High-density lipoprotein subfractions display proatherogenic properties in overweight and obese children

Abstract

Background:In adults, obesity-driven inflammation can lead to increased cardiovascular disease (CVD). However, information regarding childhood obesity and its inflammatory sequelae is less well defined. Serum amyloid-A (SAA) is an inflammatory molecule that rapidly associates with highdensity lipoproteins (HDLs) and renders them dysfunctional. Therefore, SAA may be a useful biomarker to identify increased CVD potential in overweight and obese children. Methods: Young Hearts 2000 is a cross-sectional cohort study in which 92 children who were obese were matched for age and sex with 92 overweight and 92 lean children. HDL 2 and HDL 3 (HDL 2&3 ) were isolated from plasma by a three-step rapid-ultracentrifugation procedure. SAA was measured in serum and HDL 2&3 by an enzyme-linked immunosorbent assay procedure, and the activities of cholesterol ester transfer protein (CETP) and lecithin cholesteryl acyltransferase (LCAT) were measured by fluorimetric assays. results: Trends across the groups indicated that SAA increased in serum and HDL 2&3 as BMI increased, as did HDL 2 -CETP and HDL 2 -LCAT activities. conclusion: These results have provided evidence that overweight and obese children are exposed to an inflammatory milieu that impacts the antiatherogenic properties of HDL and that could increase CVD risk. This supports the concept that it is important to target childhood obesity to help minimize future cardiovascular events.

Impaired antioxidant HDL function is associated with premature myocardial infarction

“…This mechanism might also explain the observed association between impaired HDL function and hypertension, which is strongly linked to oxidative stress [32]. In line with other studies demonstrating a negative effect of obesity on HDL function [33], we also detected a correlation between body mass index and antioxidant HDL function in premature AMI patients. The deleterious impact of smoking on HDL function has been previously shown and might be caused by oxidative modifications of HDL-associated proteins as well as a shift in particle size distribution towards smaller HDL particles [34,35].…”

“…Generally, oxidative stress is regarded as crucial player in the development of dysfunctional HDL [30,31]. In line with other studies demonstrating a negative effect of obesity on HDL function [33], we also detected a correlation between body mass index and antioxidant HDL function in premature AMI patients. In line with other studies demonstrating a negative effect of obesity on HDL function [33], we also detected a correlation between body mass index and antioxidant HDL function in premature AMI patients.…”

High density lipoprotein subfractions and paraoxonase 1 in children

“…Pietiläinen et al (2009) investigated HDL subfractions in young twin and found in abdominal overweight children decreased HDL2b and increased HDL3c subfractions independent of genetic influences. A marker for cardiovascular disease, serum amyloid-A was found to be positively correlated with small HDL subfractions in overweight children McEneny et al (2013).…”

A Pro-Atherogenic HDL Profile in Coronary Heart Disease Patients: An iTRAQ Labelling-Based Proteomic Approach

“…ApoA-I in HDL has been identified as being responsible for reverse cholesterol transport and reverse atherosclerosis, and paraoxonase 1 in HDL has been found to have anti-oxidant properties [9]. In addition, studies have indicated that elevated amounts of serum amyloid A (SAA) in HDL render it pro-atherogenic [10], [11]. It has also been demonstrated that overexpression of apoA-II in HDL fractions advanced atherosclerosis even though the plasma levels of HDL-C were elevated [12].…”