Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Hypertriglyceridemia”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 325 records · Page 18Linked to original sources
PubMed2000

Coagulofibrinolytic assessment of effects of bezafibrate on hypertriglyceridemia in postmenopausal women.

The present study investigates the effect of bezafibrate on lipid levels and coagulofibrinolytic factors. Subjects enrolled in the study included 124 postmenopausal women with hypertriglyceridemia. We examined the levels of tissue plasminogen activator (t-PA), plasminogen activator inhibitor type-1 (PAI-1), and blood coagulation factors VII and X as parameters of coagulofibrinolysis. After 12 weeks of bezafibrate therapy, mean serum triglyceride (TG) and remnant-like particle lipoprotein cholesterol (RLP-C) levels significantly decreased from baseline. Activated factor X levels decreased significantly by 11.3% (P < 0.01) and the ratio of tPA/PAI-1 (0.146+/-0.07) increased significantly by 37.7% from baseline (P < 0.05). The rates of change in activated factor VII and PAI-1 showed a significant positive correlate with the rates of change in TG and RLP-C (P = 0.001). These present findings suggest that bezafibrate improves triglyceride-rich lipoprotein metabolism and coagulofibrinolytic activity by increasing fibrinolysis in postmenopausal women with hypertriglyceridemia.

Bezafibrate↗
PubMed1992

Reliability of in vivo mixed venous oximetry during experimental hypertriglyceridemia.

BACKGROUND AND METHODS: The spectral absorbance of iv lipid emulsion produces interference in the in vitro spectrophotometric measurement of hemoglobin saturation. Therefore, we investigated in vivo mixed venous oximetry during lipid emulsion infusions. Boluses of lipid emulsion, increasing by 0.1-g/kg increments, were infused every 30 mins into nine anesthetized dogs. After each lipid bolus, laboratory and hemodynamic data measurements were repeated, and arterial and mixed venous blood gases were analyzed on a laboratory cooximeter that was equipped for canine blood. The in vivo mixed venous oxygen saturation was continuously monitored via an indwelling, optically equipped pulmonary artery catheter. RESULTS: As expected, increasing concentrations of lipid emulsion increased (r2 = .92) serum triglyceride concentration. As a result, the in vitro measurements of percentage methemoglobin increased artifactually, reducing in vitro measurements of arterial (r2 = .74) and mixed venous (r2 = .44) oxygen saturations. The in vivo mixed venous oxygen saturation, however, remained constant during hypertriglyceridemia (r2 less than .01). CONCLUSIONS: In vivo mixed venous oximetry remained constant during hypertriglyceridemia, while in vitro measurements of arterial and mixed venous saturations were artifactually reduced.

Animals↗
PubMedDate not supplied

Tumor necrosis factor mediates hypertriglyceridemia during thermal injury in mice genetically susceptible to lipopolysaccharides.

A rise in plasma triglycerides has been noted after thermal injury in a number of animal species including humans. In this study we identified a factor, tumor necrosis factor, which was responsible for increased plasma triglycerides during thermal injury that was induced by scalding. Two strains of mice that differed genetically in susceptibility to lipopolysaccharides were used. These were CH3HEB/HeJ (LPS-) and CH3HEB/FeJ (LPS+). A 15% total body surface area was burned; this resulted in an increase of plasma triglycerides of 126% of preburn levels in the LPS+ strain 24 hours after burn injury. No change in triglycerides was noted in the LPS- mice at any time after burn injury. Sera from LPS+ mice at 1 to 2 hours after burn injury was injected into nonburned animals of the same strain; this caused a 62% +/- 5% increase in plasma triglycerides 24 hours after injection. When thermally injured LPS+ mice were injected with anti-tumor necrosis factor-alpha at 1 hour after injury, they did not show a rise in plasma triglycerides at any time between 24 to 72 hours after injury. Hepatic secretion of triglycerides was also measured 1 day after burn; the average secretion of triglycerides was significantly reduced (2.69 +/- 0.36 mg/kg/hr, compared with 3.83 +/- 0.15 mg/kg/hr for the control). We conclude that tumor necrosis factor, a cytokine that inhibits lipoprotein lipase, causes hypertriglyceridemia during thermal injury in spite of a decreased secretion of triglycerides. This is the first report that demonstrates that hypertriglyceridemia that is secondary to thermal injury is induced by tumor necrosis factor.

Animals↗
PubMed1996

Prevention of recurrent acute pancreatitis in patients with severe hypertriglyceridemia: value of regular plasmapheresis.

The association between acute pancreatitis and severe hypertriglyceridemia has long been recognized. We report two cases of severe primary hypertriglyceridemia (types 1 and V) with recurrent acute pancreatitis. In both patients, observance of appropriate diet and drug therapy was insufficient. Recurrent episodes of pancreatitis were precipitated by dietary fat or alcohol abuse. A plasmapheresis was performed every 4 weeks to decrease the incidence of pancreatitis. It appears that plasmapheresis is a safe and highly effective method for quickly removing serum triglycerides. Moreover, plasma-pheresis may be useful for preventing acute pancreatitis.

Acute Disease↗
PubMed1999

Drug-induced hypertriglyceridemia with and without pancreatitis.

We describe two cases of drug-induced hypertriglyceridemia, one associated with interferon alfa-2b and the other with asparaginase, each of which is mediated through a different mechanism. Hypertriglyceridemia caused by these medications is not listed as an adverse reaction in the Physicians' Desk Reference, one of the most popular pharmacologic reference sources used in the United States. We emphasize the importance of early recognition of this metabolic effect and the potential life-threatening complication, acute pancreatitis.

Adolescent↗
PubMedDate not supplied

Effect of probucol therapy on plasma fatty acid composition during postprandial lipemia in hypertriglyceridemia.

OBJECTIVE: To determine the effect of probucol (PR) on fatty acid composition of plasma lipids in patients with hypertriglyceridemia during the fasting and postprandial states. DESIGN: Open-label, single-center, 6-week treatment, baseline-controlled trial. SETTING: Outpatient clinical research center. PATIENTS: Six patients with established hypertriglyceridemia and no complicating medical conditions. INTERVENTION: Step 1 American Heart Association diet and no lipid-lowering medications for at least 4 weeks. Lead to a baseline standarized meal ingestion with postprandial blood samplings. After 6 weeks of treatment with 500-mg of PR twice daily and diet, the meal tests were repeated. MEASUREMENTS: The clinical status, 3-day food records, postprandial blood samplings (0, 2, 4, 6, and 8 hours) for lipid and fatty acids in whole plasma, triglyceride (TG), phospholipid (PL), and cholesteryl ester (CE) fractions. RESULTS: PR had the following effects: (1) In plasma, cholesterol, high-density lipoprotein cholesterol, apolipoprotein (Apo) A1, and ApoB were decreased postprandially. ApoC111 ratio (heparin-treated plasma versus precipitate) was decreased in the fasting state. (2) The saturated/unsaturated (S/U) fatty acid ratios in the PL, TG, and CE fractions were elevated postprandially and increased in CE in the fasting state. In the PL fraction it was due to an increase in the percentage of myristic, palmitic, stearic, and oleic acids and a decrease in linolenic, eicosatrienoic, and arachidonic acids. In the TG and CE fractions the changes were not due to any particular patterns of fatty acids. The ratio of arachidonic/eicosatrienoic acid was decreased postprandially in PL and CE fractions. The ratio of eicosatrienoic/linoleic acid was decreased in PL and increased in CE fractions. (3) The S/U ratio in the lipoprotein (Lp) B and LP(a) lipid components decreased in PL and CE. Lp(a) was more saturated with respect to fatty acids than LpB. CONCLUSION: PR treatment for 6 weeks increased postprandial S/U fatty acid ratios. This was due to a combination of an increase in saturated and monounsaturated levels and a decrease in polyunsaturated levels. The effect was most notable in the PL fraction. In those systems dependent on the pattern of fatty acids, the fatty acid compositional change could modify biological responses in clinically important ways during lipid-lowering therapy. The change toward saturation of fatty acids in the postprandial state may contribute to the antioxidant properties of probucol.

Anticholesteremic Agents↗
PubMed2006

Lipodystrophy is an independent predictor of hypertriglyceridemia during pregnancy in HIV-infected women.

Lipid values were measured during pregnancy in HIV-infected, treatment-experienced women. A previous history of lipodystrophy was associated with significantly higher triglyceride values at all pregnancy trimesters. In multivariate analyses lipodystrophy independently increased the risk of hypertriglyceridemia by threefold at the first trimester, and by eightfold at the second and third trimesters. Protease inhibitor treatment was also independently associated with hypertriglyceridemia.

Adult↗
PubMedDate not supplied

Substitution of transdermal estradiol during oral estrogen-progestin therapy in postmenopausal women: effects on hypertriglyceridemia.

OBJECTIVE: We investigated effects of changing from oral estrogen to transdermal estradiol on the lipid and lipoprotein profile of postmenopausal women who developed hypertriglyceridemia (serum concentrations exceeding 150 mg/dL) during estrogen-progestin therapy. DESIGN: Sixty-one postmenopausal Japanese women receiving 0.625 mg of conjugated equine estrogen plus 2.5 mg of medroxyprogesterone acetate daily for 12 months had developed serum triglyceride concentrations exceeding 150 mg/dL after 12 months of treatment. Thirty-six of them, chosen randomly for study, were assigned at random to either a group that continued this oral regimen or another that changed to transdermal estradiol while continuing 2.5 mg of oral medroxyprogesterone acetate for the next 3 months (n = 18 for each). Blood lipids were compared between groups. RESULTS: Serum concentrations of triglyceride and very-low-density lipoprotein triglyceride decreased significantly after changing to transdermal estradiol (triglyceride, from 226.0 +/- 43.9 to 110.5 +/- 44.1 mg/dL, P < 0.01). No changes were seen in concentrations of low-density lipoprotein cholesterol or high-density lipoprotein cholesterol. CONCLUSION: Changing to transdermal estradiol may improve triglyceride metabolism in women who developed hypertriglyceridemia during oral estrogen-progestin therapy, with minimal effect on cholesterol profiles.

Administration, Cutaneous↗
PubMed1989

Selective removal of triglyceride-rich lipoproteins by plasmapheresis in diabetic patients with severe hypertriglyceridemia.

Two diabetic patients with marked intractable hypertriglyceridemia under treatment with hemodialysis for chronic renal failure were treated by either an apolipoprotein B-dependent removal of lipoproteins using dextran sulfate cellulose column plasmapheresis or a size-dependent removal of lipoproteins using hollow-fiber filtration plasmapheresis. In one patient, a column packed with hollow fibers was used as a plasma separator and a dextran sulfate cellulose column as an adsorbent. In another patient, because the hollow-fiber column did not separate plasma from whole blood, a centrifuge-type blood cell separator was used for the plasma separation. The amounts of plasma cholesterol, triglycerides, and phospholipids removed by plasmapheresis were 30%, 33%, and 30%, respectively, when the combination of a hollow-fiber column and a dextran sulfate cellulose column was used. Corresponding values were 31%, 29%, and 27%, respectively, when the combination of the centrifuge-type blood cell separator and the hollow-fiber column was used. The efficiency of lipid removal was almost the same with both techniques. As for plasma separation, the centrifuge-type blood cell separator was more efficient than the hollow-fiber column. Some losses of albumin and platelets were observed when combination plasmapheresis using the centrifuge-type blood cell separator and the hollow-fiber column was performed. In conclusion, we prefer the centrifuge-type blood cell separator to the hollow-fiber column for plasma separation of marked hypertriglyceridemia. The second filter must be chosen for each patient according to the size of the lipoproteins.

Adult↗
PubMed1993

Insulin resistance and compensatory insulin secretion in middle-aged persons with hypertriglyceridemia.

Insulin secretion and insulin sensitivity were measured in hypertriglyceridemic patients using the frequently sampled intravenous glucose tolerance test. Three groups of men who were matched for age and body mass index were studied: eight healthy control subjects (C), seven patients with mild hypertriglyceridemia and normal glucose tolerance (TG), and seven with well-controlled type 2 diabetes with hypertriglyceridemia (TG-DM). The first-phase insulin response was increased by 116% in the TG group and decreased by 59% in the TG-DM group. The second phase of insulin secretion was increased in both TG groups (TG by 310% and TG-DM by 250%). The mean insulin sensitivity index (SI) was reduced by 50% in the TG group and by 60% in the TG-DM group. Glucose effectiveness (SG) was reduced by 30% in the TG-DM group compared with the control subjects.

Adult↗
PubMed1995

Effect of hypertriglyceridemia on endotoxin responsiveness in humans.

Triglyceride-rich lipoproteins can inhibit endotoxin activity in vitro and in rodents. We sought to determine whether Intralipid, a triglyceride-rich fat emulsion which in contact with plasma functions similarly to endogenous lipoproteins, can alter the human response to endotoxin. Intralipid inhibited endotoxin-induced cytokine production in human whole blood in vitro in a dose-dependent manner, with maximal inhibition (up to 70%) being achieved at a concentration of 10 g/liter. In healthy men, a bolus intravenous injection of endotoxin (lot EC-5; 20 U/kg of body weight) was given midway through a 4-h infusion (125 ml/h) of either 5% glucose (n = 5) or 20% Intralipid (n = 5). The infusion of Intralipid led to an increase in triglyceride levels in serum from 95 +/- 16 to 818 +/- 135 mg/dl prior to endotoxin administration, i.e., levels that importantly reduced cytokine production in endotoxin-stimulated whole blood. However, in vivo hypertriglyceridemia did not influence inflammatory responses to endotoxin (fever, release of tumor necrosis factor and soluble tumor necrosis factor receptors, and leukocytosis) or even potentiated endotoxin responses (release of interleukins 6 and 8 and neutrophil degranulation). Hypertriglyceridemia does not inhibit the in vivo responses to endotoxin in humans.

Adult↗
PubMed1994

Hypertriglyceridemia in experimental diabetes: relationship to cardiac dysfunction.

The incidence of mortality from cardiovascular disease is higher in diabetic patients. The objective of the present investigation was to test the hypothesis that the diabetes-induced depression in cardiac function may be due to hypertriglyceridemia. Hyperlipidemia and a depressed left ventricular developed pressure and rate of increase and decrease of ventricular pressure (+/- dP/dt) were produced in isolated hearts from rats made diabetic with streptozotocin compared with hearts from control animals. This depressed cardiac performance was successfully prevented by hydralazine treatment (for 3 weeks), which also lowered plasma triglyceride levels and suggested that hyperlipidemia may be important in altering cardiac function in experimental diabetic rats. The beneficial effects of clofibrate, verapamil, prazosin, enalapril, and benazepril administration were then studied in diabetic rats. The treatments (with the exception of enalapril) significantly reduced plasma triglyceride levels but did not prevent the onset of heart dysfunction in chronically diabetic rats. These studies suggest that in the chronically diabetic rat, hypertriglyceridemia may not be as important as previously suggested, in the development of cardiac dysfunction. Since acute dichloroacetate perfusion improves cardiac function in 6 week (but not 24 week) diabetic rats, it appears more likely that improving myocardial glycose utilization is more critical than triglyceride lowering, in preventing cardiac dysfunction in the diabetic rat at this time point.

Animals↗
PubMed2003

Multiple eruptive dermatofibromas with CD34+ cells in a patient with hypertriglyceridemia.

Multiple eruptive dermatofibromas (MEDF) are rare and have been thought to be associated with altered immunity. It has been reported that dermatofibromas (DFs) are positive for factor X IIIa but not for CD34. In this report, we describe a 34-year-old Japanese woman with MEDF and persistent hypertriglyceridemia. Histopathological examination revealed that several areas in larger nodules, showing higher cellularity and storiform growth pattern, had CD34+ cells. Our case and the review of previous reports suggest that hyperlipidemia, including hypertriglyceridemia, could induce MEDF and that highly cellular areas in DFs are sometimes positive for CD34.

Adult↗
PubMed2005

Endogenous hypertriglyceridemia intensifies the course of cerulein-induced pancreatitis in rat: relation with changes in the VLDL composition.

AIMS: To study if the course of cerulein-induced pancreatitis in rats changes in a state of triglyceride-rich lipoprotein metabolism alteration. METHODS: Two groups of rats received control diet during a 90-day period (A) and sucrose-rich diet to induce endogenous hypertriglyceridemia (B). Subgroups A2 and B2 received i.p. 45 microg cerulein/kg body weight (to induce acute pancreatitis). Histological examination of pancreas tissue, serum pancreatic lipase, lipoprotein profile and VLDL chemical composition were assessed. Then, pancreatic lipase hydrolytic activity on VLDL-triglycerides was evaluated in vitro. RESULTS: Cellular vacuolization was observed in all of the cerulein-injected rats, but only in subgroup B2 fat necrosis was present. Serum triglycerides were higher in subgroup B1 than in subgroup A1 (mean +/- SEM, mg/dl 123,77 +/- 25.7 vs. 65.8 +/- 7, p < 0.01). Triglycerides from rats fed with sucrose-rich diet, decreased after cerulein-induced pancreatitis (80.38 +/- 11.3 vs. 123,77 +/- 25.7, p < 0.02). Moreover, the endogenous hypertriglyceridemic rats showed an increment of VLDL triglyceride content, which decreased when rats were injected with cerulein. A negative correlation was found between VLDL-triglyceride content and serum pancreatic lipase activity (r = 0.58, p < 0.02). The in vitro assay showed a decrease in VLDL-triglyceride content post incubation with pancreatic lipase enriched serum (mean +/- SD: 59.2 +/- 27.7%, p < 0.01). CONCLUSIONS: The endogenous hypertriglyceridemia intensifies the course of cerulein-induced pancreatitis and it could be related to the decrease in VLDL-triglycerides as a consequence of pancreatic lipase hydrolytic activity.

Acute Disease↗
PubMed1992

Hypertriglyceridemia: cause or consequence of insulin resistance?

An overproduction of VLDL by the liver and a slower clearance of these lipoproteins are usually seen in diabetic patients. There is correlation between insulin resistance and plasma triglyceride concentration. Triglyceride may influence an early step in the insulin action pathway and alternatively, insulin resistance may cause hypertriglyceridemia. Hyperinsulinemia and/or hypertriglyceridemia may play a strong role in the cardiovascular risk of patients with type II diabetes. There is an important need to conduct trials to define therapy that can reduce the risk of cardiovascular complications.

Cardiovascular Diseases↗
PubMed2003

Short-term triglyceride lowering with fenofibrate improves vasodilator function in subjects with hypertriglyceridemia.

OBJECTIVE: The objective of this study was to investigate the effects of lowering plasma triglycerides (TGs) on endothelial function and gain insight into the role played by free fatty acids (FFAs) in hypertriglyceridemia-associated vascular dysfunction. METHODS AND RESULTS: Eleven hypertriglyceridemic subjects without coronary artery disease, diabetes, elevated low-density lipoprotein cholesterol, tobacco use, or hypertension were studied using a randomized, double-blinded, crossover design (fenofibrate and placebo, 14 days). After each regimen, forearm blood flow was assessed by plethysmography in response to arterial acetylcholine, nitroprusside, and verapamil infusion. Hourly plasma TGs, FFA, glucose, and insulin were measured during a 24-hour feeding cycle to characterize the metabolic environment. Changes in plasma FFA after intravenous heparin were used to estimate typical FFA accumulation in the luminal endothelial microenvironment. Fenofibrate lowered plasma TG (P<0.001), total cholesterol (P<0.01), and apolipoprotein B (P<0.01) without altering high-density lipoprotein or low-density lipoprotein cholesterol concentrations. Forearm blood flow in response to acetylcholine (P<0.0001), nitroprusside (P<0.001), and verapamil (P<0.0001) improved after fenofibrate. Fenofibrate lowered 24-hour (P<0.0001) and post-heparin (P<0.001) TG and tended to lower 24-hour (P=0.054) and post-heparin (P=0.028) FFA. CONCLUSIONS: Vascular smooth muscle function significantly improves after lowering plasma TG without changes in confounding lipoproteins or insulin resistance. The data raise additional questions regarding the role of FFA in hypertriglyceridemia-associated vascular dysfunction.

Adult↗
PubMedDate not supplied

Apolipoprotein E polymorphism association with lipoprotein profile in endogenous hypertriglyceridemia and familial hypercholesterolemia.

Apolipoprotein (apo) E polymorphism was among the first-reported genetic polymorphisms that explained part of the normal variation in plasma cholesterol concentrations in humans. The aim of this study was to assess the influence of allelic variation at the apo E gene locus on the plasma lipoprotein profile in hyperlipidemia. The lipoprotein levels of hyperlipidemic subjects of the major apo E phenotypes (E3/2, E3/3, and E4/3) were compared. One hundred eighty-two subjects with endogenous hypertriglyceridemia and 98 subjects with familial hypercholesterolemia due to a 10-kb deletion in their low density lipoprotein (LDL) receptor genes were compared with 424 normolipidemic controls from the same environmental background. LDL concentrations were lower in the E3/2 subset than in the E3/3 or E4/3 subset in the control, hypertriglyceridemic, and familial hypercholesterolemic groups. In absolute values, the magnitude of the effect was greatest in the familial hypercholesterolemic group. However, the direction and percentage change were identical in the presence or absence of the LDL receptor defect, indicating that the apo E phenotype effect is independent of LDL receptor status. Triglyceride and very low density lipoprotein (VLDL) cholesterol concentrations were higher in E3/2 than in E3/3 or E4/3 hypertriglyceridemic subjects, but this difference was not found in the familial hypercholesterolemic or control group. Thus, there seems to be a specific interaction between apo E isoforms and VLDL metabolism in hypertriglyceridemia; allelic variation at the apo E gene locus seems to be associated with specific alterations in the plasma lipoprotein profile of subjects with well-defined types of hyperlipidemia.

Adult↗
PubMedDate not supplied

Will a high-carbohydrate, low-fat diet lower plasma lipids and lipoproteins without producing hypertriglyceridemia?

A sudden increase in dietary carbohydrate invariably increases the plasma levels of very low density lipoprotein (VLDL) and triglyceride. The present studies were designed to test the hypothesis that dietary carbohydrate-induced hypertriglyceridemia need not occur. In the first study we fed gradually increasing amounts of carbohydrate and gradually decreasing amounts of fat to eight subjects. The usual American diet (40% fat, 45% carbohydrate, and 15% protein) was followed in sequence by four diets in a phased regimen, the carbohydrate increasing by 5% of total calories and the fat content decreasing by 5% for each dietary period. In the last dietary period (phase 4), 20% of the energy was in the form of fat and 65% in the form of carbohydrates; the cholesterol content was 100 mg/day. Throughout the study, plasma triglyceride and VLDL triglyceride levels did not change significantly. The plasma total and low density lipoprotein (LDL) cholesterol levels were greatly reduced, by 15% and 22%, respectively (p = 0.004). Plasma high density lipoprotein (HDL) cholesterol levels decreased concomitantly. In the second study, after a washout period six of the subjects were initially fed the phase 4 high-carbohydrate diet for a 10-day period. The plasma triglyceride concentration increased over baseline levels by 47%, and VLDL triglyceride levels increased by 73%. We conclude that although a sudden increase in dietary carbohydrate increases the plasma triglyceride level, patients gradually introduced to a high-carbohydrate, low-fat diet may achieve a significant reduction of plasma total and LDL cholesterol without developing carbohydrate-induced hypertriglyceridemia.

Adult↗