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 595 records · Page 33Linked to original sources
PubMed2006

Hypertriglyceridemia: management of atherogenic dyslipidemia.

Elevated triglycerides are now considered an independent risk factor for coronary heart disease and continue to be a major risk for acute pancreatitis, especially when levels exceed 1000 mg/dL (SOR: B). Elevated triglycerides are a component of atherogenic dyslipidemia and often signal the presence of other conditions (eg, metabolic syndrome, type 2 diabetes mellitus) associated with an increased cardiovascular risk (SOR: A). When evaluating a patient with elevated triglycerides, it is important to be cognizant of all atherogenic lipoproteins to more accurately determine the risk of coronary heart disease (SOR: C). Patients with hypertriglyceridemia should first achieve their low-density lipoprotein cholesterol goal, followed by their non-high-density lipoprotein cholesterol goal (SOR: C). Fibrates, niacin, and omega-3 acid ethyl esters are highly effective at reducing triglycerides, while statins are considered moderately efficacious (SOR: A).

Acute Disease↗
PubMed2006

[Analysis of cholesterol ester transfer protein gene Taq IB and -629 C/A polymorphisms in patients with endogenous hypertriglyceridemia in Chinese population].

OBJECTIVE: To investigate the variations of cholesterol ester transfer protein (CETP) gene and its relation to endogenous hypertriglyceridemia (HTG) in Chinese population. METHODS: One hundred and thirty-five endogenous hypertriglyceridemics and 214 healthy subjects from a population of Chinese Han nationality in Chengdu area were studied using restriction fragment length polymorphism (RFLPs) amplified by polymerase chain reaction (PCR). The polymorphic sites studied included Taq IB and -629 C/A polymorphism in CETP gene. RESULTS: The frequencies of B(2) allele at Taq IB site in normal group and HTG group were 0.418 and 0.382, respectively. The frequencies of A allele at -629 C/A site in the two groups were 0.479 and 0.489, respectively. No significant difference between normal control and HTG groups were found in both allele frequency of the two polymorphism. Linkage disequilibrium was observed between Taq IB and -629 C/A polymorphic sites (D'=0.881). In the normal control group, subjects with genotype B(2)B(2) of Taq IB site had a higher serum mean concentration of HDL-C and lower LDL-C when compared with that of genotype B(1)B(1) and B(1)B(2), respectively (both P< 0.05), while those with genotype CC of -629 C/A site had a lower LDL-C level and higher Apo A II level when compared with that of genotype AC (P< 0.01 and P< 0.05, respectively). The changes of the lipid and lipoprotein levels were only observed in normal male subjects when male and female groups were further separated. No significant changes of lipid and lipoprotein levels were observed in both polymorphism in HTG group. Combined genotype analysis of the two sites, subjects with genotype B(2)B(2)CC in normal controls had higher HDL-C levels but lower serum triglyceride (TG) when compared with B(1)B(1)CC. CONCLUSION: These results suggest that Taq IB and -629 C/A polymorphisms in CETP gene are associated with healthy control subjects to some extent in Chinese population, but not with endogenous hypertriglyleridemia in the population group.

Adult↗
PubMed1991

Effects of exercise training on glucose control, lipid metabolism, and insulin sensitivity in hypertriglyceridemia and non-insulin dependent diabetes mellitus.

Exercise training has potential benefits for patients with hyperlipidemia and/or non-insulin dependent diabetes mellitus. In nondiabetic, nonobese subjects with hypertriglyceridemia, exercise training alone increased insulin sensitivity, improved glucose tolerance, and lowered serum triglyceride and cholesterol levels. These improvements did not occur when exercise training alone was given to similar patients with impaired glucose tolerance. In severely obese (X = 125 kg) subjects without diabetes melitus, a 600 calorie diet alone decreased glucose and insulin concentrations and improved glucose tolerance but did not increase insulin sensitivity. The addition of exercise training improved insulin sensitivity. Obese, non-insulin dependent diabetes mellitus subjects on sulfonylurea therapy alone increased insulin levels but failed to improve insulin sensitivity or glucose levels. In contrast, the addition of exercise training to this medication resulted in improved insulin sensitivity and lowered glucose levels. We conclude that exercise training has major effects on lowering triglyceride levels in hyperlipidemic subjects and can potentiate the effect of diet or drug therapy on glucose metabolism in patients with non-insulin dependent diabetes mellitus.

Blood Glucose↗
PubMed1990

Lymphadenopathy associated with severe hypertriglyceridemia.

The clinical recognition of diffuse lymphadenopathy generates a variety of important differential diagnostic considerations. We describe a woman with severe hypertriglyceridemia (type V hyperlipidemia) associated with diffuse lymphadenopathy. This association has not been described previously and should be included in the differential diagnosis of diffuse lymphadenopathy.

Female↗
PubMedDate not supplied

[Properties of plasma low density lipoproteins in patients with hypertriglyceridemia and ischemic heart disease].

It has been shown that low-density plasma lipoproteins in patients with ischemic heart disease and hypertriglyceridemia are heavier in density, smaller in size, more negatively charged and more inclined to peroxide modification and aggregation than in healthy persons. The protein in the composition of such lipoproteins deviates towards the water phase, which may result in the masking of the domen, recognized by the BE-receptor and may lead to hyperlipidemia of a retaining character.

Chemical Phenomena↗
PubMed1989

The status of hypertriglyceridemia as a risk factor for coronary heart disease.

The three-decade long controversy surrounding the status of triglycerides as an independent risk factor for coronary heart disease is presented. The studies that reported an association and the clinical trials of cholesterol-lowering medications are examined. Because of the inconsistency between the observational findings and the consistently negative clinical trial findings, treatment of isolated hypertriglyceridemia cannot be recommended at present.

Coronary Disease↗
PubMed1989

Hypertriglyceridemia in bone marrow transplant recipients: another side effect of cyclosporine A.

The incidence and duration of hypertriglyceridemia (HTG) associated with allogeneic HLA-identical bone marrow transplantation (BMT) were investigated in 38 patients with normal triglyceride levels (TG) before BMT and without any evidence of prior liver disorder. Twenty-two (58%) patients developed HTG. The median of TG peak values was 350 mg/dl (range 215-908) and the median actuarial time for HTG appearance was 7 weeks (range 1-12). Among several variables analysed (age, sex, hyperglycemia, total parenteral nutrition, treatment with methylprednisolone, estrogens or cyclosporine A) only cyclosporine A administration was significantly associated with HTG development.

Adolescent↗
PubMed1989

A novel explanation for the reduced LDL cholesterol in severe hypertriglyceridemia.

When [3H]cholesteryl ester-labeled low density (LDL) and intermediate density lipoproteins (IDL) from a normotriglyceridemic, hypercholesterolemic rabbit were injected into severely hypertriglyceridemic, hypercholesterolemic rabbits, 60% of the label appeared in very low density lipoproteins (VLDL) at 3 hr. A similar experiment showed that 40% of injected 131I-protein-labeled LDL appeared in the IDL fraction at 4 hr. Taken together, these data suggest that the exchange of LDL cholesteryl ester for VLDL triglyceride results in a density shift of injected LDL to the IDL density range. Furthermore, the percent of injected 131I-labeled LDL from normotriglyceridemic rabbits that appeared in the IDL fraction increased in rabbits with increasing levels of plasma triglyceride. This LDL density shift was reproduced in vitro by incubating iodinated LDL from normotriglyceridemic, hypercholesterolemic rabbits with concentrations of VLDL from hypertriglyceridemic, hypercholesterolemic rabbits similar to those in plasma. With such a system, it was shown that the percentage of LDL that appeared in the IDL fraction increased with time, was enhanced fourfold by the addition of plasma lipid transfer protein, increased with increasing molar ratio of triglyceride to cholesteryl ester in VLDL, but apparently did not increase with increasing VLDL particle number. These studies suggest that a pronounced decrease in density of lipoproteins that would normally appear in the LDL density range, resulting from loss of cholesteryl ester in exchange for VLDL triglyceride, may explain, at least in part, the reduced LDL levels in severe hypertriglyceridemia.

Animals↗
PubMed1989

Incides of lipid peroxidation in patients with hypercholesterolemia and hypertriglyceridemia.

Peroxidation of lipoproteins has received attention recently in connection with its possible initiation and propagation of atherosclerosis. We studied indices of lipid peroxidation in plasma of 30 patients with either hypercholesterolemia or both hypercholesterolemia and hypertriglyceridemia, and compared them with those of 19 healthy subjects. In the patients lipid hydroperoxides measured both iodometrically and as thiobarbituric acid-reactive substances (TBA-RS) were significantly increased, while concentrations of thiol groups remained unchanged. There was no correlation between concentrations of hydroperoxides and TBA-RS, possibly because the two methods assessed different breakdown products of lipid peroxidation. Lipid hydroperoxide levels, but not those of TBA-RS were correlated with LDL-cholesterol and triglyceride levels. In 6 patients administration of vitamin E at a daily dosage of 300 mg for 4 to 6 weeks depressed elevated hydroperoxides by 33%, and TBA-RS by 44% on average.

Adult↗
PubMed1994

HMG-CoA reductase activity in the liver of rats with hereditary hypertriglyceridemia: effect of dietary fish oil.

To assess the possible participation of liver microsomal 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase in the hypocholesterolemic effect of fish oil (FO) in rats with hereditary hypertriglyceridemia (derived from the Wistar strain, obtained from VELAZ, Prague, Czech Rep.), male animals were fed a basal diet (BD) or a high sucrose diet (SD-63 cal %) with or without FO supplement (30 wt% n-3 polyunsaturated fatty acids) for 21 days. The feeding with high sucrose diet resulted in increased HMG-CoA reductase activity; (P < 0.05). However, FO added to the diet suppressed this stimulated enzymatic activity (919.05 +/- 76.86 vs. 614.05 +/- 48.53 pmol/min/mg prot.; P < 0.05) and decreased cholesterol (CH) content in both serum and the liver of HTG rats fed basal as well as sucrose diet; (P < 0.05). The results of the study demonstrated that the hypocholesterolemic effect of FO added to the diet was mediated under certain conditions, by affecting of HMG-CoA reductase activity and not only by its effect on specific receptors as demonstrated before.

Animals↗
PubMed1994

In vivo metabolism of apolipoprotein A-IV in severe hypertriglyceridemia: a combined radiotracer and stable isotope kinetic study.

Apolipoprotein (apo) A-IV is an intestinally derived apolipoprotein that plays a potentially important role in lipoprotein metabolism and reverse cholesterol transport. However, the factors that regulate its plasma concentrations are not well understood. Plasma apoA-IV levels have been previously shown to correlate with fasting triglyceride (TG) levels in humans with TG levels less than 300 mg/dl (Lagrost et al. 1989. J. Lipid Res. 30: 701-710). In this study, we established that apoA-IV levels were significantly elevated (mean 29.3 mg/dl) in a group of 15 hypertriglyceridemic patients (TG > 300 mg/dl) compared with normolipidemic controls (mean 13.4 mg/dl). In order to investigate the relationship between hypertriglyceridemia and apoA-IV metabolism, we then studied the in vivo kinetics of apoA-IV in two healthy hypertriglyceridemic patients (mean TG = 1297 mg/dl) compared with normolipidemic control subjects. Combined studies using endogenous stable isotope labeling (with a primed constant infusion of deuterated L-leucine) and exogenous radiolabeling (with 125I) of apoA-IV were performed. Both stable isotope and radiotracer studies demonstrated substantially decreased apoA-IV fractional catabolic rates (FCR) in the hypertriglyceridemic patients (1.24 +/- 0.13 day-1) compared with controls (2.33 +/- 0.08 day-1). The apoA-IV production rate was not significantly different between the two groups. Gel filtration chromatography of plasma indicated an increased proportion of apoA-IV in the triglyceride-rich lipoproteins (TRL) of the hypertriglyceridemic patients compared with controls and delayed catabolism of this TRL-associated apoA-IV. The rate of apoA-IV catabolism from the lipid deficient fraction was not different between the hypertriglyceridemic patients and controls. In summary, plasma levels of apoA-IV are significantly elevated in hypertriglyceridemic patients due to delayed catabolism of apoA-IV as demonstrated by both endogenous stable isotope labeling and exogenous radiotracer techniques.

Apolipoproteins A↗
PubMed1994

Association of etretinate and fish oil in psoriasis therapy. Inhibition of hypertriglyceridemia resulting from retinoid therapy after fish oil supplementation.

We studied the main papers concerning treatment with fish oil (EPA and DHA) of patients with psoriasis vulgaris, psoriatic arthritis and pustular psoriasis. In our investigation, 25 patients with psoriasis vulgaris evidenced a statistically significant increase in triglyceride serum levels, compared with controls. 10 of these patients underwent therapy with etretinate 0.75-1.0 mg/kg daily for 2 months followed by 2-3 months of etretinate 0.35-0.50 mg/kg daily associated with fish oil 1.5 g (EPA and DHA) daily. According with several authors, fish oil is able not only to produce good clinical results, but also to minimize the side effects of retinoid therapy, especially hypertriglyceridemia.

Adult↗
PubMed1993

Overexpression of human lipoprotein lipase in transgenic mice. Resistance to diet-induced hypertriglyceridemia and hypercholesterolemia.

Lipoprotein lipase (LPL) is a key enzyme in the hydrolysis of triglyceride-rich lipoproteins. To determine the role of LPL in lipoprotein metabolism, we established three transgenic mouse lines overexpressing the human LPL gene; the highest expressor line, which transcribed human LPL mRNA in the heart, skeletal muscles, and adipose tissue, was used in this study. The transgenic mice had 5- and 1.7-fold higher LPL activity in adipose tissue and post-heparin plasma, respectively. Plasma triglyceride levels in transgenic mice were 24.2% of that in control mice, and gel filtration chromatography showed that very low density lipoprotein (VLDL) triglycerides were much reduced in transgenic mice. In the chemical analysis of plasma lipoproteins isolated by ultracentrifugation, we found that LDL particles were cholesterol-rich and HDL2 cholesterol was increased 1.4-fold in transgenic mice as compared to control mice. When we injected 125I-VLDL intravenously into transgenic mice, the clearance of 125I-VLDL and the conversion of VLDL to LDL was markedly enhanced as compared to control mice. Furthermore, the clearance of chylomicrons, estimated by both the fat loading and retinyl palmitate loading tests, was significantly enhanced in transgenic mice. After sucrose feeding, no increase in VLDL was observed in transgenic mice. When fed a high cholesterol diet, the development of hypercholesterolemia was suppressed in transgenic mice. These results suggested that LPL determined not only hydrolysis of triglyceride-rich lipoproteins but also lipolytic conversion, and that overexpression of LPL acted to protect against diet-induced hypertriglyceridemia as well as hypercholesterolemia.

Actins↗
PubMed1993

Central obesity in rhesus monkeys: association with hyperinsulinemia, insulin resistance and hypertriglyceridemia?

Total body fat and anthropometric assessments of fat distribution were examined in 23 lean and obese rhesus monkeys (Macaca mulatta). In addition, the relationships of central obesity to hyperinsulinemia, insulin resistance, glucose intolerance and hyperlipidemia were studied. Total body fat (as determined by the tritiated water dilution method), plasma glucose, insulin, lipoproteins (triglyceride, cholesterol and HDL- and LDL-cholesterol) and free fatty acids (FFA), and glucose disappearance rate (KG) and peripheral insulin-stimulated glucose uptake (M) were obtained. Results showed that abdominal circumference was the best predictor of body fat (r = 0.90; P < 0.001). There were strong linear relationships between abdominal circumference and plasma insulin (r = 0.66), glucose tolerance (r = -0.53), and M rate (r = -0.59) (all P < 0.05) but not to plasma glucose, lipoprotein fractions, or free fatty acids. When the subjects were grouped according to degree of obesity and insulin resistance (lean normals, obese insulin sensitive, and obese insulin resistant), the obese resistant monkeys had significantly higher plasma insulin levels, lower glucose tolerance, and significantly higher plasma triglyceride levels. We conclude that the spontaneously obese rhesus monkey is an excellent model of central obesity. Furthermore, in this model upper body obesity appears to be facilitative in the development of hyperinsulinemia, glucose intolerance and hypertriglyceridemia but does not appear to be causally related. In the rhesus monkey and in humans as well, we propose that the link between central obesity and these metabolic abnormalities may be peripheral insulin resistance.

Adipose Tissue↗
PubMed1993

Effect of hypertriglyceridemia correction by omega-3 fatty acids on peritoneal transport in continuous ambulatory peritoneal dialysis patients.

Lipid abnormalities, both hypercholesterolemia and particularly hypertriglyceridemia (hyperTg), are common in long-term continuous ambulatory peritoneal dialysis (CAPD) patients. Hyperviscosity and rheological alterations have been proposed as major hemodynamic problems in hyperTg patients. The aim of this study was to evaluate whether a hyperTg correction by employing omega-3 fatty acids (omega-3) affects peritoneal transport. Six hyperTg (> 700 mg/dL) CAPD patients were treated with 2-3 g/day of omega-3 until normal Tg values were achieved. The assessment of peritoneal dialysis efficacy was performed by evaluating the peritoneal equilibration test (PET) before omega-3 supplementation, when normal Tg levels were reached, and 3 weeks after stopping therapy when hyperTg returned. When normal Tg levels were reached, a small but significant improvement of urea and creatinine D/P was noted: 0.85 +/- 0.05 versus 0.93 +/- 0.03 (p < 0.05) and 0.78 +/- 0.03 versus 0.86 +/- 0.05 (p < 0.05), respectively, with negative correlation between D/P of urea and Tg. These preliminary data demonstrate that a hyperTg correction with omega-3 may induce an increase in peritoneal transport of small molecules in CAPD.

Aged↗
PubMed1996

Efficacy and safety of a new HMG-CoA reductase inhibitor, atorvastatin, in patients with hypertriglyceridemia.

OBJECTIVE: To assess the lipid-lowering effect of atorvastatin (a new 3-hydroxy-3-methylglutaryl coenzyme A [HMG-CoA] reductase inhibitor) on levels of serum triglycerides and other lipoprotein fractions in patients with primary hypertriglyceridemia, determine if atorvastatin causes a redistribution of triglycerides in various lipoprotein fractions, and assess its safety by reporting adverse events and clinical laboratory measurements. DESIGN: Randomized double-blind, placebo-controlled, parallel-group, multicenter trial. SETTING: Community- and university-based research centers. PATIENTS: A total of 56 patients (aged 26 to 74 years) with a mean baseline triglyceride level of 6.80 mmol/L (603.3 mg/dL) and a mean baseline low-density lipoprotein cholesterol (LDL-C) level of 3.07 mmol/L (118.7 mg/dL). INTERVENTIONS: Cholesterol-lowering diet (National Institutes of Health National Cholesterol Education Program Step I Diet) and either 5 mg, 20 mg, or 80 mg of atorvastatin, or placebo. MAIN OUTCOME MEASURES: Percent change from baseline in total triglycerides for three dose levels of atorvastatin compared with placebo. RESULTS: Mean reductions in total triglycerides between 5 mg, 20 mg, and 80 mg of atorvastatin and placebo after 4 weeks of treatment were -26.5%, -32.4%, -45.8%, and -8.9%, respectively. Mean reductions in LDL-C were -16.7%, -33.2%, -41.4%, and -1.4%, respectively, and very low-density lipoprotein cholesterol (VLDL-C) were -34.3%, -45.9%, -57.7%, and -5.5%, respectively. Similar mean changes in total apolipoprotein B (apo B) (-16.9%, -32.8%, -41.7%, and +1.0%), apo B in LDL (-14.8%, -29.8%, -42.0%, and -3.1%), and apo B in VLDL (-23.8%, -35.8%, -34.4%, and +11.7%) were observed. In addition, comparable mean changes in LDL triglycerides (-22.5%, -30.7%, -39.9%, and +3.9%) and VLDL triglycerides (-28.1%, -34.0%, -47.3%, and -10.8%) were seen. CONCLUSIONS: In atorvastatin treatment groups, total serum triglyceride levels decreased in a dose-dependent manner, reductions in the 20-mg and 80-mg groups were statistically significant (P < .05) compared with placebo. Atorvastatin did not cause a redistribution of triglycerides but consistently lowered triglycerides in all lipoprotein fractions. Atorvastatin was well tolerated.

Adult↗
PubMed1994

[Hypertriglyceridemia].

The hypertriglyceridemias comprise a heterogenous group of lipoprotein disorders varying with respect to etiology, lipoprotein pattern, and its major clinical sequelae, i.e. pancreatitis and atherosclerosis. Therefore goals and modalities of treatment should be individualized to a large extent. Behavioral measures like diet, weight control, exercise, reduced alcohol consumption and smoking cessation form the cornerstone of medical management. Lipid lowering drugs should be considered when triglyceride levels exceed 1000 mg/dl to reduce the risk of pancreatitis and in patients at high risk for atherosclerosis, often characterized by a high total cholesterol/HDL ratio, to reduce cardiovascular endpoints.

Combined Modality Therapy↗
PubMed1996

Heterozygosity for Asn291-->Ser mutation in the lipoprotein lipase gene in two Finnish pedigrees: effect of hyperinsulinemia on the expression of hypertriglyceridemia.

We describe two Finnish kindreds with the Asn291 --> Ser mutation (A291S) of the lipoprotein lipase (LPL) gene. Sixteen subjects (9 male, 7 female) heterozygous for this mutation were studied and compared with 17 unaffected family members or spouses (family controls) and 19 unrelated healthy subjects (population controls). In the group of subjects heterozygous for the A291S mutation, postheparin plasma LPL activity was on average 23% lower than in the family controls and 29% lower than in the population controls. In agreement, in vitro expression studies with COS-7 cells showed that the mutant protein exhibits approximately 50% of the lipolytic activity of the wild-type protein. Median serum triglyceride concentration was 2.90 mmol/l in the group of heterozygotes, compared with 1.14 mmol/l in the family controls (P < 0.01) and 0.99 mmol/l in the population controls (P < 0.001). The heterozygotes also had a marked preponderance of small dense low density lipoproteins (LDL) as assessed by gradient gel electrophoresis. Nine of the heterozygous subjects were hypertriglyceridemic (serum triglyceride concentration > 2.0 mmol/l). Age or body mass index were not related to the presence of hypertriglyceridemia. By contrast, all hypertriglyceridemic subjects were either hyperinsulinemic (serum insulin concentration > 10 mU/l, n = 7) or had diabetes (n = 2). In a multivariate regression analysis, very low density lipoprotein (VLDL) triglyceride level was significantly and independently related to serum apolipoprotein B concentration, the presence of the A291S mutation, serum insulin concentration, and postheparin plasma LPL activity. The Asn291-->Ser mutation of the LPL gene results in reduced lipolytic activity. However, dyslipidemia appears to manifest only if VLDL production is also increased. Hyperinsulinemia was the major determinant of excessive VLDL synthesis and dyslipidemia among the subjects heterozygous for the A291S mutation in this study.

Adolescent↗