Impact of hormone replacement therapy on postprandial lipoproteins and lipoprotein(a) in normolipidemic postmenopausal women

In 43 normolipidemic postmenopausal women we studied fasting and postprandial (oral fat load with 50 g fat per square meter; blood sampling for 5 h) lipoprotein components and lipoprotein(a) levels before and with the administration of conjugated equine estrogens opposed by medrogestone (on days 11–21). Data was compared intraindividually; the second testing was performed during the last 5 days of the combined estrogen/progestogen phase of the third cycle. Fasting low-density lipoprotein (LDL) and total cholesterol concentrations decreased significantly; high-density lipoprotein (HDL) cholesterol, including subfractions HDL₂ and HDL₃, was not changed. Fasting triglyceride concentrations increased. All lipoprotein fractions measured showed a postprandial elevation with the exception of chylomicron cholesterol concentrations. There was a significant effect of hormone replacement therapy on the postprandial course of total cholesterol (decrease; P < 0.001), VLDL cholesterol (increase; P = 0.025), and the triglyceride proportion in the LDL plus HDL fraction (increase; P < 0.001). With hormone replacement therapy the postprandial curve of total triglycerides was increased only 1 h after the fat load while chylomicron triglyceride concentrations were lowered after 5 h. VLDL triglycerides were not influenced. In all patients with lipoprotein(a) levels above 10 mg/dl, this parameter decreased (about 25%). Although increasing fasting triglyceride concentrations, hormone replacement therapy does not bring about an exaggerated postprandial increase in triglycerides. Postprandial chylomicron clearance is evidently promoted. Hormone replacement therapy leads to a small increase in triglycerides in the LDL plus HDL fraction by inhibiting hepatic lipase activity. Moreover, the decrease in lipoprotein(a) levels may contribute to the antiatherosclerotic effect.Abbreviations: CEE conjugated equine estrogens - HDL high-density lipoproteins - HRT hormone replacement therapy - LDL low-density lipoproteins - TG triglycerides - VLDL very low density lipoproteins Correspondence to: U. Julius     

Role of hepatic and lipoprotein lipase in lipoprotein metabolism and atherosclerosis: studies in transgenic and knockout animal models and somatic gene transfer

Hepatic lipase (HL) and lipoprotein lipase (LPL) are the two major lipolytic enzymes responsible for the hydrolysis of triglycerides and phospholipids present in circulating plasma lipoproteins. Both lipases are attached to the vascular endothelium via cell surface proteoglycans. HL is primarily involved in the metabolism of chylomicron remnants, intermediate density lipoproteins and high-density lipoproteins whereas LPL catalyzes the hydrolysis of triglycerides from chylomicrons and very low-density lipoproteins. In addition to their traditional function as lipolytic enzymes, HL and LPL appear to serve as ligands that mediate the interaction of lipoproteins to cell surface receptors and/or proteoglycans. Over the past several years significant advances have been made in our understanding of new, alternative mechanisms by which HL and LPL modulate lipoprotein metabolism and the development of atherosclerosis in vivo. This review will summarize some of the new insights generated from the study of transgenic and knockout HL and LPL animal models as well as somatic gene transfer of these two lipases.     

Lipoprotein lipase activity in patients with combined hyperlipidaemia

The aetiology of familial combined hyperlipidaemia remains obscure, with both genetic and environmental factors contributing to the phenotype, which is frequently associated with premature coronary heart disease. We have studied lipoprotein lipase (LPL) activity and hepatic lipase (HL) activity in patients with coronary heart disease to determine whether variation in lipase activities contributes to this phenotype. Forty-one patients (mean age 50 years; 30 male) were selected on the basis of cholesterol levels above 6.5 mmol/l and triglyceride levels above 2.2 mmol/1, with apoprotein B values over the 90th percentile. There was a family history of premature coronary heart disease in 78% and a personal history in 64%, at mean age 44, the patient group therefore predominantly corresponded to the common definition of familial combined hyperlipidaemia, appropriate in the absence of molecular markers. None of the patients was diabetic; hypertension and smoking were not over represented. Blood samples were taken following intravenous administration of heparin (100IU/kg body wt), and LPL and HL activities were measured. Mean post-heparin LPL was significantly lower in patients than controls 10 min after heparin administration (2.98 ± 1.04 and 3.86 ± 0.93 mol ml^-1 h^-1, respectively, P = 0.001), and 37% patients had values below the 10th percentile of controls. Both male and female patients had significantly higher HL activities than their respective controls at 5, 10, 20 and 30 minutes postheparin. As expected, both female patients and controls had lower HL activities than males, although this sex difference did not reach statistical significance in the patient group. Mean lipid and lipoprotein results were: cholesterol 8.2 mmol/1; triglycerides 4.2 mmol/l; high-density lipoprotein cholesterol 0.90 mmol/1; apoprotein Al 122 mg/dl; apoprotein B 171 mg/dl; lipoprotein (a) 23 mg/dl (median 10 mg/dl). High-density lipoprotein cholesterol and triglycerides were negatively correlated (r = -0.26, P = 0.05). HL was significantly related to body mass index at all time points whereas the negative correlation between post-heparin LPL and body mass index was significant only 30 min after heparin administration. Post-heparin LPL was only weakly correlated with triglycerides 10 and 20 min after heparin administration. These lipid and lipoprotein results are clearly potentially atherogenic as indicated by the extent of premature coronary heart disease in the group described. A decrease in LPL activity may contribute to this pattern.Abbreviations FCHL familial combined hyperlipidaemia - CHD coronary heart disease - LPL lipoprotein lipase - HL hepatic lipase - HDL high-density lipoprotein - VLDL very low density lipoprotein; - apo apoprotein - TG triglyceride - BMI body mass index Correspondence to: M. Seed     

Effects of a brisk walk on lipoprotein lipase activity and plasma triglyceride concentrations in the fasted and postprandial states

This study aimed to determine whether changes in plasma heparin-releasable lipoprotein lipase (LPL) activity following a brisk walk were associated with decreases in fasting and/or postprandial triglyceride (TG) concentrations. Two groups of pre-menopausal women participated. In one group (fasting study group, n=10), TG concentrations and post-heparin plasma LPL activity were measured in the fasted state on two occasions: ~18 h after a 2-h treadmill walk at 50% maximal oxygen uptake (exercise trial); and after a day of no exercise (control trial). The other group (postprandial study group, n=9) undertook two oral fat tolerance tests (blood samples taken fasting and for 6 h after a high-fat meal), with plasma LPL activity measured 6 h after meal ingestion. Pre-conditions were the same as for the fasting study group (i.e. control and prior exercise). Prior exercise reduced fasting TG concentrations by 23 (7)% (fasting study group) [mean (SEM)] and by 18 (9)% (postprandial study group) (both P<0.05), and the postprandial TG response by 23 (6)% (postprandial study group) (P<0.01). Plasma LPL activity was not significantly increased by exercise in either the fasting or postprandial study groups. However, exercise-induced changes in both fasting and postprandial LPL activity were significantly correlated with the respective exercise-induced changes in fasting TG concentration and the postprandial TG response (r=−0.70 and −0.77 respectively, P<0.05 for both). These data suggest that increased LPL activity may contribute to the hypotriglyceridaemic effect of moderate exercise, although other mechanisms are also likely to be involved. Electronic Publication     

Chronic hyperprolactinemia and plasma lipids in women

Summary Plasma total cholesterol (TC), triglycerides (TG), high-density lipoprotein-cholesterol (HDL-C), and low-density lipoprotein-cholesterol (LDL-C) were studied in 15 hyperprolactinemic women who had a prolactin (PRL) adenoma, in comparison to 15 age-matched control women. In the hyperprolactinemic group, plasma lipids were also correlated to age, excess body weight (EBW), plasma PRL, and estradiol-17 (E2). Plasma TC, TG, and LDL-C were similar in both hyperprolactinemic and control women, while plasma HDL-C was significantly lower (P<0.01) in the hyperprolactinemic group. The correlation study showed a significant negative correlation between HDL-C and EBW (r=–0.64;P<0.02) and a slightly significant positive correlation between TG and PRL (r=0.54;P<0.05). The direct effect of PRL on plasma lipids is difficult to establish since many factors influencing lipid metabolism are altered during hyperprolactinemia.Abbreviations EBW excess body weight - E2 estradiol-17 - GH growth hormone - HDL-C high-density lipoprotein-cholesterol - LDL-C low-density lipoprotein-cholesterol - LPL lipoprotein lipase - PRL prolactin - RIA radioimmunoassay - TC total cholesterol - TG triglycerides     

Selective deficiency of hepatic triglyceride lipase in uremic patients.

To investigate the pathogenesis of hypertriglyceridemia in patients with renal disease we measured plasma lipoprotein composition as well as hepatic triglyceride lipase and lipoprotein lipase in post-heparin plasma. Three groups with renal disease were studied: conservatively treated chronic uremia; patients undergoing maintenance hemodialysis; and renal-allograft recipients. A selective decrease of hepatic triglyceride lipase with normal lipoprotein lipase was found in conservatively treated uremia and in patients undergoing hemodialysis. Elevated levels of very-low-density lipoproteins and increased triglycerides in low-density lipoproteins occurred in these patients. In contrast, hepatic triglyceride lipase and lipoprotein lipase were both normal in patients after renal transplantation who had Type II hyperlipoproteinemia as a common lipoprotein pattern with increased low-density-lipoprotein cholesterol and decreased high-density-lipoprotein cholesterol concentrations. The accumulation of a triglyceride-rich low-density lipoprotein in the majority of patients with renal disease may be the consequence of low hepatic triglyceride lipase.     

Relationship of high-density lipoprotein subfractions and cholesteryl ester transfer protein in plasma to carotid artery wall thickness

High plasma concentrations of high-density lipoprotein (HDL) cholesterol are a powerful indicator of low vascular risk. By decreasing HDL cholesterol, cholesteryl ester transfer protein (CETP) could perhaps constitute an atherogenic protein. We measured HDL cholesterol and HDL subfractions and quantified CETP mass in fasting plasma in 21 asymptomatic probands, and related these variables to the mean intima media thickness of the extracranial carotid arteries. HDL₂ cholesterol, the less dense HDL subfraction, was inversely related to carotid wall thickness (r=–0.378; P<0.05), and CETP was directly related to carotid wall thickness (r=0.436; P<0.05). In plasma CETP is associated mostly with the HDL₃ subfraction. We therefore calculated from our measurements the relative CETP content of HDL₃, i.e., CETP/HDL₃ cholesterol. This ratio was correlated with carotid wall thickness stronger than any other variable measured (r=0.718, P<0.001). We conclude that variation in HDL subfractions and CETP may be more closely associated with carotid intima media thickness than the accepted strong risk factor of HDL cholesterol.Abbreviations HDL High-density lipoprotein - CETP Cholesteryl ester transfer protein - LDL Low-density lipoprotein     

Alterations in serum lipids and lipoproteins profile of pregnant camels (Camelus dromedarius) at term

Concentration of serum lipids and lipoproteins was determined on 32 pregnant camels (Camelus dromedarius) at term and was compared with those of 31 non-pregnant camels. Variations in the serum concentrations of total cholesterol, triglycerides, total lipid, and some lipoproteins such as high-density lipoprotein cholesterol, low-density lipoprotein cholesterol (LDL-C), and very low-density lipoprotein were investigated. Sera from pregnant group had significantly higher mean triglycerides and very low-density lipoprotein concentrations. However, total cholesterol and high-density lipoprotein showed significantly low concentrations. Total lipid and LDL-C did not differ significantly.     

Postprandial dyslipidemia in insulin resistant states in adolescent populations

Obesity and the metabolic syndrome are becoming increasingly prevalent not only in adults, but also in adolescents. The metabolic syndrome, a complex cluster of metabolic abnormalities, increases one's risk of developing type 2 diabetes and cardiovascular disease (CVD). Dyslipidemia, a key component of the metabolic syndrome, is highly associated with insulin resistance and contributes to increased CVD risk. Dyslipidemia has traditionally been assessed using a fasting lipid profile [i.e. fasting triglycerides, total cholesterol, low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C)]. However, the postprandial state predominates over the course of a day and non-fasting triglycerides independently predict CVD risk. In insulin resistant states, the intestine overproduces triglyceride-rich lipoprotein (TRL) particles, termed chylomicrons (CMs), following ingestion of a fat-containing meal, as well as in the fasting state. Along with elevated hepatic TRLs (i.e. very-low density lipoproteins), CMs contribute to remnant lipoprotein accumulation, small dense LDL particles, and reduced HDL-C, which collectively increase CVD risk. Given the early genesis of atherosclerosis and physiological metabolic changes during adolescence, studying postprandial dyslipidemia in the adolescent population is an important area of study. Postprandial dyslipidemia in the pediatric population poses a significant public health concern, warranting a better understanding of its pathogenesis and association with insulin resistance and CVD. This review discusses the metabolic syndrome, focusing on the link between insulin resistance, postprandial dyslipidemia, and CVD risk. Furthermore, the clinical significance and functional assessment of postprandial dyslipidemia, specifically in the adolescent population, is discussed in more detail.     

Atypical type III hyperlipoproteinemia in a patient with Ig A myelomatosis

Summary We studied a 58-year-old woman with severe therapy-refractory hyperlipidemia, xanthomatosis, and multiple myeloma (immunoglobulin A, lambda light chain). The lipid disorder became evident about half a year prior to the expression of myelomatosis. Clinical symptoms were similar to those found in classical type III hyperlipoproteinemia but the underlying metabolic defect was different from the one described in this primary dyslipoproteinemia. The patient has the heterozygous apolipoprotein E3/2 phenotype and her VLDL-cholesterol/serum-triglyceride ratio is unusually low at 0.05. Evidence is given that the hyperlipoproteinemia is due to an impaired catabolism of intermediate density lipoproteins probably because of a reduced hepatic triglyceride lipase activity.Abbreviations AIH autoimmune hyperlipidemia - Chol cholesterol - HDL high density lipoproteins - HLP hyperlipoproteinemia - HTGL hepatic triglyceride lipase - IDL intermediate density lipoproteins - IEF isoelectric focusing - Ig immunoglobulin - LDL low density lipoproteins - LPL lipoprotein lipase - PL phospholipids - TG triglycerides - VLDL very low density lipoproteins     

Variability in the response of different male subjects to the effect of marathon running on the increase in plasma high density lipoprotein

Summary The acute effects of running a 42.2 km marathon race on the concentration and composition of the plasma lipoproteins were studied in 56 men of varying fitness, training experience, age and physical characteristics. There was no change in the mean concentration of total serum cholesterol, but a 10.9% increase (P<0.001) in the mean concentrations of high-density lipoprotein cholesterol (HDL-TC), representing an 11.1% increase (P<0.001) in the cholesteryl ester (CE) and 9.9% increase (P<0.001) in the unesterified cholesterol (UC) moieties of HDL. The ratio of total serum cholesterol to HDL-TC decreased significantly (P<0.001) during the exercise. Changes in lipoprotein concentrations during the marathon varied considerably between individual subjects, with a small proportion of subjects exhibiting relatively large increases or decreases in HDL-TC, HDL-CE and HDL-UC. Small sub-populations of runners were identified who showed abnormally large decreases in HDL-UC and abnormally small increases in HDL-CE relative to HDL-UC. A correlation (P<0.05) was found between the average weekly mileage of training and the increase in HDL-TC, whilst faster runners (finishing time <3 h; n=13) had a significantly greater (P<0.02) increase in HDL-TC than slower runners (>4 h; n=14). The observed alterations in the lipoproteins are consistent with increased rates of lipolysis of triacylglycerol-rich lipoproteins and of cholesterol esterification during the marathon and suggest that the effect of exercise on the activities of the enzymes that catalyse these processes may vary considerably between different subjects and may be modulated by training and other factors.Abbreviations VLDL very low density lipoproteins - LDL low density lipoproteins - HDL high density lipoproteins - HDL-TC high-density lipoprotein-total cholesterol - HDL-CE cholesteryl ester - HDL-UC unesterified cholesterol     

Genetic contributions to quantitative lipoprotein traits associated with coronary artery disease: Analysis of a large pedigree from the Bogalusa heart study

A pedigree of a large family with high prevalence of heart disease is subjected to association and sib-pair linkage analysis to investigate the role of 5 candidate genes in the regulation of lipoprotein metabolism and the development of coronary artery disease. At the 5% nominal significance level, the apolipoprotien B locus (APOB) was found to be linked to high-density lipoprotein cholestrol level (HDL-C), low-density lipoprotein cholestrol level (LDL-C), the ratio HDL-C/LDL-C, and apolipoprotein AI level times this ratio (apoAI × LDL-C/HDL-C). APOB (PvuII) was strongly associated with apolipoprotein B levels (apoB) (P = 0.006) and the VNTR region of the APOB locus showed highly significant association between allele 7 and low triglyceride levels (P = 0.004). No significant linkage results were found with cholesterol ester transfer protein (CETP). At the 1% nominal significance level, CETP [TaqI(B)] showed significant association with LDL-C, apoB, and HDL-C/LDL-C. There was significant linkage of lipoprotein lipase (LPL) with very-low-density lipoprotein cholestrol and the ratio apoAI/HDL-C, and strong association results between LPL (HindIII) and triglyceride levels (P = 0.005). At the 5% nominal significance level, haptoglobin (HPA) was associated with HDL-C, HDL-C/LDL-C, apoAI/HDL-C and apoAI × LDL-C/HDL-C. The apolipoprotein AI locus did not show any significant linkages or associations. The study thus indicated that genetic variation of APOB, LPL, CETP, and lecithin cholestrol acyl transferase (which is linked to HPA and CETP) may play an important role in the regulation of lipoprotein metabolism and could contribute to the risk of coronary artery disease. © 1993 Wiley-Liss, Inc.     

Lecithin-cholesterol acyltransferase activity in patients with coronary artery disease examined by coronary angiography

This study grew out of observations of certain lecithin:cholesterol acyltransferase (LCAT) abnormalities in patients with atherosclerosis. We studied the interrelationships among LCAT, and total cholesterol, free and esterified cholesterol, cholesterol in individual lipoprotein fractions, triglycerides, phospholipids, free fatty acids, L-lactates in 90 angiographically examined patients with coronary artery disease and 30 control subjects without clinical manifestations of coronary artery disease. Results of the study showed LCAT activity to be significantly decreased (P<0.05) in patients with single-, double-, or triple-vessel disease than in disease-free subjects. LCAT was also found to follow the stage of coronary artery disease in angiographically examined patients. Decreased LCAT activity was accompanied by lower high-density lipoprotein cholesterol, elevated ratio of unesterified to esterified cholesterol, and increased levels of L-lactates, free fatty acids, and low-density lipoprotein cholesterol. Total cholesterol and triglycerides were within or slightly above the normal limits. The results show LCAT to be a significantly better indicator of the risk of coronary artery disease than either total cholesterol or triglycerides.Abbreviations LCAT lecithin:cholesterol acyltransferase - CAD coronary artery disease - UC/EC ratio of esterified to unesterified cholesterol - MI myocardial infarction - HDL high-density lipoprotein Correspondence to: A. Stavljenic-Rukavina     

Effects of short-term melatonin administration on lipoprotein metabolism in normolipidemic postmenopausal women

OBJECTIVE: To investigate the effects of short-term administration of melatonin on lipoprotein metabolism in normolipidemic postmenopausal women. METHODS: Fifteen such women received 6.0 mg melatonin daily for 2 weeks. Blood was sampled before and after treatment. We measured concentrations of total cholesterol and total triglyceride in the plasma, as well as the levels of cholesterol, triglyceride, and protein in the very low-density lipoprotein (VLDL), low-density lipoprotein (LDL), and high-density lipoprotein (HDL). Plasma apolipoprotein levels were determined by immunoturbidimetric assay. Activities of lipoprotein lipase, hepatic triglyceride lipase, and lecithin cholesterol acyltransferase were also determined by enzymatic analysis. RESULTS: Melatonin administration significantly increased the plasma levels of triglyceride by 27.2% (P < 0.05), of VLDL-cholesterol by 37.2% (P < 0.01), of VLDL-triglyceride by 62.2% (P < 0.001), and of VLDL-protein by 30.0% (P < 0.05). However, the plasma total cholesterol level and the concentration of lipid and protein in LDL and HDL were not significantly affected. Melatonin significantly increased the plasma levels of apolipoprotein C-II by 29.5% (P < 0.005), of C-III by 17.1% (P < 0.001), and of E by 7.6% (P < 0.05). The plasma levels of apolipoprotein A-I, A-II, and B were not altered. Melatonin significantly inhibited the activity of lipoprotein lipase by -14.1% (P < 0.05), but did not significantly affect the activities of hepatic triglyceride lipase or of lecithin cholesterol acyltransferase. CONCLUSIONS: Findings indicate that melatonin increases the plasma level of VLDL particles by inhibiting the activity of lipoprotein lipase, but may not affect the plasma levels of LDL and HDL particles in postmenopausal women with normolipidemia.     

Glucose tolerance,plasma lipoproteins and tissue lipoprotein lipase activities in body builders

Summary Oral glucose tolerance, insulin binding to erythrocyte receptors, serum lipids, and lipoproteins, and lipoprotein lipase activities of adipose tissue and skeletal muscle were measured in nine body builders (relative body weight (RBW) 118±4%), eight weight-matched (RBW 120±5%) and seven normal-weight controls (RBW 111±3%). The body builders had 50% higher relative muscle mass of body weight (% muscle) and 50% smaller relative body fat content (% fat) than the two other groups (P<0.005). Maximal aerobic power was comparable in the three groups. In the oral glucose tolerance test (OGTT), blood glucose levels, and plasma insulin levels were lower (P<0.05) in the body builders than in weight-matched controls. Insulin binding to erythrocytes was similar in each group. On the basis of multiple linear regression analysis, 87% of the variation in plasma insulin response could be explained by body composition (% muscle and % fat) and .Plasma total cholesterol, low-density lipoprotein (LDL) cholesterol, and very low-density lipoprotein (VLDL) triglyceride concentrations were significantly lower in the body builders than in weight-matched controls. In comparison with the normal-weight group, the body builders had a lower total cholesterol level. High density lipoprotein (HDL) cholesterol, its subfractions (HDL₂ and HDL₃ cholesterol) and lipoprotein lipase (LPL) activities of adipose tissue and skeletal muscle were comparable in all three groups. Partial correlation analysis showed a positive relationship between plasma total triglyceride, total cholesterol and LDL cholesterol on the other hand and the % fat on the other.The results indicate that a shift in body composition from the adipose to the muscular type is associated with 1) lower glucose and insulin levels during the OGTT and 2) decrease in total and VLDL triglyceride and in total and LDL cholesterol levels but unchanged HDL cholesterol level. Thus, body builders are characterized by some metabolic features which decrease the risk of coronary heart disease. In contrast to aerobic training, body building does not influence HDL or its subfractions.     

Effect of pravastatin on metabolic parameters of apolipoprotein B in patients with mixed hyperlipoproteinemia

Summary 3-Hydroxy-3-methylgluratyl coenzyme A reductase inhibitors reduce plasma cholesterol in different forms of hyperlipoproteinemia. Although an increase in low-density lipoprotein (LDL) receptor activity is the proven mechanism of this therapy in familial hypercholesterolemia, the mechanism remains controversial in mixed hyperlipoproteinemia. A decreased production of apolipoprotein B (apoB) and/or an increased removal of lipoproteins could mediate the hypocholesterolemic effect of these drugs. The effect of pravastatin on the metabolism of apoB was evaluated in a randomized, double blind, placebo controlled, cross-over study in five men with mixed hyperlipoproteinemia. Metabolic parameters for apoB were determined using endogenous labeling with [1^t3C]leucine and [¹⁵N]glycine and multicompartmental modeling. During pravastatin therapy cholesterol, LDL cholesterol, apoB, and LDL apoB levels were significantly reduced (P < 0.01) by 18%, 20%, 27%, and 29%, respectively, while triglyceride and high-density lipoprotein cholesterol levels remained unchanged. Pravastatin therapy increased the fractional catabolic rate of very low density lipoprotein apoB from 3.9±0.6 to 5.1±1.7 per day (P = 0.08) and that of LDL apoB from 0.37±0.09 to 0.46±0.10 per day (P<0.01). The apoB production (placebo 35.2±11.9 mg/kg per day; pravastatin 25.8±8.7 mg/kg per day) and conversion of very low density lipoprotein apoB to LDL apoB (placebo 65%, pravastatin 57%) remained stable. Thus, also in mixed hyperlipoproteinemia 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors increase the catabolism of apoB-containing lipoproteins without significantly affecting the production of apoB.Abbreviations apoB apolipoprotein B - FCR fractional catabolic rate - HMG hydroxy-methylglutaryl - CoA coenzyme A - FH familial hypercholesterolemia - HDL high-density lipoprotein - IDL intermediate-density lipoprotein - LDL low-density lipoprotein - VLDL very low density lipoprotein Dedicated to Prof. Dr. G. Paumgartner on the occasion of his 60th birthday     

Lipoprotein Metabolism in Dogs and Cats

High-density lipoproteins (HDL) are the predominant lipoproteins in plasma of dogs and cats and are the major cholesterol-carrying particles. Two HDL subfractions are identifiable in dog: small, dense particles (equivalent to human HDL₃) and large, buoyant particles called HDL₁, which overlap in hydrated density with low-density lipoproteins (LDL). The HDL₁ are enriched in cholesterol and apolipoprotein (apo) E, and are prevalent in dogs fed high amounts of cholesterol and, or, saturated fat, when they are also referred to as HDL_c. Lipoproteins similar to human HDL₂ and HDL₃ are identifiable in feline plasma, along with trace HDL₁. Lipoprotein lipase (LPL), hepatic lipase (HL) and lecithin: cholesterol acyl transferase (LCAT) activities are present in dogs and cats. Both species lack significant cholesteryl ester transfer protein activity, and reverse cholesterol transport is probably accomplished by receptor-mediated hepatic uptake of HDL₁. Methods for the measurement of canine and feline plasma lipoprotein-cholesterol concentrations, apolipoprotein concentrations, and the activities of LPL, HL and LCAT have been developed. Together with oral and intravenous fat tolerance tests, these methods provide the basis for studying lipoprotein metabolism in cats and dogs.Originally presented at ECCP 95.     

Serum lipid profiles and their correlation with thyroid hormones in clinically healthy Turkoman horses

 Blood samples were collected from the jugular vein of 50 clinically healthy Turkoman horses according to their age (2–3, 3–5 and >5 years) and sex. Variations in the serum concentrations of cholesterol, triglyceride, total lipid, very low-density lipoprotein (VLDL cholesterol), low-density lipoprotein (LDL cholesterol) and high-density lipoprotein (HDL cholesterol), and their correlations with the concentrations of triiodothyronine (T₃) and thyroxine (T₄) were investigated. With an increase in the age of animals, there were significant increases (p=<0.05) in the cholesterol, triglyceride, total lipid, HDL cholesterol, LDL cholesterol and VLDL cholesterol concentrations. However, sex showed no significant differences on the concentrations of these parameters. The concentrations of T₃ and T₄ were significantly different in male and female Turkoman horses (p=<0.05). There were no significant correlations between thyroid hormones (T₃ and T₄) and serum lipids and cholesterol concentations in lipoproteins. Received: 11 June 2002 / Accepted: 6 November 2002     

The apolipoprotein CIII T2854G variants are associated with postprandial triacylglycerol concentrations in normolipidemic Korean men

This study investigated associations between the apolipoprotein (apo) CIII polymorphism and triacylglycerol (TAG) concentrations in fasting and postprandial plasma. Polymerase chain reaction followed by a restriction fragment length genotyping was conducted to assess the allele frequency of the apo CIII T2854G variants in healthy and normolipidemic Korean men (n=262). Waist circumference, body mass index (kilograms per meter squared), fasting plasma concentrations of TAG, total cholesterol, high-density lipoprotein cholesterol (HDLC), low-density lipoprotein cholesterol (LDLC), glucose, and insulin were compared across the genotypes. Compared to TT homozygotes and TG heterozygotes, GG homozygotes had 22% higher fasting TAG concentrations, respectively (p<0.05). A subgroup of 60 subjects (TT homozygotes=20, TG heterozygotes=22, GG homozygotes= 18) were further invited to participate in a high-fat meal test to assess postprandial TAG concentrations. During the high-fat meal test, the GG homozygotes had 21% higher TAG area under the curve (AUC) than the TT homozygotes (p<0.05) and 22% higher TAG AUC than the TG heterozygotes (p<0.05). In conclusion, this is the first study to show that the apo CIII T2854G variants are associated with elevated postprandial TAG concentrations in the study population of Korean men.     

Effects of fish oil concentrate on lipoproteins and apolipoproteins in familial combined hyperlipidemia

Summary The effects of two moderate doses of long-chain n-3 fatty acids (3.0 and 4.5 g EPA + DHA per day for 4 weeks each) on serum lipids and lipoproteins of patients with familial combined hyperlipidemia (FCH) were studied in a double-blind, placebo-controlled clinical trial. In nine patients with FCH n-3 fatty acids led to a statistically significant, dose-dependent fall in very low density lipoprotein (VLDL) triglycerides (3 g/day: –42%, 4.5 g/day: –55%) VLDL cholesterol (3 g/day: –41%, 4.5 g/day: –47%), and VLDL apolipoprotein (apo) B-100 (3 g/day: –40%, 4.5 g/day: –56%). No overall change in low-density lipoprotein (LDL) cholesterol was found, as confirmed statistically. However, when analyzing the data of single patients LDL cholesterol and LDL apo B did not change in five patients but increased dose dependently (from pretreatment 4.80±0.93 mmol/l to 5.70+0.93 mmol/l LDL cholesterol after 4.5 g/day) in four. LDL and VLDL composition as indicated by cholesterol/apo B-100 and triglyceride/apo B-100 ratios did not change significantly. High-density lipoprotein (HDL) cholesterol was unchanged; the HDL cholesterol/apo A-I+apo A-II ratio increased by 19% (P<0.05) during fish oil treatment. We conclude that in FCH moderate doses of long-chain n-3 fatty acids are highly effective in lowering pathological VLDL triglycerides, VLDL cholesterol, and VLDL apo B. LDL cholesterol must, however, be monitored during treatment as it may rise substantially in some although not in all patients with this disease.Abbreviations EPA eicosapentaenoic acid - DHA docosahexaenoic acid - FCH familial combined hyperlipidemia - VLDL very low density lipoprotein - LDL low-density lipoprotein - HDL high-density lipoprotein - apo apolipoprotein Dedicated to Prof. Dr. N. Zöllner on the occasion of his 70th birthday