An Expert Panel group of scientists and clinicians met to consider several aspects related to non-fasting and postprandial triglycerides (TGs) and their role as risk factors for cardiovascular disease (CVD). In this context, we review recent epidemiological studies relevant to elevated non-fasting TGs as a risk factor for CVD and provide a suggested classification of non-fasting TG concentration. Secondly, we sought to describe methodologies to evaluate postprandial TG using a fat tolerance test (FTT) in the clinic. Thirdly, we discuss the role of non-fasting lipids in the treatment of postprandial hyperlipemia. Finally, we provide a series of clinical recommendations relating to non-fasting TGs based on the consensus of the Expert Panel: 1). Elevated non-fasting TGs are a risk factor for CVD. 2). The desirable non-fasting TG concentration is < 2 mmol/l ( < 180 mg/dl). 3). For standardized postprandial testing, a single FTT meal should be given after an 8 h fast and should consist of 75 g of fat, 25 g of carbohydrates and 10 g of protein. 4). A single TG measurement 4 h after a FTT meal provides a good evaluation of the postprandial TG response. 5). Preferably, subjects with non-fasting TG levels of 1-2 mmol/l (89-180 mg/dl) should be tested with a FTT. 6). TG concentration ≤ 2.5 mmol/l (220 mg/dl) at any time after a FTT meal should be considered as a desirable postprandial TG response. 7). A higher and undesirable postprandial TG response could be treated by aggressive lifestyle modification (including nutritional supplementation) and/or TG lowering drugs like statins, fibrates and nicotinic acid.

Background/Aim: Triglycerides (TGs) are measured in studies evaluating changes in non-fasting lipid profiles after a fat tolerance test (FTT); however, the optimal timing for TG measurements after the oral fat load is unclear. The aim of this study was to evaluate how non-fasting TG levels vary after an oral FTT in healthy subjects. Methods: This meta-analysis included 113 studies with > 5 participants of Caucasian race that were indexed in PubMed from its inception through March 2010, using the search term “postprandial lipemia”. We only included studies that provided mean values and standard deviation (SD) (or standard error of the mean) for TG measurements at baseline (=fasting) and for at least one other time-point. Exclusion criteria included uncommon sampling time-points after the FTT, baseline TGs≥2.0 mmol/L (≥177mg/dl), and a body mass index ≥30kg/m2. Results: All studies combined, weighted mean±SD TG values in mmol/L were 1.25±0.32 fasting, 1.82±0.40 at 2 h, 2.31±0.62 at 4 h, 1.87±0.63 at 6 h, and 1.69±0.80 at 8 h. After stratifying studies based on fat quantity in the test meal ( < 40,≥40- < 50, ≥50- < 60, ≥60- < 70, ≥70- < 80, ≥80- < 90, ≥90- < 100, ≥100- < 110, ≥110-120, ≥120 g), the highest standardized mean difference in TG levels from fasting levels was found in those having an oral fat load of ≥70 g and < 80 g, and at 4 h (difference=1.74 mmol/L; p < 0.001). Conclusion: The 4 h time-point after an oral fat load during a FTT was the most representative measurement of TGs. The highest standardized mean difference of TGs was found after a meal containing 70-79g of fat. The relevance of these two key parameters determined in healthy subjects should be considered for further developments of an oral FFT for clinical purposes.

Dietary intervention is the first and usually successful approach in the treatment of high LDL cholesterol (LDL-C) concentration, but it is frequently accompanied by a decrease in HDL concentration. We studied 14 male volunteers on two different diets, high saturated fatty acid (SFA) and high PUFA, in a crossover design to test whether a decrease in HDL can affect reverse cholesterol transport from relabeled macrophages. A significant decrease of LDL-C (in mmol/l) after a PUFA diet compared with an SFA diet from 3.15 ± 0.65 to 2.80 ± 0.56 (P < 0.01) was accompanied by a significant decrease of HDL cholesterol (HDL-C) (in mmol/l) from 1.21 ± 0.30 to 1.10 ± 0.32 (P < 0.05). These changes did not affect cholesterol efflux (CHE) from macrophages (9.74 ± 1.46% vs. 9.53 ± 1.41%). There was no correlation between individual changes of HDL-C and changes of CHE. It is concluded that the decrease of HDL-C after successful dietary intervention of LDL-C is not accompanied by a decrease of CHE.

Cholesterol 7α-hydroxylase (CYP7A1), the key regulatory enzyme of bile acid synthesis, displays a pronounced diurnal variation. To better understand the regulation of CYP7A1 activity, three daylong examinations were carried out in 12 healthy men. The concentrations of 7α-hydroxycholest-4-en-3-one (C4), a surrogate marker of CYP7A1 activity, bile acids (BA), insulin, glucose, nonesterified fatty acids, triglycerides, and cholesterol were measured in serum in 90-min intervals from 7 AM till 10 PM. To lower and to increase BA concentration during the study, the subjects received cholestyramine and chenodeoxycholic acid (CDCA), respectively, in two examinations. No drug was used in the control examination. There was a pronounced diurnal variation of C4 concentration with a peak around 1 PM in most of the subjects. The area under the curve (AUC) of C4 concentration was five times higher and three times lower when subjects were treated with cholestyramine and CDCA, respectively. No relationship was found between AUC of C4 and AUC of BA concentration, but AUC of C4 correlated positively with that of insulin. Moreover, short-term treatment with cholestyramine resulted in about 10 % suppression of glycemia throughout the day. Our results suggest that insulin is involved in the regulation of diurnal variation of CYP7A1 activity in humans.