Relation of triglyceride metabolism and coronary artery disease. Studies in the postprandial state.

Abstract

The status of fasting triglycerides as a risk factor for coronary artery disease (CAD) has been considered weak because in multivariate analyses, triglycerides tend to be eliminated by high density lipoprotein (HDL) cholesterol. To further evaluate the role of triglycerides in CAD, we employed postprandial lipemia as a more informative means of characterizing triglyceride metabolism. In 61 male subjects with severe CAD and 40 control subjects without CAD as verified by angiography, we measured cholesterol; triglycerides; HDL cholesterol; HDL 2 cholesterol; and apolipoproteins A-I, A-II, and B in fasting plasma and triglycerides before and 2, 4, 6, and 8 hours after a standardized test meal. Both the maximal triglyceride increase and the magnitude of postprandial lipemia (area under the triglyceride curve over 8 hours after the meal) were higher in cases than in control subjects. Single postprandial triglyceride levels 6 and 8 hours after the meal were highly discriminatory (p<0.001), and by logistic-regression analysis displayed an accuracy of 68% in predicting the presence or absence of CAD. In this respect, accuracy was higher than that of HDL 2 cholesterol (64%) and equal to that of apolipoprotein B (68%), the most discriminatory fasting parameter. Multivariate logistic-regression analysis was performed to reduce the number of risk factors to those that were statistically independent. This statistical procedure selected postprandial but not fasting triglycerides into the most accurate multivariate model, which also contained the accepted risk factors HDL 2 cholesterol, apolipoprotein B, and age. This model classified 82% of subjects correctly. We conclude that triglycerides are independent predictors of CAD in multivariate analyses including HDL cholesterol, provided that a challenge test of triglyceride metabolism such as postprandial lipemia is used. The study suggests that the metabolism of triglycerides is a critical determinant of cholesterol metabolic routing. The findings support the concept that the negative association between HDL cholesterol levels and CAD actually originates in part from a positive relation between CAD and plasma triglycerides, as ascertained in the postprandial state. (

Methodology for studying postprandial lipid metabolism

“…In that case, a similar standardized test meal is to be used in every subject. (Weintraub et al, 1988(Weintraub et al, , 1989Lopez-Miranda et al, 1997Patsch et al, 1992;Mekki et al, 1999;Minihane et al, 2000;Tiret et al, 2000;Sharrett et al, 2001;Robertson et al, 2002;Jackson et al, 2003;Harbis et al, 2004).…”

“…As shown in Table 1, during the early sets of postprandial studies in the 1980s, investigators used test meals providing high amount of nutrient/energy, usually more than 50 g fat per test meal (Cohn et al, 1988a(Cohn et al, , 1993Patsch et al, 1983Patsch et al, , 1992Weintraub et al, 1988). These were called 'fat load' or 'fat-tolerance tests' and resembled the glucose-tolerance tests used to detect underlying defects in glucose metabolism in diabetes.…”

1H NMR metabonomics can differentiate the early atherogenic effect of dairy products in hyperlipidemic hamsters

“…This is indicated by the reciprocal 25 changes in the concentrations among glycerol, plasma lipids and VLDL (R 2 range from 0.51 26 to 0.65 according to the multiple NMR chemical shifts, not shown). High plasma glycerol was 27 associated with lower atherogenesis, which could emphasize the importance of the 28 postprandial blood lipid clearance in the etiology of atherogenesis 34 . We identified 29 resonances that corresponded to N-acetyl-glycoproteins, clustering with plasma lipids and 30 VLDL.…”

Overproduction of intestinal lipoprotein containing apolipoprotein B-48 in Psammomys obesus: impact of dietary n-3 fatty acids

“…by a huge meta-analysis [5], as well as by intervention [6] and observational long-term [1] studies. In addition, postprandial hyperlipidaemia has been linked to atherosclerosis, even in fasting normocholesterolaemic subjects [7][8][9][10].…”