HDL biology
A review revisiting a 40-year-old study names the CETP, VLDL-triglyceride, and hepatic lipase cluster as drivers of atherogenic HDL and LDL remodeling (Rom J Intern Med 2008)
Original title: Lipolytic enzymes, metablic syndrome and atherosclerosis (revisiting and revising a 40 years old study)
Revisiting a study from more than 40 years earlier reporting decreased post-heparin lipolytic activity in patients with severe atherosclerotic disease, this review notes that data limitations at the time hampered interpretation. Reviewing recent literature, pre-heparin lipoprotein lipase mass by ELISA was significantly lower in insulin-resistant coronary patients than in those without lesions, correlating negatively with lesion severity, and hypoadiponectinemia, a hallmark of insulin resistance, was associated with decreased lipoprotein lipase and increased hepatic lipase activities. Clustering of increased plasma VLDL-triglyceride, cholesteryl ester transfer protein (CETP), and hepatic lipase would remodel HDL and LDL particles into an atherogenic lipoprotein profile, whereas hypertriglyceridemia from deficient lipolytic clearance carries relatively low coronary risk, suggesting the decreased lipoprotein lipase seen in atherosclerotic patients reflects inflammation rather than a major pathogenic mechanism.
Original abstract
More than 40 years ago, our laboratory reported that post-heparin lipolytic activity was decreased in patients with severe atherosclerotic disease, while values recorded in obese and hyperlipidemic subjects without clinically detectable atherosclerotic lesions did not significantly differ from normal weight normolipidemic controls. Because in 1967 data on pathophysiology of lipolytic enzymes were rather scarce, and mainly because our information facilities were limited in those years, we had difficulties in interpreting these results, and the study was to some extent awkwardly approached, as the investigated subjects were not considered according to their gender, body fat patterning and type of hyperlipoproteinemia, and the lipolytic activities of lipoprotein lipase and hepatic lipase had not been selectively assessed. Reviewing recent data in the literature it was noted that pre-heparin lipoprotein lipase mass assessed by ELISA was indeed significantly lower in insulin resistant coronary patients than in patients with no lesions, and correlated negatively with the severity of atherosclerotic lesions. Noteworthy hypoadiponectinemia, a hallmark of insulin resistance, was associated with decreased lipoprotein lipase and increased hepatic lipase activities. Clustering of increased plasma VLDL-triglyceride, cholesteryl-ester transfer protein and hepatic lipase would remodel HDL and LDL particles, generating an atherogenic lipoprotein profile. In opposition to atherogenic dyslipidemia related to an enhanced hepatic secretion of VLDL, cases with important hypertriglyceridemia subsequent to deficient lipolytic clearance are at a rather low risk for coronary artery disease. It may therefore be suggested that the decreased lipoprotein lipase noted in atherosclerotic patients is not a major pathogenic link, being rather related to the inflammatory component of the disease, its expression being reduced by proinflammatory cytokines.
Summary written by cetpinhibition.org from the published abstract; figures as published. Page updated 19 August 2026. Methods.