María Fátima Garcés1, Yamil Guarin1, Yenny Carrero1, Hilda Stekman1, Celsy Hernández1, María Luisa Núñez1, Rafael Apitz2, Germán Camejo3. 1. Associated Research Laboratory of Basic and Applied Research, Department of Biochemistry at the School of Bioanalysis, Faculty of Medicine, Central University of Venezuela, Caracas, Venezuela. 2. National Academy of Medicine, Caracas, Venezuela. 3. Germán Camejo, Clinical Chemistry Laboratory, Department of Laboratory Medicine, Karolinska Institute, Stockholm, Sweden.
Abstract
BACKGROUND: Postprandial increase of triglyceride-rich lipoproteins augments the risk of atherosclerotic cardiovascular disease and all-cause mortality. We explored the hypothesis that a simplified oral fat tolerance test can uncover differences in postprandial triglyceride response associated with potentially atherogenic lipoprotein characteristics, even in a cohort of apparently healthy 31-year-old [mean (SD), 31 (11)] nonobese individuals with normal fasting lipids and lipoproteins. METHODS: We used a fat tolerance test in 96 females and 62 males with blood sampled at 0, 2, and 4 h after a breakfast containing 26.3 g of fats. The postprandial triglyceride response was used to classify the individuals in apparently fat-tolerant and apparently fat-intolerant participants. RESULTS: The intolerant individuals were found to have at 0 h significantly higher body mass index, plasma triglycerides, remnant cholesterol, VLDL cholesterol, and LDL cholesterol and lower apolipoprotein (apo) AI and HDL cholesterol than the tolerant individuals. More than 70% of the variability (r2) of the postprandial response in tolerant and intolerant individuals measured as area under the curve or, at a single point at 4 h after the oral fat load, was linearly correlated with 0-h triglycerides (P < 0001). Fasting lipoprotein parameters, proposed to be markers of cardiovascular risk, as the ratios apo B/apo AI, total cholesterol/HDL cholesterol, and triglycerides/HDL cholesterol, were increased in the intolerant individuals. CONCLUSIONS: A simplified oral fat tolerance test, even when used in an apparently healthy, nonobese, normolipidemic cohort, detected that an increased postprandial triglycerides response was associated with augmented lipoprotein markers of increased cardiovascular risk.
BACKGROUND: Postprandial increase of triglyceride-rich lipoproteins augments the risk of atherosclerotic cardiovascular disease and all-cause mortality. We explored the hypothesis that a simplified oral fat tolerance test can uncover differences in postprandial triglyceride response associated with potentially atherogenic lipoprotein characteristics, even in a cohort of apparently healthy 31-year-old [mean (SD), 31 (11)] nonobese individuals with normal fasting lipids and lipoproteins. METHODS: We used a fat tolerance test in 96 females and 62 males with blood sampled at 0, 2, and 4 h after a breakfast containing 26.3 g of fats. The postprandial triglyceride response was used to classify the individuals in apparently fat-tolerant and apparently fat-intolerant participants. RESULTS: The intolerant individuals were found to have at 0 h significantly higher body mass index, plasma triglycerides, remnant cholesterol, VLDL cholesterol, and LDL cholesterol and lower apolipoprotein (apo) AI and HDL cholesterol than the tolerant individuals. More than 70% of the variability (r2) of the postprandial response in tolerant and intolerant individuals measured as area under the curve or, at a single point at 4 h after the oral fat load, was linearly correlated with 0-h triglycerides (P < 0001). Fasting lipoprotein parameters, proposed to be markers of cardiovascular risk, as the ratios apo B/apo AI, total cholesterol/HDL cholesterol, and triglycerides/HDL cholesterol, were increased in the intolerant individuals. CONCLUSIONS: A simplified oral fat tolerance test, even when used in an apparently healthy, nonobese, normolipidemic cohort, detected that an increased postprandial triglycerides response was associated with augmented lipoprotein markers of increased cardiovascular risk.