Apolipoprotein A-V plays an important role in the determination of plasma triglyceride (TG) concentration. We aimed to determine whether polymorphisms -1131T>C (rs662799) and 56C>G (rs3135506) of the APOA5 gene have an impact on the course of postprandial lipemia induced by a fat load and a fat load with added glucose. Thirty healthy male volunteers, seven heterozygous for the -1131C variant and three for the 56G variant (HT) carriers, and 20 wild-type (WT) carriers underwent two 8-hour tests of postprandial lipemia – one after an experimental breakfast consisting of 75 g of fat and second after a breakfast consisting of 75 g of fat and 25 g of glucose. HT carriers had a higher postprandial response after fat load than WT carriers (AUC TG: 14.01±4.27 vs. 9.84±3.32 mmol*h/l,
respectively, p=0.016). Glucose added to the test meal suppressed such a difference. Heterozygous carriers of the variants of APOA5 (-1131C and 56G) display more pronounced postprandial lipemia after pure fat load than WT carriers. This statistically significant difference disappears when glucose is added to a fat load, suggesting that meal composition modulates the effect of these polymorphisms on the magnitude of postprandial lipemia.
The review aims to summarize current knowledge on the effects of moderate alcohol consumption ( 1 standard drink a day for women; 2 drinks a day for men) on triglyceride concentration in circulation. Current evidence suggests that the relationship between alcohol consumption and triglyceridemia is J -shaped. Triglyceridemia is lowest in subjects who drink 10 -20 g/alcohol a day. Such a J -shaped association is comparable with that described for the relationship between alcohol and cardiovascular risk. On the contrary, alcohol taken with a meal increases and prolongs postprandi al triglyceridemia. Such effects of alcohol consumption may be at least partially explained by the effects of ethanol on lipoprotein lipase (LPL) activity. Long -term moderate alcohol consumption increases LPL activity, which may explain its TG -lowering effect. On the other hand, LPL activity is acutely downregulated by ethanol, which explains increased postprandial triglyceridemia., J. Kovář, K. Zemánková., and Obsahuje bibliografii
The treatment of hypercholesterolemia with bile acid (BA)
sequestrants results in upregulation of BA synthesis through the
classical pathway initiated by cholesterol 7α-hydroxylase (CYP7A1). To characterize the detailed dynamics of serum lipid and BA concentrations and the BA synthesis rate in response to treatment with BA sequestrants and to determine whether the -203A/C promoter polymorphism of the CYP7A1 encoding gene (CYP7A1) affects such a response, this pilot study was carried out in healthy men (8
h omozygous for the -203A allele and 8 homozygous for the -203C allele of CYP7A1). The subjects were treated for 28 days with colesevelam
and blood was drawn for analysis before and on days 1, 3, 7, 14 and 28 of treatment. The response of lipids, BA, fibroblast growth factor-19 (FGF19) and 7α-hydroxy-4-cholesten-3-one (C4) to colesevelam did not differ between carriers of -203A and -203C alleles; their data were then aggregated for further analysis. Colesevelam treatment caused immediate suppression of FGF19 concentration and a fivefold increase in CYP7A1 activity, as assessed from C4 concentration, followed by a 17% decrease in LDL-cholesterol. Although total plasma BA concentrations were not affected, the ratio of cholic acid/total BA rose from 0.25±0.10 to 0.44±0.16 during treatment at the expense of decreases in chenodeoxycholic and deoxycholic acid.
Increased and prolonged postprandial lipemia has been identified as a risk factor of cardiovascular disease. However, there is no consensus on how to test postprandial lipemia, especia lly with respect to the composition of an experimental meal. To address this question of how glucose, when added to a fat load, affects the selected parameters of postprandial lipemia, we carried out a study in 30 healthy male volunteers. Men consumed an experimental meal containing either 75 g of fat + 25 g of glucose (F+G meal) or 75 g of fat (F meal) in a control experiment. Blood was taken before the meal and at selected time points within the following 8 h. Glucose, when added to a fat load, induced an increase of glycemia and insulinemia and, surprisingly, a 20 % reduction in the response of both total and active glucagon -like peptide -1 (GLP -1) concentration. The addition of glucose did not affect the magnitude of postprandial triglyceridemia and TRL -C and TRL -TG concentrations but stimulated a faster response of chylomicrons to the test meal, evaluated by changes in apolipoprotein B -48 concentrations. The addition of glucose induced the physiological response of insulin and the lower response of GLP -1 to the test meal during the early postprandial phase, but had no effect on changes of TRL -cholesterol and TRL -TG within 8 h after the meal., K. Zemánková, J. Mrázková, J. Piťha, J. Kovář., and Obsahuje bibliografii