApoA-1 glycation was associated with waist circumference, abdominal visceral fat (VFA) and abdominal subcutaneous fat. In multivariate analyses, VFA was identified as a critical contributor for low CEC and LCAT. When stratified into groups based on the presence of cardiometabolic risk factors, we found a prominent reduction in CEC and LCAT as a function of the progressive increase of cardiometabolic risk from 0-2, 0-3 to 0-4/5, whereas an increase in Pre-beta-HDL and ApoA-1 glycation was observed between the lowest and highest risk groups. These findings confirm the connection between MS and its predisposing conditions to an impairment of atheroprotective efflux-promoting function of HDLs. Furthermore, we have identified the bona fide pathogenically contribution of abdominal obesity to profound alterations of key metrics of RCT.
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