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At least 793 records · Page 44Linked to original sources
PubMed2000

Current perspectives on the management of hypertriglyceridemia.

BACKGROUND: Observational studies have demonstrated that triglycerides are an independent risk factor for coronary heart disease. Atherothrombosis may be mediated by uptake and incorporation of triglyceride-rich lipoproteins by macrophages and through an association with small, dense LDL and HDL particles. There are considerable data that lowering LDL cholesterol reduces cardiovascular events. However, the importance of triglyceride lowering remains elusive. METHODS: A summary of major arteriographic and clinical end point trials is reviewed. Studies evaluating various strategies, including dietary and hygienic measures as well as pharmacologic therapies, are discussed. RESULTS: Dietary reduction of saturated fat, coupled with aerobic activity, reduces triglyceride levels approximately 20% to 24%. Omega-3 fatty acids may also reduce triglyceride levels appreciably. Effective pharmacologic therapies that lower triglyceride levels include nicotinic acid (20% to 40%), fibrates (20% to 55%), and statins (10% to 30%). Nevertheless, an independent benefit of triglyceride lowering on coronary event rate has not been demonstrated. CONCLUSIONS: There are little data that triglyceride reduction improves cardiovascular event rate. In contrast, lowering LDL cholesterol and, more recently, raising HDL cholesterol are proven therapies in coronary heart disease prevention. As such, these modalities remain the top priority in the management of dyslipidemia with triglyceride reduction as an adjunctive consideration.

Clinical Trials as Topic↗
PubMed2006

A randomised controlled trial of omega-3 fatty acid supplementation for the treatment of hypertriglyceridemia in HIV-infected males on highly active antiretroviral therapy.

BACKGROUND: Hypertriglyceridaemia is a recognised metabolic abnormality in HIV-infected people, increasing in severity in people treated with highly active antiretroviral therapy (HAART). An alternative treatment for hypertriglyceridaemia in non-HIV-infected populations is omega-3 fatty acid supplementation. This study aimed to compare the effectiveness of omega-3 fatty acid supplementation and placebo in lowering fasting triglyceride levels in HIV-infected patients on HAART. METHODS: A placebo-controlled, randomised, double-blind trial in participants on stable HAART with fasting triglycerides of >3.5 mm to 10.0 mm using 9 g of omega-3 fatty acids versus placebo (olive oil) after a 6-week lead in on dietary therapy. RESULTS: Eleven patients were enrolled. The mean triglyceride level for the population decreased from 5.02 mm at baseline to 4.44 mm (-11.6%) after dietary intervention and 3.37 mm (-32.9%) after the 8-week treatment period. In the omega-3 fatty acid arm of the study, triglycerides fell from 5.34 mm to 5.02 mm (-6%) after dietary intervention and to 2.30 mm (-56.9%) after the treatment period. In the placebo arm of the study, triglycerides fell from 4.77 mm to 4.05 mm (-15.1%) after dietary intervention and to 4.08 mm (-14.5%) after the treatment period. Using the random effects model, a statistically significant effect on triglycerides of omega-3 fatty acid versus placebo was found (chi(2) = 6.04, P = 0.0487). The estimated difference between groups for change in mean triglycerides over 8 weeks was -2.32 mm (95% CI -4.52, -0.12 mm). CONCLUSIONS: Omega-3 fatty acids are likely to be an effective treatment for hypertriglyceridaemia in HIV-infected males on HAART.

Adult↗
PubMed2006

A genetic variant at the fatty acid-binding protein aP2 locus reduces the risk for hypertriglyceridemia, type 2 diabetes, and cardiovascular disease.

Obesity and the associated pathologies including dyslipidemia, insulin resistance, type 2 diabetes, and cardiovascular disease constitute a major threat to global human health. Yet, the genetic factors that differentially predispose individuals to this cluster of pathologies are unclear. The fatty acid-binding protein aP2 is a cytoplasmic lipid chaperon expressed in adipocytes and macrophages. Mice with aP2 deficiency are partially resistant to obesity-induced insulin resistance and type 2 diabetes, have lower circulating triglycerides, and exhibit marked protection against atherosclerosis. Here, we demonstrate a functionally significant genetic variation at the aP2 locus in humans that results in decreased adipose tissue aP2 expression due to alteration of the CAAT box/enhancer-binding protein binding and reduced transcriptional activity of the aP2 promoter. In population genetic studies with 7,899 participants, individuals that carry this T-87C polymorphism had lower serum triglyceride levels and significantly reduced risk for coronary heart disease and type 2 diabetes compared with subjects homozygous for the WT allele. Taken together, our results indicate that reduction in aP2 activity in humans generate a metabolically favorable phenotype that is similar to aP2 deficiency in experimental models.

Adipose Tissue↗
PubMed1988

Rabbit serum hypertriglyceridemia after administration of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin) caused a dose-dependent decrease of adipose tissue lipoprotein lipase (LPL) activity and caused a concomitant increase in serum triglyceride concentration in the rabbit 10 d after single ip administration of either 1 or 50 micrograms/kg. Hepatic low-density lipoprotein (LDL) binding was markedly depressed and serum cholesterol concentrations were modestly increased relative to pair-fed control animals. Serum glucose concentrations were significantly lower in the rabbit administered TCDD compared to ad libitum or pair-fed control animals, although little change was observed in serum insulin concentration. Electron microscopic examination of aortic arches 20 d after a single ip administration of 50 micrograms TCDD/kg revealed ruffling, denudation, and sloughing off of the cell surface and the appearance of macrophage-like structures in the intima and media of the endothelial cells. These alterations resemble preatherosclerotic lesions typical in animals with hyperlipidemia. It is proposed that TCDD causes hyperlipidemia in the rabbit through suppression of LPL activity and LDL receptor binding.

Animals↗
PubMed1990

Fish oils in hypertriglyceridemia: a dose-response study.

The effects of three supplemental doses of fish oil on plasma lipids, lipoproteins, and bleeding times were studied in ten hypertriglyceridemic patients. After a 3-wk baseline period each patient was given 15, 25, or 40 mL fish oil/d (containing 4.5, 7.5, and 12 g n-3 fatty acids) for three successive 6-wk periods, each separated by a 4-wk period of no supplementation. Plasma cholesterol concentrations decreased from 7.40 mmol/L to 6.35, 6.55, and 6.40 mmol/L with increasing doses of fish oil (p less than 0.01 vs baseline for each). Plasma triglyceride concentrations decreased from 6.10 mmol/L to 2.90, 2.80, and 2.35 mmol/L (p less than 0.01 vs baseline for each). Low-density-lipoprotein cholesterol concentrations increased significantly (by 23% and 28%) with the two higher doses, respectively. Bleeding times increased only with the largest dose. The lowest dose was the most hypolipidemic per gram n-3 fatty acids.

Adult↗
PubMed1996

Effect of high-amylose starch and oat bran on metabolic variables and bowel function in subjects with hypertriglyceridemia.

We compared the effects of a diet in which approximately 25% of the carbohydrate was replaced by high-amylose starch with those of a similar diet high in oat bran or low-amylose starch in 23 hypertriglyceridemic subjects who were overweight mostly because of abdominal adiposity. Each diet was consumed for 4 wk in random order and in a crossover fashion. Overall, the diets were high in carbohydrate (> 55% of energy) and low in fat (< 30% of energy); the amount of resistant starch in the foods containing high-amylose starch was 17 g in women and 25 g in men. The metabolic effects of specific starches on plasma lipids, fasting and postprandial glucose and insulin profiles, and bowel function were assessed at the end of each intervention. Plasma triacylglycerols (triglycerides) were significantly lower after the oat bran diet than after the other two diets (P < 0.02). No other effects on fasting plasma lipids, glucose, or insulin were noted. However, when the high-amylose starch comprised 33% of the carbohydrate content in a test meal, there was a significant but biologically small reduction in the overall postprandial plasma insulin concentration by 17% relative to the low-amylose diet (P < 0.01). Both the oat bran and the high-amylose diet resulted in an increased frequency of bowel actions and lower fecal pH (P < 0.02) relative to the low-amylose diet. However, unlike the oat bran diet, the high-amylose diet increased short-chain fatty acid concentrations in fecal water by 32% (P < 0.001).

Adult↗
PubMed1993

Molecular cloning and characteristics of a new apolipoprotein C-II mutant identified in three unrelated individuals with hypercholesterolemia and hypertriglyceridemia.

A new rare mutant form of apolipoprotein C-II (apoC-II), designated apoC-IISF, was identified in three unrelated hyperlipidemic patients. The first was a Caucasian male with a total cholesterol (TC) of 313 mg/dl and total triglyceride (TG) of 282 mg/dl, the second an African-American female (TC 345 mg/dl, TG 203 mg/dl) and the third, an African-American male (TC 345 mg/dl, TG 1000 mg/dl). Each subject was found to be heterozygous for a G to A substitution in the codon for residue 38, resulting in a Lys for Glu exchange. This accounts for the increased pl value of 5.3. The third patient, in addition to apoC-IISF, had apoC-II2, another charge variant. This was determined by DNA sequencing, confirming the Gln for Lys change at residue 55 previously predicted by analysis of peptide fragments in this laboratory. Similar Michaelis constants of activation and activation energies were observed when the ability of apoC-IISF to activate lipoprotein lipase was compared to normal apoC-II. This indicates that major changes in charge around residue 38 lack effect on the activation properties. The variant may be altered in some other property, such as lipid binding, but since the distribution of apoC-IISF revealed no simple co-inheritance with lipid levels, it is unclear to what extent it plays a role in the observed hyperlipidemia. The presence of other factors acting together with the variant may predispose to elevated lipid levels.

Amino Acid Sequence↗
PubMed2003

Identification of a novel lipase gene mutated in lpd mice with hypertriglyceridemia and associated with dyslipidemia in humans.

Triglyceride (TG) metabolism is crucial for whole body and local energy homeostasis and accumulating evidence suggests an independent association between plasma TG concentration and increased atherosclerosis risk. We previously generated a mouse insertional mutation lpd (lipid defect) whose phenotype included elevated plasma TG and hepatic steatosis. Using shotgun sequencing (approximately 500 kb) and bioinformatics, we have now identified a novel lipase gene lpdl (lpd lipase) within the lpd locus, and demonstrate the genetic disruption of exon 10 of lpdl in the lpd mutant locus. lpdl is highly expressed in the testis and weakly expressed in the liver of 2-week old mice. Human LPDL cDNA was subsequently cloned, and was found to encode a 460AA protein with 71% protein sequence identity to mouse lpdl and approximately 35% identity to other known lipases. We next sequenced the human LPDL gene exons in hypertriglyceridemic subjects and normal controls, and identified seven SNPs within the gene exons and six SNPs in the adjacent introns. Two hypertriglyceridemic subjects were heterozygous for a rare DNA variant, namely 164G>A (C55Y), which was absent from 600 normal chromosomes. Two other coding SNPs were associated with variation in plasma HDL cholesterol in independent normolipidemic populations. Using bioinformatics, we identified another novel lipase designated LPDLR (for 'LPDL related lipase'), which had 44% protein sequence identity with LPDL. Together with the phospholipase gene PSPLA1, LPDL and LPDLR form a new lipase gene subfamily, which is characterized by shortened lid motif. Study of this lipase subfamily may identify novel molecular mechanisms for plasma and/or tissue TG metabolism.

Amino Acid Sequence↗
PubMed2000

Dietary oligofructose lessens hepatic steatosis, but does not prevent hypertriglyceridemia in obese zucker rats.

We studied the influence of oligofructose (OFS), a nondigestible fructan, on lipid metabolism in obese fa/fa Zucker rats. The addition of 10 g/100 g OFS to the diet slowed the increase in body weight without modifying serum triglycerides or glucose concentrations after 7 wk of treatment. However, an oral load of 2 g glucose and 5 g corn oil/kg body weight increased triglyceridemia more in OFS-fed rats than in control rats. After 10 wk, OFS decreased the hepatic concentration of triglycerides 57% relative to controls. The less severe steatosis was confirmed by histologic analysis. Among the key enzymes involved in fatty acid synthesis and esterification, only malic enzyme activity was significantly lower in OFS-fed rats than in controls. The epididymal fat mass was significantly lower in OFS-fed rats. In conclusion, dietary enrichment with OFS can counteract both the fat mass development and the hepatic steatosis that occur in obese Zucker rats. Future studies will be designed to clarify in obese animals the influence of dietary OFS on postprandial triglyceridemia, which is an important variable associated with the development of atherosclerosis in humans, and to analyze the biochemical mechanism underlying the "hepatoprotective" effect of OFS.

Analysis of Variance↗