retinol-palmitate and Coronary-Disease

Topics: Apolipoprotein B-100; Apolipoprotein B-48; Apolipoproteins B; Arteriosclerosis; Biomarkers; Blood Chemical Analysis; Breath Tests; Cholesterol; Coronary Disease; Diterpenes; Electrophoresis, Polyacrylamide Gel; Humans; Hyperlipidemias; Lipoproteins; Receptors, LDL; Retinyl Esters; Triglycerides; Vitamin A

Postprandial lipaemia, whether measured using levels of triglyceride of retinyl palmitate, is more severe in patients with coronary heart disease; however, little improvement in the discrimination between individuals with and without coronary heart disease can be made using postprandial measurements rather than measuring levels of high-density-lipoprotein2 cholesterol of apolipoproteins B. Retinyl palmitate levels occasionally reveal differences not apparent from triglyceride measurements. Elevated fasting and postprandial triglyceride levels may produce clinical disease partly by enhancing coagulation and by interfering with fibrinolysis.

Topics: Anticarcinogenic Agents; Clinical Trials as Topic; Coronary Disease; Diterpenes; Eating; Factor VII; Fasting; Humans; Hyperlipidemias; Lipoproteins; Retinyl Esters; Risk Factors; Triglycerides; Vitamin A

Although a low plasma high-density lipoprotein cholesterol (HDL-C) level is a well-accepted risk factor for coronary artery disease (CAD), it is unclear whether pharmacologic agents can effectively increase HDL-C levels and/or reduce the incidence of CAD in patients with isolated low HDL-C levels. An important determinant of HDL levels is the efficiency of postprandial lipoprotein catabolism. The purpose of the present study was to evaluate the efficacy of bezafibrate therapy in increasing HDL-C levels in these patients and to examine its effect on postprandial lipoprotein levels. Fasting and postprandial lipid and lipoprotein levels were studied in 23 patients with isolated low HDL-C levels before and during 3 and 6 months of bezafibrate treatment. Postprandial lipoprotein levels were evaluated using the vitamin A-fat loading test, in which these intestinally derived lipoproteins are specifically labeled with retinyl palmitate (RP). Patients with isolated low HDL had significantly higher levels of chylomicron RP than a control group of 19 normolipidemic subjects. The area below the chylomicron RP curve was 17,773 +/- 6,821 versus 13,936 +/- 6,217 micrograms/L.h, respectively (P < .005). No differences were found in chylomicron remnant levels between the groups. Bezafibrate therapy reduced the chylomicron RP area by 27%, from 17,773 +/- 6,821 to 12,895 +/- 2,576, and the nonchylomicron RP area by 25%, from 6,059 +/- 3,310 to 4,430 +/- 1,963 (P < .0001). It increased fasting HDL-C levels from 35 +/- 3 to 38 +/- 1.4 mg/dL after 3 months (P < .001) and to 40 +/- 2.2 mg/dL after 6 months (P < .001).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Aged; Bezafibrate; Cholesterol, HDL; Chylomicrons; Coronary Artery Disease; Coronary Disease; Diterpenes; Eating; Fasting; Humans; Hypolipidemic Agents; Hypolipoproteinemias; Lipoproteins; Male; Middle Aged; Retinyl Esters; Triglycerides; Vitamin A

Prolonged and exaggerated postprandial plasma triacylglycerol (TAG) concentrations are considered as an independent risk factor for coronary artery disease. Western populations eat many meals at regular intervals, and can be in a postprandial state for at least 17 h of a 24 h period. After consuming 2 meals an early plasma TAG peak has been observed after the second meal, the origin of which is unclear.. To test the hypothesis that the early TAG peak observed following sequential meals was of intestinal origin and represented fat derived from the previous meal.. Postprandial plasma lipaemic responses of 17 healthy postmenopausal women were studied by giving a test breakfast followed by a lunch. Watermiscible retinyl palmitate (RP) was added to the breakfast, but not the lunch test meal. Plasma TAG, retinyl esters (RE) and apo B-48 were determined for a 10 h period following breakfast.. In response to the test meals, RE, apo B-48 and TAG showed multiple peaks. Despite omission of RP from the lunch, RE showed an early peak response after ingestion of lunch in 15 of 17 subjects. The peak response after lunch of all three markers appeared significantly earlier compared with their respective peak responses after the breakfast (P < 0.0001). The area of RE response after lunch was significantly correlated with the RE lipaemic response to the breakfast (r = 0.67; P < 0.004) and to the fasting TAG concentration (r = 0.48; P < 0.05).. Since the lunch did not contain RP, the distinctive second influx of RE after lunch was believed to have originated from the breakfast. This, together with the fact that all three markers showed an earlier response to the lunch than the breakfast, supports the view that ingestion of a second meal provokes entry of fat from the previous meal, from an as yet unidentified site (gut, enterocytes, lymph). The results indicate that the degree of TAG "storage" from previous meals might be a function of TAG tolerance and provide a possible site of regulation of the entry of fat into the systemic circulation.

Topics: Aged; Apolipoprotein B-48; Apolipoproteins B; Area Under Curve; Chylomicrons; Coronary Disease; Dietary Fats; Digestion; Diterpenes; Female; Humans; Middle Aged; Postmenopause; Postprandial Period; Retinyl Esters; Risk Factors; Triglycerides; Vitamin A

Dyslipidemia is common among patients receiving antiretroviral therapy for HIV infection. The purpose of this study was to determine whether postprandial lipemia contributes to the dyslipidemia observed in HIV-positive patients taking antiretroviral therapy.. A standardized fat load was administered to 65 subjects (group 1 35 HIV-positive subjects receiving protease inhibitors [PIs]; group 2 20 HIV-positive subjects not receiving PIs; group 3 10 HIV-negative controls). Serum triglycerides, retinyl palmitate, and lipoproteins were measured using enzymatic and nuclear magnetic resonance spectroscopic techniques. Compared with HIV-negative controls, peak postprandial retinyl palmitate and large very low-density lipoprotein (VLDL) levels occurred later in both HIV-positive groups, and a delayed decrease in serum triglycerides was observed. However, postprandial areas under the curve (AUCs) for triglycerides, retinyl palmitate, chylomicrons, and large VLDL were similar. Postprandial AUCs for intermediate-density lipoproteins (IDLs) and low-density lipoproteins (LDLs) were higher in group 1 than groups 2 and 3 (all P<0.035).. Postprandial clearance of triglyceride-rich lipoproteins is delayed in HIV-positive individuals receiving antiretroviral therapy. Compared with HIV-positive individuals not on PIs, those taking PIs do not have increased postprandial triglyceride-rich lipoproteins but do have increased postprandial IDLs and LDLs. An oral fat load was administered to 55 HIV-positive and 10 HIV-negative individuals. Postprandial clearance of triglyceride-rich lipoproteins was delayed in HIV-positive individuals. Compared with HIV-positive subjects not on PIs, those taking PIs do not have increased postprandial triglyceride-rich lipoproteins but do have increased postprandial intermediate-density and low-density lipoproteins.

Topics: Adult; Anti-HIV Agents; Antiretroviral Therapy, Highly Active; Apolipoproteins E; Area Under Curve; Blood Glucose; Chylomicrons; Coronary Disease; Dietary Fats; Diterpenes; Female; HIV Infections; HIV Protease Inhibitors; Humans; Hyperlipidemias; Hypertension; Insulin; Lipoproteins; Lipoproteins, IDL; Lipoproteins, LDL; Lipoproteins, VLDL; Male; Postprandial Period; Retinyl Esters; Risk Factors; Smoking; Triglycerides; Vitamin A

It is not known in detail whether postprandial lipaemia is associated with coronary artery disease (CAD) in women. To investigate this, we administered an oral vitamin A/squalene/fat meal to 24 post-menopausal women with angiographically proven CAD who were not taking hormone replacement therapy, and to 30 healthy controls (18 without and 12 with hormone replacement therapy) to evaluate the effects of CAD on postprandial lipoprotein metabolism. This was done by assessing squalene, triacylglycerols, retinyl palmitate and apolipoprotein B-48 (apoB-48) during the subsequent 24 h. The subjects with CAD had significantly higher fasting concentrations of squalene and apoB-48 in triacylglycerol-rich lipoproteins (TGRL) compared with the controls. The postprandial areas under the incremental curve of TGRL apoB-48, chylomicrons, very-low-density lipoprotein (VLDL) and TGRL squalene, and of retinyl palmitate in VLDL only, were significantly higher in women with CAD than in controls. Adjustment for fasting values did not eliminate the differences in postprandial squalene and apoB-48 between CAD and controls. The postprandial responses of control subjects were not influenced by hormone replacement therapy. The peaks of squalene and retinyl palmitate of the controls, but not of the women with CAD, occurred significantly earlier (P<0.01 for both) in chylomicrons than in VLDL. The findings suggest that lipoproteins that accumulate postprandially are labelled by dietary squalene, and that these lipoproteins may be atherogenic in post-menopausal women.

Topics: Apolipoprotein B-48; Apolipoproteins B; Coronary Disease; Diterpenes; Estrogen Replacement Therapy; Female; Humans; Lipoproteins, VLDL; Middle Aged; Postmenopause; Postprandial Period; Retinyl Esters; Squalene; Triglycerides; Vitamin A

To assess the importance of postprandial lipemia and delayed chylomicron clearance as early atherogenic risk factors, 60 male offspring of parents with early coronary artery disease (CAD) and 41 controls were administered a fat-rich meal containing vitamin A. There were no significant differences between CAD-positive (CAD+) offspring and CAD-negative controls for areas under the postprandial curves for triglyceride and plasma, chylomicron, and chylomicron remnant retinyl palmitate. Older CAD+ offspring, aged 31-45 yr, had significantly increased very low density lipoprotein (VLDL) cholesterol, VLDL triglyceride, VLDL apoprotein B, and areas under postprandial curves for triglyceride and plasma, chylomicron, and chylomicron remnant retinyl palmitate than younger CAD+ offspring, aged 15-30 yr. Correcting for waist/hip ratio eliminated significant differences between the two groups for VLDL and areas under the triglyceride and chylomicron remnant curves, but this was not the case for the insulin sensitivity index. We conclude that neither increased postprandial lipemia nor abnormalities of chylomicron clearance are important early atherogenic risk factors in this population. An increase in age is associated with increased VLDL and postprandial lipemia and decreased chylomicron remnant clearance. This is due mainly to an increase in the waist/hip ratio and not to a change in insulin sensitivity.

Topics: Adolescent; Adult; Analysis of Variance; Case-Control Studies; Cholesterol; Chylomicrons; Coronary Disease; Diterpenes; Humans; Male; Metabolic Clearance Rate; Middle Aged; Parents; Postprandial Period; Reference Values; Retinyl Esters; Triglycerides; Vitamin A

We studied the effect of a single oral fat load, supplemented with retinyl palmitate (RP), on high density lipoprotein (HDL) lipids in six normolipidemic men with coronary artery disease (CAD) and in six age- and lipid-matched controls. All subjects were selected from a study group which underwent the same protocol 2 years earlier. Post-prandial total plasma lipids, plasma RP levels, and HDL lipids were evaluated at 2-h intervals up till 10 h after the meal. In most subjects the post-prandial response of plasma triglyceride (TG) and plasma RP was identical in the first and second tests. Following the fat load, control subjects showed no change in HDL total cholesterol (TC) or HDL cholesteryl ester (CE) and showed an increase in HDL-TG. CAD subjects however showed a decrease in HDL-TC and HDL-CE and an increase in HDL-TG, similar to the increase in control subjects. In control subjects an increase in HDL phospholipid (PL) was apparent between 0 and 8 h after the fat load. By contrast, in CAD subjects the increase in HDL-PL was only found after as long as 6 h. The magnitude of the post-prandial response of HDL-PL measured during the test was significantly lower in the CAD group. The effects of the fat load on HDL free cholesterol (FC) were similar to the changes in HDL-PL. These data support the hypothesis that PL and FC released during the degradation of chylomicrons as surface remnants are taken up by HDL. This process is clearly delayed in normolipidemic CAD subjects compared with controls. The data suggest that differences in the post-prandial response to an oral fat load in normolipidemic CAD patients and control subjects are not confined to the clearance of TG-rich lipoproteins, but also involve a difference in the uptake of chylomicron surface material by HDL.

Topics: Adult; Aged; Carrier Proteins; Cholesterol Ester Transfer Proteins; Cholesterol, HDL; Chromatography, High Pressure Liquid; Coronary Disease; Dietary Fats; Diterpenes; Follow-Up Studies; Glycoproteins; Humans; Male; Middle Aged; Phospholipids; Postprandial Period; Retinyl Esters; Triglycerides; Vitamin A

A 49 year-old hypercholesterolemic male with marked electrocardiographic ST segment depression on exercise testing was found to have an apo E E3/3 phenotype by isoelectric focusing, but an APOE E4/3 genotype using HhaI restriction isotyping. DNA sequence analysis of the proband's APOE gene found a G-->C point mutation at codon 251. This predicted a change in the amino acid encoded by codon 251, from arginine to glycine. The mutation occurred on an allele that encoded arginine at position 112 and this variant was named APOE R112; R251G. The R251G change altered a recognition site for the endonuclease StuI and was the basis for a restriction isotyping method to rapidly screen for this mutation. In relatives of the proband, APOE R112; R251G was consistently found in subjects with both hyperlipidemia and atherosclerosis. Apo E R112; R251G-containing very low density lipoproteins bound normally to macrophages in vitro. However, the proband had an abnormal post-prandial lipoprotein response to a dietary fat challenge. The association of APOE R112; R251G with abnormal phenotypes suggests that the amino acid change in the carboxy-terminal, perhaps in combination with the common amino acid polymorphism at codon 112, has a functional impact upon lipoprotein metabolism in members of this family.

Topics: Animals; Apolipoproteins E; Cell Line; Cholesterol; Cholesterol Esters; Coronary Disease; Diterpenes; Female; Humans; Hyperlipidemia, Familial Combined; Hyperlipoproteinemia Type II; Isoelectric Focusing; Lipoproteins, VLDL; Macrophages; Male; Mice; Middle Aged; Oleic Acid; Pedigree; Polymorphism, Restriction Fragment Length; Postprandial Period; Retinyl Esters; Sequence Analysis, DNA; Triglycerides; Vitamin A

Because remnants of triglyceride-rich lipoproteins (TRLP) are potentially atherogenic, the postprandial lipoprotein metabolism was studied in 12 normocholesterolemic, normotriglyceridemic women, aged 60 +/- 2 years, with angiographically proven coronary artery disease (CAD+; cholesterol 5.7 +/- 0.1 (S.E.) mmol/l, triglyceride 1.35 +/- 0.10 mmol/l) and in 12 individually matched controls, aged 59 +/- 2 years, without angiographical abnormalities (CAD-; cholesterol 5.1 +/- 0.2 mmol/l and triglyceride 1.16 +/- 0.13 mmol/l). Following an oral retinyl palmitate-fat load, the CAD+ women showed a significantly higher triglyceride response in the chylomicron, or Sf > 1000, fraction (P < 0.05 vs. controls). Total plasma apolipoprotein (apo) B and retinyl palmitate concentrations were similar in both groups. Fasting apo B-48 levels in the d < 1.006 g/ml fraction were significantly higher in CAD+ cases (0.25 +/- 0.03 integrated optical density (iod) units) than CAD- controls (0.15 +/- 0.03; P < 0.05). Furthermore, after the fat load, a greater absolute and incremental apo B-48 response in the intermediate density lipoprotein (IDL) fraction (d = 1.006-1.019 g/ml) was observed in CAD+ cases (incremental area under the curve (Delta-AUC)8: 0.40 +/- 0.12 h.iod) than CAD- controls (0.01 +/- 0.06 h.iod; P = 0.01). Post-heparin hepatic lipase (HL) activities were higher in the CAD+ group: 422 +/- 22 mU/l vs 288 +/- 20 mU/ml in the CAD- group (P < 0.001) while lipoprotein lipase (LPL) activities were identical. The results provide evidence that the metabolism of intestinal TRLP is significantly different in normolipidemic women with angiographically proven CAD compared with individually matched controls without coronary disease. Fasting apo B-48 levels in d< 1.006 g/ml fractions represent a potentially useful marker in women at risk for CAD.

Topics: Analysis of Variance; Anticoagulants; Apolipoprotein B-48; Apolipoproteins B; Case-Control Studies; Cholesterol; Coronary Angiography; Coronary Disease; Diterpenes; Electrophoresis, Polyacrylamide Gel; Female; Heparin; Humans; Lipoprotein Lipase; Lipoproteins; Lipoproteins, IDL; Liver; Middle Aged; Postprandial Period; Radioimmunoassay; Retinyl Esters; Retrospective Studies; Risk Factors; Triglycerides; Ultracentrifugation; Vitamin A

A low HDL cholesterol level is frequently but not consistently associated with inefficient postprandial fat clearance. We studied triglycerides, retinyl palmitate and squalene and apolipoprotein B-48 after a fat loading test in one subject heterozygous for a novel point mutation of apolipoprotein A-I (A-IFIN, Leu 159-->Arg) and low HDL cholesterol level without coronary artery disease, and in 16 healthy controls with the same apolipoprotein E phenotype, 3/3, as the proband. HDL cholesterol and apolipoprotein A-I levels were 0.32 mmol/l and 57 mg/dl in the proband, and 1.29 +/- 0.12 mmol/l (mean +/- S.E.) and 126 +/- 4 mg/dl in the controls. The peak concentration for triglycerides in plasma, chylomicrons and VLDL occurred at 4 h both in the case and controls. However, the peak concentrations for retinyl palmitate and squalene in chylomicrons and VLDL were delayed to 12 h in the proband compared with 4 and 9 h in the controls. The peak of apolipoprotein B-48 occurred at 6 h in the proband and at 4 h in the controls, so that triglycerides, apolipoprotein B-48 and retinyl palmitate and squalene peaked differently. After 24 h, retinyl palmitate, squalene, and apolipoprotein B-48 had returned to the baseline levels. The results show for the first time an impaired postprandial lipoprotein removal in a case heterozygote with moderately low HDL cholesterol due to an apolipoprotein A-1 mutation not associated with coronary artery disease.

Topics: Adult; Anticarcinogenic Agents; Apolipoprotein A-I; Apolipoprotein B-48; Apolipoproteins B; Cholesterol, HDL; Cholesterol, VLDL; Chromatography, Gas; Chylomicrons; Coronary Disease; Dietary Fats; Diterpenes; Electrophoresis, Polyacrylamide Gel; Female; Heterozygote; Humans; Middle Aged; Point Mutation; Postprandial Period; Retinyl Esters; Risk Factors; Squalene; Triglycerides; Vitamin A

Blood lipid alterations after a fatty meal may be atherogenic, but there is little information regarding their associations with disease independent of fasting lipids. Asymptomatic atherosclerosis cases (n = 229) and 373 control subjects free of atherosclerosis, as defined by carotid intima-media thickness on ultrasound images, were given a fatty meal with vitamin A, followed by 3.5- and 8-hour measurements of triglycerides (TGs), TG-rich lipoprotein TGs, apoproteinB48, and retinyl palmitate. Among white men and women but not among blacks, case status was associated with greater postprandial responses of TGs and TG-rich lipoprotein TGs, but only in nonobese persons (body mass index < 30 kg/m2). The associations were strong and significant after controlling for coronary risk factors (odds ratio, approximately 2.0) and fasting TGs (odds ratio, 1.5). Associations with other postprandial lipid measurements did not persist after controlling for fasting lipids. Elevated postprandial TGs appear to be an independent risk factor for carotid intimal thickening in nonobese whites. The lack of such a relation in obese subjects and the lipid profile they manifest suggest that postprandial TGs must be accompanied by accumulation of TG-rich lipoprotein remnants to be atherogenic.

Topics: Apolipoprotein B-48; Apolipoproteins B; Arteriosclerosis; Black People; Carotid Artery Diseases; Carotid Stenosis; Coronary Disease; Dietary Fats; Diterpenes; Female; Humans; Male; Middle Aged; Obesity; Retinyl Esters; Triglycerides; Vitamin A; White People

Although strong evidence exists linking fasting plasma levels of LDL cholesterol (LDL-C) and HDL cholesterol (HDL-C) to risk for development of coronary artery disease (CAD), the data in support of an independent role for fasting triglyceride (TG) concentrations are weak. Humans are in the postprandial state most of the day, however, and results from both basic and clinical studies suggest that postprandial TG levels may be atherogenic. Previous studies have not, however, attempted to determine if postprandial TG levels are associated with CAD independent of other traditional risk factors or plasma lipid levels, particularly fasting plasma concentrations of TG and HDL-C. Ninety-two men and 113 women (mean age, 51.6 and 53.6 years, respectively) were recruited from populations undergoing diagnostic exercise electrocardiographic or thallium stress tests at our medical centers. Twenty-six men and 24 women had positive tests. We chose exercise-induced myocardial ischemia (EIM) as the criterion for defining case and control subjects because we wanted participants who did not have a prior diagnosis of CAD. Blood samples were obtained for measurement of plasma TG, TG-rich lipoprotein TG, and retinyl palmitate (RP) levels 2, 3.5, 5, and 8 hours after the subjects had consumed a fatty test meal. Logistic regression models were developed to test for associations between each variable and case-control status. Among men but not women postprandial TG and RP responses were associated with EIMI independent of age, race, and smoking status. In the male group, the odds ratio (OR) for an increase in postprandial TG response of approximately 1 SD was 1.69 (P = .007); the OR for an increase in RP response of 1 SD was 2.47 (P = .011). However, when fasting TG was added to the model, the OR for postprandial TG area in the men was reduced to 1.44 (P = .17); the OR postprandial RP area in the men was reduced to 1.88 (P = .12). There was no effect of adding other risk factors, including LDL-C and HDL-C, to the model. Significant effect modification by body mass index (BMI) on the relationship between postprandial responses and case-control status was observed. In men with BMI < 30, the OR was 1.83 for postprandial TG (P = .041) and 2.77 for postprandial RP (P = .032) in models that included fasting TG, LDL-C, and hypertension.

Topics: Age Factors; Case-Control Studies; Coronary Disease; Diterpenes; Exercise Test; Female; Food; Humans; Male; Middle Aged; Myocardial Ischemia; Retinyl Esters; Risk Factors; Sex Factors; Triglycerides; Vitamin A

Topics: Adult; Apolipoprotein B-100; Apolipoproteins B; Chylomicrons; Coronary Disease; Diterpenes; Eating; Fasting; Humans; In Vitro Techniques; Lipids; Macrophages; Middle Aged; Retinyl Esters; Time Factors; Vitamin A

To investigate whether abnormalities in alimentary lipemia explain the increased risk of coronary artery disease (CAD) in subjects with non-insulin-dependent diabetes mellitus (NIDDM), we performed an oral vitamin A fat-load test in four groups of men (each n = 15): 1) NIDDM and angiographically verified CAD (DM+CAD+): 2) CAD but no diabetes (DM-CAD+); 3) NIDDM but no CAD, excluded by an exercise thallium scan (DM+CAD-); and 4) healthy control subjects (DM-CAD-). The groups were matched for age and body mass index. Plasma obtained after an overnight fast and 2, 3, 4, 6, 9, 12, and 24 h after a fatty meal (78 g fat, 345,000 IU retinyl palmitate [RP]) was separated by density gradient ultracentrifugation into six fractions of triglyceride (TG)-rich lipoproteins: Svedberg flotation units (Sf) > 3200, Sf 1100-3200, Sf 400-1100, Sf 60-400, Sf 20-60, and Sf 12-20. TG, RP, and cholesterol concentrations were measured in plasma and in each lipoprotein fraction. Postprandial plasma TG responses were significantly larger in both NIDDM groups than in the healthy control group. The most marked differences were observed in the Sf 60-400 lipoproteins, whether measured as TG or RP responses. However, there were no differences between the DM+CAD+ and DM+CAD- groups. The between-group differences in alimentary lipemia were only partially explained by fasting TG levels. In contrast to the healthy subjects, no significant negative correlation was observed in the NIDDM patients between alimentary lipemia and lipoprotein lipase activity, implying an abnormality of the lipolysis of TG-rich particles in NIDDM. Levels of atherogenic postprandial remnant lipoproteins are increased in NIDDM. However, in this study the magnitude of alimentary lipemia did not distinguish NIDDM patients with CAD from those without CAD symptoms and normal exercise thallium scans.

Topics: Aged; Apolipoproteins E; Blood Glucose; Cholesterol; Coronary Disease; Diabetes Mellitus, Type 2; Dietary Fats; Diterpenes; Humans; Hypertriglyceridemia; Insulin; Lipase; Lipoprotein Lipase; Lipoproteins; Lipoproteins, HDL; Lipoproteins, IDL; Lipoproteins, VLDL; Male; Middle Aged; Plasminogen Activator Inhibitor 1; Retinyl Esters; Triglycerides; Vitamin A

This report describes the response of patients with severe coronary artery disease to a dynamic fat load test and monitors the change induced by fenofibrate therapy. The presence of disease was associated with prolonged and exaggerated hypertriglyceridemia following the meal and with lower basal HDL cholesterol and HDL subfraction masses. A further indicator of risk was the persistence of increased amounts of retinyl palmitate in the plasma of severely affected individuals 24 h after its ingestion with the meal. These observations are consistent with the proposal that the clearance of chylomicrons and their remnants is impaired in coronary atherosclerosis. Fenofibrate reduced alimentary lipemia following the fat load in both normo- and hypercholesterolemic subjects. This was associated with a 10% rise in plasma HDL cholesterol levels. The improvement in chylomicron catabolism probably derived from a 37% increase (P less than 0.001) in lipoprotein lipase activity induced by fenofibrate. Hepatic lipase on the other had was only slightly affected by treatment.

Topics: Adult; Cholesterol; Cholesterol, HDL; Cholesterol, VLDL; Coronary Disease; Dietary Fats; Diterpenes; Fenofibrate; Heparin; Humans; Lipase; Lipids; Lipoprotein Lipase; Liver; Middle Aged; Retinyl Esters; Triglycerides; Vitamin A