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Published on: October 12, 2017
High-density lipoprotein subfractions display proatherogenic properties in overweight and obese children
Jane McEneny1, Sarah Blair, Jayne V Woodside
1Centre for Public Health, Nutrition and Metabolism Group, Queen's University Belfast, Belfast, UK. j.mceneny@qub.ac.uk
Insights
Childhood obesity is linked to inflammation that impairs high-density lipoprotein (HDL) function, increasing cardiovascular disease (CVD) risk. Serum amyloid-A (SAA) may indicate this risk in children.
Area of Science:
- Pediatric Endocrinology
- Cardiovascular Research
- Inflammation Biology
Background:
- Childhood obesity is increasingly recognized as a contributor to chronic inflammation.
- Inflammation associated with obesity can negatively impact cardiovascular health.
- Serum amyloid-A (SAA) is an acute-phase reactant protein that alters high-density lipoprotein (HDL) function.
Purpose of the Study:
- To investigate the association between childhood obesity, inflammation, and HDL functionality.
- To evaluate Serum amyloid-A (SAA) as a potential biomarker for cardiovascular disease (CVD) risk in overweight and obese children.
Main Methods:
- Cross-sectional study of 92 obese, 92 overweight, and 92 lean children (Young Hearts 2000 cohort).
- Isolation of HDL subfractions (HDL(2) and HDL(3)).
- Measurement of SAA levels in serum and HDL, and activities of cholesterol ester transfer protein (CETP) and lecithin cholesteryl acyltransferase (LCAT).
Main Results:
- Serum and HDL-associated SAA levels increased with rising Body Mass Index (BMI).
- Activities of HDL(2)-CETP and HDL(2)-LCAT also increased with increasing BMI.
- These findings indicate an inflammatory state in overweight and obese children impacting HDL properties.
Conclusions:
- Overweight and obese children exhibit an inflammatory profile that compromises the antiatherogenic capacity of HDL.
- Elevated SAA and altered HDL activity in obese children suggest an increased potential for cardiovascular disease (CVD).
- Targeting childhood obesity is crucial for mitigating future cardiovascular events.
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 high-density 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.
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