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PubMed1985

Impaired catabolism of very low-density lipoprotein-triglyceride in a family with primary hypertriglyceridemia.

In this report, kinetic studies of plasma very low-density lipoprotein-triglyceride (VLDL-TG) were examined in five brothers (three affected and two unaffected) from a family with primary hypertriglyceridemia. Synthesis and catabolism of VLDL-TG were studied by in vivo labelling of plasma TG with 3H-glycerol, and multicompartmental analysis of the plasma die-away curves. Results of the kinetic studies revealed the following information: (1) one brother, who had the highest plasma TG level and was obese, had both overproduction and a reduced fractional catabolic rate (FCR) of VLDL-TG; (2) second brother, who had moderate hypertriglyceridemia, had a low FCR and high-normal synthesis of VLDL-TG; (3) a third, who had only mildly elevated TG, had a low FCR and normal synthesis of VLDL-TG; and (4) the two normolipidemic brothers had neither overproduction nor decreased FCR of VLDL-TG. The composition of the soluble apoproteins of VLDL was normal. The apoprotein E phenotypes were E4/3 in four brothers, and E3/2 in the fifth. We have reached the following conclusions regarding this family: (1) the common kinetic abnormality of VLDL-TG metabolism in the hypertriglyceridemic brothers was a low clearance of VLDL-TG; (2) impaired catabolism of VLDL could not be explained by the apoprotein C or E patterns; and (3) the most severe hypertriglyceridemia occurred when the decreased FCR was present in conjunction with VLDL-TG overproduction due to obesity. Thus, a moderate defect in catabolism of plasma TG appears to be responsible for one familial form of primary hypertriglyceridemia.

Adult↗
PubMed1988

Hypertriglyceridemia and hyperuricemia: effects of two fibric acid derivatives (bezafibrate and fenofibrate) in a double-blind, placebo-controlled trial.

The effects of bezafibrate and fenofibrate on serum lipoproteins and serum urinary uric acid were compared. In a double-blind, placebo-controlled, cross-over study, each drug was administered in random order for 6 weeks followed by a 3-week drug-free phase to ten men with primary hypertriglyceridemia. Serum triglyceride and cholesterol concentrations decreased significantly with both fenofibrate and bezafibrate, although no significant change in serum apolipoprotein B, serum low density lipoprotein (LDL) cholesterol or serum high density lipoprotein (HDL) cholesterol concentrations was apparent. Serum uric acid levels, which were elevated on placebo and bezafibrate, were significantly reduced by 20% by fenofibrate. This was associated with an increase in renal uric acid clearance of 30% during fenofibrate therapy. Because it seems likely that hypertriglyceridemia and hyperuricemia are linked by a common carbohydrate inducibility, we studied the acute hyperuricemic response to orally administered fructose. Fructose (50 g) caused the anticipated rise in serum urate reaching a peak between 60 and 90 minutes, which was quantitatively greater in the men with hypertriglyceridemia than in healthy controls. The serum uric response to fructose was unaffected by bezafibrate, but was converted to normal by fenofibrate. The hyperuricemic action of fenofibrate is of sufficient magnitude to be of therapeutic value in the management of patients whose hypertriglyceridemia is associated with gout.

Bezafibrate↗
PubMedDate not supplied

Induction of hypertriglyceridemia in rabbits by thermal injury: I. Time course of elevated plasma triglyceride levels.

Thermal injury was produced in rabbits to determine (1) whether hypertriglyceridemia was inducible by thermal injury and, if so, (2) what was its time course and (3) how were the levels of apolipoproteins B, E, and A-I affected. In this study, seven New Zealand-specific pathogen-free male rabbits were inflicted with a burn to 27% of the total body surface area; another seven rabbits underwent a sham procedure. Plasma triglyceride levels rose markedly in the thermally injured group, and the hypertriglyceridemia persisted for ten days. Total plasma apolipoprotein B levels increased markedly by three days postburn and remained elevated for a period longer than the hypertriglyceridemia. In contrast, apolipoprotein E levels slowly increased, reaching a peak by day 10, and declined thereafter. Plasma levels of apolipoprotein A-I increased rapidly and remained elevated for two months. Thus, hypertriglyceridemia and concomitant changes in levels of apolipoproteins B, E, and A-I could be induced in rabbits by thermal injury. Plasma triglyceride levels were elevated for some time and then returned to normal, whereas apolipoprotein levels remained elevated for a longer time. These abnormalities may impair normal lipid transport in the postburn phase.

Animals↗
PubMedDate not supplied

Plasma lipoproteins, apolipoproteins, and triglyceride metabolism in familial hypertriglyceridemia.

Several parameters of lipoprotein metabolism were examined in 38 men with primary hypertriglyceridemia (phenotype IV). Family investigation showed that 17 men had familial combined hyperlipidemia (FCH), seven had familial hypertriglyceridemia (FHT), and 14 had unclassified hypertriglyceridemia (UNC). In all three groups, plasma high density lipoprotein (HDL) cholesterol and the concentrations of apolipoprotein A-I and A-II were decreased, and apolipoprotein B was increased, each to the same extent. These results are compatible with an increased risk of cardiovascular disease in both FCH and FHT patients. The mean concentration of LDL cholesterol and the ratio of LDL to HDL cholesterol were significantly higher in FCH subjects, which could explain their increased risk. Postheparin lipoprotein lipase and hepatic lipase were the same in both groups. Determination of apolipoprotein C composition, which may modulate lipoprotein lipase activity, did not reveal any abnormalities in the different groups. In both FCH and FHT, the mean turnover rate of plasma triglycerides was almost twice normal, indicating that overproduction of plasma triglyceride plays an important role in both disorders. However, there was an overlap with normal controls, indicating impaired triglyceride removal in some subjects. The underlying mechanism of hypertriglyceridemia in FCH and FHT therefore seems to be heterogeneous.

Aged↗
PubMed1967

Role of insulin in endogenous hypertriglyceridemia.

Dietary carbohydrate accentuation of endogenous triglyceride production has been studied in 33 patients. A broad and relatively continuous spectrum of steady-state plasma triglyceride concentrations was produced in 31 of the 33 subjects during 3 wk of a high carbohydrate (fat-free) liquid formula diet. Two patients developed plasma triglyceride concentrations in excess of 2000 mg/100 ml, and these were the only patients we have studied in which carbohydrate induction of hypertriglyceridemia seemed to be associated with a defect in endogenous plasma triglyceride removal mechanisms. In the remaining 31 patients the degree of hypertriglyceridemia was highly correlated with the insulin response elicited by the ingestion of the high carbohydrate formula (P < 0.005). No significant correlation existed between fasting plasma triglyceride concentration and either plasma glucose or free fatty acid concentrations after the high carbohydrate diet, nor was the degree of hypertriglyceridemia related to degree of obesity. It is suggested that hypertriglyceridemia in most subjects results from an increase in hepatic triglyceride secretion rate secondary to exaggerated postprandial increases in plasma insulin concentration.

Adult↗
PubMed1995

Common genetic variation in the promoter of the human apo CIII gene abolishes regulation by insulin and may contribute to hypertriglyceridemia.

Overexpression of plasma apolipoprotein CIII (apo CIII) causes hypertriglyceridemia in transgenic mice. A genetically variant form of the human apo CIII promoter, containing five single base pair changes, has been shown to be associated with severe hypertriglyceridemia in a patient population. In animals and in cultured cells the apo CIII gene is transcriptionally downregulated by insulin. In this study we demonstrate that, unlike the wild-type promoter, the variant promoter was defective in its response to insulin treatment, remaining constitutively active at all concentrations of insulin. The loss of insulin regulation was mapped to polymorphic sites at -482 and -455, which fall within a previously identified insulin response element. Loss of insulin regulation could result in overexpression of the apo CIII gene and contribute to the development of hypertriglyceridemia. The variant apo CIII promoter is common in the human population and may represent a major contributing factor to the development of hypertriglyceridemia.

Alleles↗
PubMedDate not supplied

Severe hypertriglyceridemia and acute pancreatitis during pregnancy: treatment with gemfibrozil.

OBJECTIVE: To describe the effect of gemfibrozil therapy during pregnancy in a woman with severe hypertriglyceridemia. METHODS: We present a case report, with details of lipid levels throughout several attempted pregnancies, and discuss other similar published studies. RESULTS: In a 22-year-old woman, severe acute pancreatitis due to hypertriglyceridemia developed during her first pregnancy. After a prolonged hospital course, the outcome was fetal demise. The patient was subsequently treated with gemfibrozil, which controlled the hypertriglyceridemia. A second pregnancy ended with a therapeutic abortion at 1 month because of the possible risk of pancreatitis. Gemfibrozil therapy was instituted but subsequently discontinued when she was discovered to be pregnant again, at approximately 10 weeks of gestation; the potential risks involved with the use of this drug during pregnancy were unknown. Because of the patient's strong desire to maintain the pregnancy, gemfibrozil treatment was resumed 1 week later in order to help prevent recurrent pancreatitis. The patient ultimately delivered a fullterm healthy boy, and she had no recurrence of pancreatitis or other complications. CONCLUSION: In selected patients at high risk for pancreatitis, the potential risk of gemfibrozil use during pregnancy may be offset by its benefits in the management of severe hypertriglyceridemia.

Journal Article↗
PubMed1975

The spectrum of electrophoretic mobility of very low density lipoproteins: role of slower migrating species in endogenous hypertriglyceridemia (type IV hyperlipoproteinemia) and broad-beta disease (type III).

To test whether beta-migrating very low-density lipoproteins (VLDL, d less than 1.006) might not be unique to broad-beta disease (with a Type III lipoprotein pattern) but rather a caricature of an intermediate species in the catabolism of triglyceride-rich lipoproteins of normal composition and electrophoretic mobility in nonretarding media, VLDL from subjects with endogenous hypertriglyceridemia (with a Type IV pattern) or broad-beta disease were analyzed under varying dietary and pharmacologic conditions following starch-block electrophoresis. These studies revealed a spectrum in electrophoretic mobility and lipid composition throughout the Sf20 to 400 range: the more buoyant, triglyceride-rich VLDL migrated faster and the denser, triglyceride-poor VLDL more slowly, but the VLDL were broadly and continuously distributed throughout the entire beta to alpha2 regions in both disorders. However, in each subfraction of VLDL (Sf100 to 400, 60 to 100 and 20 to 60) as well as in the whole Sf20 to 400 class, the relative proportion of slower species was greater in the subjects with broad-beta disease than in those with endogenous hypertriglyceridemia. Under conditions of acutely stimulated VLDL production (following an oral fat load), a late increase in the slower species was observed as alimentary lipemia resolved. During chronic VLDL hypersecretion (with high carbohydrate feeding) both faster and slower species increased in a subject with broad-beta disease. In the same subject during clofibrate therapy, the faster species were decreased more than the slower on both normal and high carbohydrate diets. Acute acceleration of VLDL catabolism by heparin administration increased the slower VLDL at the expense of the faster, both in this subject and in a counterpart with endogenous hypertriglyceridemia. These studies are consistent with the hypothesis that slower migrating, triglyceride-poor VLDL are normal intermediate (or remnant) forms in a continuous catabolic process. The concentration of these remnants is dwarfed by that of the faster species in subjects with endogenous hypertriglyceridemia. However, in subjects with broad-beta disease they accumulate as the beta-VLDL characteristic of this disorder, most likely as a result of a relative blockade in their further catabolism.

Adult↗
PubMed1989

Strong association of a single nucleotide substitution in the 3'-untranslated region of the apolipoprotein-CIII gene with common hypertriglyceridemia in Arabs.

A potential genetic marker for hypertriglyceridemia and coronary disease, an apolipoprotein-CIII gene allele displaying a single nucleotide substitution, was found in 71% of Arabs with primary hypertriglyceridemia. Over 96% of the unrelated adults possessing this allele showed hypertriglyceridemia. The same allele was found rarely among normotriglyceridemic subjects. In further support of involvement in hypertriglyceridemia, this allele was co-inherited with increased serum triglycerides in a three-generation family. Moreover, a gene dosage effect was also found. A mechanism of action for the allele is suggested by the findings that the subjects possessing the allele show markedly increased very-low-density lipoproteins, decreased high-density lipoproteins, and borderline chylomicronemia demonstrable by lipoprotein electrophoresis. Electrophoresis of the selectively amplified-restricted apolipoprotein-CIII DNA on agarose gel provides a rapid diagnostic test that allows identification of the subjects with this allele in less than a day.

Adult↗
PubMed1984

Studies on the mechanism of hypertriglyceridemia in the genetically obese Zucker rat.

The possibility that impaired removal of lipoprotein triglyceride from the circulation may be a participating factor in the hypertriglyceridemia of the obese Zucker rat was examined. We found no significant differences in the heparin-released lipoprotein lipase (LPL) activities of the adipose tissue, skeletal muscle, and heart (expressed per gram of tissue) from the lean and obese Zucker rats. Furthermore, the kinetic properties of adipose tissue and heart LPL from the lean and obese rats were similar, indicating that the catalytic efficiency of the enzyme was unaltered in the obese animals. The postheparin plasma LPL activities of lean and obese rats were also similar. However, the postheparin plasma hepatic triglyceride lipase (H-TGL) activity in the obese rats was elevated. The higher activity of H-TGL could not alleviate the hypertriglyceridemia in these animals. Since hypertriglyceridemia in the obese rats could also be due to the hepatic production of triglyceride-rich lipoproteins which are resistant to lipolysis, we therefore isolated very low density lipoproteins (VLDL) from lean and obese rat liver perfusates and examined their degradation by highly purified human milk LPL. Although certain differences were observed in hepatic VLDL triglyceride fatty acid composition, the kinetic patterns of LPL-catalyzed triglyceride disappearance from lean and obese rat liver perfusate VLDL were similar. The isolated liver perfusate VLDL contained sufficient apolipoprotein C-II for maximum lipolysis. These results indicate that impaired lipolysis is not a contributing factor in the genesis of hypertriglyceridemia in the genetically obese Zucker rat. The hyperlipemic state may be attributed to hypersecretion of hepatic VLDL and consequent saturation of the lipolytic removal of triglyceride-rich lipoproteins from the circulation.

Adipose Tissue↗
PubMed1982

Catabolism of very-low-density lipoproteins in subjects with broad beta disease: comparison with endogenous hypertriglyceridemia.

The catabolic rates of VLDL apo-B from subjects with broad beta disease (type III hyperlipoproteinemia) and from subjects with endogenous hypertriglyceridemia (type IV hyperlipoproteinemia) were compared in recipients with these disorders. In subjects with broad beta disease, disappearance of autologous VLDL apo-B was slower than that of isologous VLDL apo-B from subjects with a type IV lipoprotein pattern (FCR 0.049 +/- 0.03 hr-1 for autologous vs. 0.068 +/- 0.035 for isologous, n = 6, p less than 0.05). However, the FCRs of autologous and isologous VLDL apo-B in subjects with type IV hyperlipoproteinemia were the same (0.110 +/- 0.051 hr-1 for autologous vs. 0.110 +/- 0.063 for isologous, n = 4, p = NS). In vitro studies suggested that 125I-VLDL from subjects with endogenous hypertriglyceridemia retained most of the smaller peptides (87.5% +/- 1.8 apo E and 75.7% +/- 1.6 apo C) when incubated with plasma from subjects with broad beta disease. By contrast, 125I-labeled IDLs from subjects with broad beta disease exchanged these lipoproteins rapidly (retaining only 7.9% +/- 0.03 apo-E and 8.2% +/- 0.3 apo-C) when incubated with plasma from subjects with endogenous hypertriglyceridemia. Similarly, beta-VLDL isolated from a subject with broad beta disease by preparative electrophoresis, when incubated with plasma from a subject with endogenous hypertriglyceridemia, exchanged its apo-E with the normal VLDL (56% being recovered in VLDL of alpha2 mobility). Normal VLDL, however, retained most (93.3%) of its VLDL apo-E radioactivity when incubated with plasma from a subject with broad beta disease. These observations suggest that the abnormal composition of autologous VLDL may in part be responsible for its delayed clearance in subjects with broad beta disease.

Adult↗
PubMed2003

Hypertriglyceridemia in pediatrics.

Primary hypertriglyceridemias are very rare in pediatric age group. A case of 12 years old boy with hypertriglyceridemia is presented. He was being treated as a case of thalassemia major since 2 years of age and was picked up incidentally when his serum turned milky on standing. Since hypertriglyceridemia is a known risk factor for the acute pancreatitis so an early detection is helpful in adoption of a healthy life style.

Child↗
PubMed2003

Plasmapheresis for the treatment of acute pancreatitis induced by hemophagocytic syndrome related to hypertriglyceridemia.

Histiocytic cytophagic panniculitis is an unusual form of hemophagocytic syndrome related to T-cell lymphoma that can be responsible for hypertriglyceridemia. The elevation of serum triglycerides, usually in the setting of familial lipidemia or during uncontrolled diabetes mellitus, is a well-recognized cause of pancreatitis. We report here on the treatment by plasmapheresis of a patient suffering from a T-cell lymphoma-related panniculitis who presented with an acute pancreatitis induced by hypertriglyceridemia. The Ranson scoring system at day 2 was increased and predicted a poor course while clinical features worsened. The patient was treated with one plasmapheresis that allowed a dramatic (89%) decrease in the triglycerides level. The acute pancreatitis resolved and the patient was discharged from the intensive care unit at day 5 with lipids and pancreatic enzyme levels within normal range. To our knowledge, this is the first case of acute pancreatitis induced by hypertriglyceridemia in the setting of an uncontrolled cytophagic histiocytic panniculitis successfully treated by plasmapheresis.

Acute Disease↗
PubMed1994

No evidence for linkage between familial hypertriglyceridemia and apolipoprotein B, apolipoprotein C-III or lipoprotein lipase genes.

Familial hypertriglyceridemia has been suggested to be an autosomal dominant condition with age-dependent penetrance, but so far the underlying defective gene has not been elucidated. We examined the possible role of three candidate gene loci by linkage analysis in six Finnish families with familial clustering of hypertriglyceridemia. The probands were initially recruited from a group of hyperlipidemic outpatients after measurement of serum triglyceride concentrations exceeding 2.00 mmol/l on two occasions. Altogether, 71 subjects were included in the linkage analyses. Bi- or multiallelic DNA polymorphisms were used as markers for the apolipoprotein B gene (chromosome 2), lipoprotein lipase gene (chromosome 8), and apolipoprotein A-I/C-III/A-IV gene cluster (chromosome 11). Linkage analysis was performed by applying two alternative phenotyping models, one adopting quantitative serum triglyceride concentrations and another using qualitative classification of the subjects into hypertriglyceridemic, normotriglyceridemic, and borderline hypertriglyceridemic groups. Using either approach, the cumulative lod scores of each of the three candidate genes in the six families were less than -2.0 at the recombination fraction 0.0. These results suggest that none of the candidate genes investigated is involved in familial clustering of hypertriglyceridemia in our study.

Adult↗
PubMed1992

The distribution of o,p'-DDD (mitotane) among serum lipoproteins in normo- and hypertriglyceridemia.

We found that the distribution of the lipophilic chemotherapeutic agent o,p'-DDD (mitotane) among serum (lipo)proteins was altered in hypertriglyceridemia, with relatively more o,p'-DDD accumulating in the chylomicron and very-low-density lipoprotein (VLDL) fraction. Intralipid, an artificial chylomicron emulsion, or isolated VLDL could extract o,p'-DDD from the other serum (lipo)proteins. There was an inverse relationship between the relative amount of o,p'-DDD found in the fraction exhibiting a density of less than 1.006 g/ml (chylomicrons plus VLDL) and the relative amount observed in the LDL or HDL fractions of serum. Our results indicate that hypertriglyceridemia may impede the entry of o,p'-DDD into the brain or the adrenals. For therapeutic monitoring of o,p'-DDD levels in severe hypertriglyceridemia, we recommend that the chylomicron and VLDL fraction first be removed from the serum by ultracentrifugation.

Adrenal Cortex Neoplasms↗
PubMed1993

Pharmacological control of hypertriglyceridemia.

Hypertriglyceridemia has been recently recognized as a vascular risk factor, based on both clinical and experimental findings. Epidemiological studies clearly showed that elevated plasma triglycerides in subjects with low high-density lipoprotein (HDL) cholesterol (<35 mg/dl) and/or a low-density lipoprotein (LDL)/HDL cholesterol ratio > 5 are associated with an elevated risk for coronary heart disease (CHD), while intervention studies indicate that triglyceride lowering with drugs may lead to a significant CHD reduction. Elevated blood triglycerides are associated with major alterations in the structure/function of plasma lipoproteins, which become more atherogenic, and with abnormalities in the clotting system, which may predispose to coronary thrombosis. New criteria for the classification of hypertriglyceridemias and a stepwise approach to the management of patients with elevated plasma triglycerides have been recently developed. Nonpharmacological interventions, i.e., weight reduction, alcohol and smoking cessation, and physical exercise, are the first-line actions to control hypertriglyceridemia. Drug therapy should be considered when the nonpharmacological approaches are ineffective or inadequate. Fibric acid derivatives and nicotinic acid (and its derivatives) are the drugs of choice when treating hypertriglyceridemic patients; n-3 fatty acids (fish oil) and metformin (especially in diabetic patients) represent additional therapeutic agents.

Body Weight↗
PubMed2006

Treatment of hypertriglyceridemia.

Hypertriglyceridemia is a disorder commonly encountered in clinical practice. Treatment of this condition aims to prevent the major complications of hypertriglyceridemia, which differ depending on whether triglyceride elevations are moderate or severe. This review discusses the pathophysiology and clinical consequences of hypertriglyceridemia and outlines treatment approaches based on the degree of triglyceride elevation. Special consideration is given to clinical trials using medications that primarily target triglycerides.

Algorithms↗
PubMed1994

Effects of cardiac rehabilitation and exercise training on low-density lipoprotein cholesterol in patients with hypertriglyceridemia and coronary artery disease.

Substantial data suggest that elevated triglycerides are associated with increased coronary risk, and may be an independent coronary risk factor. Although it is generally accepted that patients with hypertriglyceridemia can have marked improvement in lipids after vigorous nonpharmacologic therapy, data to support this belief are lacking. This study assessed 313 consecutive patients before and after outpatient phase II cardiac rehabilitation and exercise programs to compare the response of patients with elevated triglycerides (> or = 250 mg/dl; n = 39) to vigorous nonpharmacologic therapy with the response of patients with "normal" triglyceride levels (< 150 mg/dl; n = 157). The independent effects that baseline triglycerides, as well as other variables, had on improving lipids after nonpharmacologic therapy were also determined. After cardiac rehabilitation and exercise training, patients had improvement in total cholesterol, triglycerides, high-density lipoprotein (HDL) cholesterol levels, low-density lipoprotein (LDL) cholesterol levels, LDL/HDL ratios, body mass index, percent body fat, and METs. Patients with hypertriglyceridemia were younger (p = 0.05) and had higher baseline body mass index (p < 0.001) and LDL/HDL ratios (p < 0.0001) but lower HDL cholesterol levels (p < 0.0001) than patients with low baseline triglycerides. Both groups had improvement in lipids, obesity indexes, and exercise capacity. However, patients with hypertriglyceridemia had significantly greater reductions in triglycerides (-31% vs +3%; p < 0.0001), but had less improvement in both LDL cholesterol levels (0% vs -4%; p < 0.01) and LDL/HDL ratios (-5% vs -9%; p = 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗