Key result
HDL phospholipid acquisition from TGRL correlates with HDL-C but is not associated with cardiovascular risk.
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Why the study?
It remained indeterminate whether the transfer of phospholipids from triglyceride-rich lipoproteins to HDL during lipolysis is linked to HDL-C and cardiovascular disease.
Is the capacity of HDL to acquire phospholipids during triglyceride lipolysis associated with HDL-C levels and cardiovascular risk?
Cross-Sectional
Is the capacity of HDL to acquire phospholipids during triglyceride lipolysis associated with HDL-C levels and cardiovascular risk?
Effect estimate: r = 0.58
p-value: p=<0.001
The capacity of HDL to acquire phospholipids during lipolysis correlates with HDL-C levels but does not reflect cardiovascular risk, suggesting it does not explain the U-shaped relationship between HDL-C and cardiovascular disease.
Does not support HDL phospholipid acquisition as a cardiovascular risk marker; leaves open its role in the HDL-C paradox.
BACKGROUND AND AIMS: While low concentrations of high-density lipoprotein-cholesterol (HDL-C) represent a well-established cardiovascular risk factor, extremely high HDL-C is paradoxically associated with elevated cardiovascular risk, resulting in the U-shape relationship with cardiovascular disease. Free cholesterol transfer to HDL upon lipolysis of triglyceride-rich lipoproteins (TGRL) was recently reported to underlie this relationship, linking HDL-C to triglyceride metabolism and atherosclerosis. In addition to free cholesterol, other surface components of TGRL, primarily phospholipids, are transferred to HDL during lipolysis. It remains indeterminate as to whether such transfer is linked to HDL-C and cardiovascular disease. METHODS AND RESULTS: When TGRL was labelled with fluorescent phospholipid 1,1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine perchlorate (DiI), time- and dose-dependent transfer of DiI to HDL was observed upon incubations with lipoprotein lipase (LPL). The capacity of HDL to acquire DiI was decreased by -36% (p<0.001) in low HDL-C patients with acute myocardial infarction (n = 22) and by -95% (p<0.001) in low HDL-C subjects with Tangier disease (n = 7), unchanged in low HDL-C patients with Type 2 diabetes (n = 17) and in subjects with high HDL-C (n = 20), and elevated in subjects with extremely high HDL-C (+11%, p<0.05) relative to healthy normolipidemic controls. Across all the populations combined, HDL capacity to acquire DiI was directly correlated with HDL-C (r = 0.58, p<0.001). No relationship of HDL capacity to acquire DiI with both overall and cardiovascular mortality obtained from epidemiological studies for the mean HDL-C levels observed in the studied populations was obtained. CONCLUSIONS: These data indicate that the capacity of HDL to acquire phospholipid from TGRL upon LPL-mediated lipolysis is proportional to HDL-C and does not reflect cardiovascular risk in subjects widely differing in HDL-C levels.
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Ma et al. (2021) conducted a cross-sectional in Varying HDL-C levels. HDL-C levels vs. Healthy normolipidemic controls was evaluated on HDL capacity to acquire DiI (phospholipid) from TGRL upon lipolysis (r = 0.58, p=<0.001). The capacity of HDL to acquire phospholipid from TGRL upon lipolysis directly correlated with HDL-C levels (r = 0.58, P<0.001) but was not associated with cardiovascular risk.
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