Key result
Low triglyceride metabolic capacity is proposed to increase cardiovascular disease risk by shunting cholesteryl esters into triglyceride-rich particles, creating potentially atherogenic agents.
Postprandial hyperlipidemia and low triglyceride metabolic capacity contribute to atherogenesis by altering lipoprotein composition, leading to low HDL and small, dense LDL particles.
May link impaired triglyceride clearance to atherogenic lipoproteins; leaves open need for outcome trials before clinical adoption.
Postprandial lipemia provides a daily state of challenge to triglyceride transport. A poor ability to cope with this challenge, i.e. a low triglyceride metabolic capacity, is likely to increase risk of cardiovascular disease because it provides ample opportunity for cholesteryl esters to be shunted from LDL and HDL into former triglyceride-rich particles, converting them into potentially atherogenic agents. Shunting of cholesteryl esters into triglyceride-rich lipoproteins appears to be inversely related to triglyceride metabolic capacity, and is indicated by the fasting lipoprotein constellation most frequently associated with coronary artery disease: low HDL cholesterol and a preponderance of small-sized HDL and LDL.
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ck et al. (1992) conducted a review in Postprandial hyperlipidemia. Low triglyceride metabolic capacity was evaluated. Low triglyceride metabolic capacity is proposed to increase cardiovascular disease risk by shunting cholesteryl esters into triglyceride-rich particles, creating potentially atherogenic agents.
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