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 973 records · Page 54Linked to original sources
PubMed1993

[Preliminary evaluation of an association of polyunsaturated acids in primary hypertriglyceridemia].

The above study was intended to evaluate changes in triglyceride blood level in subjects treated with a polyunsaturated fatty acid combination: docosahexanoic (DHA) and eicosapentaenoic (EPA) acid, compared to changes observed in patients treated with arachidonic acid. The results obtained show that a significant reduction of triglyceride blood level was achieved and was more marked in patients treated with the DHA-EPA combination compared to those treated with arachidonic acid only. An increase in the index of fatty acid unsaturation was observed in all patients without significant differences between treatments.

Adult↗
PubMed1995

[Baseline hypertriglyceridemia, a risk factor for non-insulin dependent diabetes mellitus: a 6-year follow-up study of 432 nondiabetics].

The relationship between baseline fasting plasma triglycerides level (FTG) and the incidence of non-insulin-dependent diabetes mellitus (NIDDM) within 6 years were investigated in 432 Chinese nondiabetics. They were identified by oral glucose tolerance test (OGTT, oral 75 g glucose) in Daqing diabetes survey in 1986. 220 subjects were men and 212 women. Among them 226 had normal glucose tolerance and 206 impaired glucose tolerance. The measurement of fasting plasma lipids and glucose were performed at the baseline examination and after 6-year follow-up. Six-year incidence of NIDDM in the highest triglycerides tertile group (top tertile Q3, mean = 2.5 mmol/L) was 2.3 times (38.6% vs 16.6%, P < 0.01) as compared with that of the lowest triglycerides tertile group (first tertile Q1, mean = 0.7 mmol/L). The difference of 2-hour blood glucose level in OGTT (OGTT BG2h level) between Q1 and Q3 was 2.4 mmol/L (mean = 7.6-10.0 mmol/L) after 6 years. Multivariate general linear regression analysis demonstrated that the FTG level was positively associated with the OGTT BG2h level after 6 years (P = 0.0335) after controlling the age, sex, fasting blood glucose (FBG) and body mass index (BMI). Therefore this result indicates that FTG level is an independent risk factor for the development of NIDDM in this population.

Adult↗
PubMed1996

Expression of a novel human apolipoprotein (apoC-IV) causes hypertriglyceridemia in transgenic mice.

The human apolipoprotein (apo) C-IV gene has been recently identified: it is closely linked to the promoter region of the apoC-II gene (Allan, C.M., D. Walker, J. Segrest, and J. M. Taylor. 1995. Genomics. 28: 291-300). To determine the effect of apoC-IV gene expression on lipoprotein metabolism, transgenic mice were generated using a human apoC-IV cDNA construct. Human apoC-IV was found associated with plasma lipoproteins (d < 1.21 g/ml), mainly in very low density lipoproteins (VLDL), and higher molecular mass isoforms were present, due to N-linked glycosylation and variable sialylation of apoC-IV. Human apoC-IV transgenic mice were hypertriglyceridemic compared to nontransgenic controls; the accumulated plasma triglycerides were present mainly in VLDL. There was little change in plasma cholesterol levels, although apoC-IV expression redistributed cholesterol to VLDL and larger particles in low density lipoprotein/large high density lipoprotein fractions. By immunoblot analysis, apoC-IV was not detected in normal adult human plasma or isolated plasma lipoproteins, a finding consistent with our previous observation of very low levels of human apoC-IV mRNA in human liver. However, our analysis of transgenic mice provides unequivocal evidence that human apoC-IV is a lipid-binding protein belonging to the apolipoprotein family and that it has the potential to alter lipoprotein metabolism.

Animals↗
PubMed1997

Alterations in serum phosphatidylcholine fatty acyl species by eicosapentaenoic and docosahexaenoic ethyl esters in patients with severe hypertriglyceridemia.

A new and sensitive method has been developed to analyze the molecular species of glycerophospholipids. This method was used to examine the effects of hypolipidemic intervention with n-3 fatty acids on the serum phosphatidylcholine species in severely hypertriglyceridemic patients. The drug treated group (n = 19) received 4 g/day of an 85% concentrate of the ethyl esters of eicosapentenoic and docosahexaenoic acids for 6 weeks. Control patients (n = 21) received 4 g/day of ethyl esters of corn oil fatty acids. To evaluate the effects of n-3 fatty acids upon serum phosphatidylcholines (PCs), sera from treated and control patients were analyzed before and after 6 weeks of intervention. PCs isolated from sera were digested with phospholipase C to diglycerides, derivatized with 7-methoxycoumarin-3-carbonyl azide, and analyzed by reverse phase high performance liquid chromatography (HPLC) with fluorescence detection. Pre-intervention serum PC species were, in order of decreasing concentration C16:0,18:2, C16:0,18:1, C18:0,18:2, C16:0,20:1, C16:0,22:0, C18:0,20:4, C16:0,16:0, C18:0,18:1, C18:1,18:2, C16:0,20:5, and C18:1,20:5. In the treated patients, mean increases of 300% in C16:0,20:5 and of 160% in C16:0,22:6 species were observed. There were no significant changes in the molecular species of the serum phosphatidylcholines in the group receiving the corn oil ethyl esters. The cumulative relative percentages for each of the individual fatty acids measured by HPLC were comparable to those determined by gas-liquid chromatography (GLC). In the treated group plasma triglycerides were reduced 26%, while they were increased by 7% in the placebo group. Our data showed that incorporation of eicosapentaenoic and docosahexaenoic acid into the serum PCs occurred within 6 weeks primarily in the C16:0,20:5 and C16:0,22:6 species and were usually accompanied by a reduction in plasma triglyceride.

Administration, Oral↗
PubMed1997

A novel apolipoprotein C-III variant, apoC-III(Gln38-->Lys), associated with moderate hypertriglyceridemia in a large kindred of Mexican origin.

Apolipoprotein C-III (apoC-III) is a major protein component of very low density lipoproteins (VLDL), chylomicrons, and a minor component of high density lipoproteins (HDL). Studies of naturally occurring human variants of apoC-III will help in adding to our understanding of the physiological function of this apolipoprotein. Using isoelectric focusing (IEF) of VLDL fractions we screened over 2500 lipid clinic patients and have identified an individual with a novel apoC-III variant. DNA sequencing revealed the variant to be a Lys for GIn exchange at amino acid residue 38 due to an A for C substitution in exon 3. This was confirmed by NH2-terminal protein sequence analysis. The mutant Lys38 variant was present in VLDL at about the same level as the normal form although the total amount of apoC-III was increased by 34%. The proband, a 16-year-old boy of Mexican origin, had a plasma level of total triglycerides above the 95th percentile for his age. Family studies revealed a further 16 individuals who were heterozygous for this apoC-III (Gln38-->Lys) variant. Compared to 21 unaffected relatives, the 17 heterozygous subjects had a statistically significant 32% elevation of their plasma levels of triglycerides when adjusted for age, sex, body mass index, and lifestyle. Other lipid and lipoprotein values were unaffected. The presence of an additional positive charge at residue 38 suggests that this residue is involved in the function of apoC-III. The elevation of plasma levels of triglycerides supports the view that apoC-III is involved in the regulation of the catabolism of triglyceride-rich lipoproteins.

Adolescent↗
PubMed1997

[Hypertriglyceridemia and plasma insulin in combined familial hyperlipidemia].

UNLABELLED: Changes in insulin secretion were investigated in a group of non obese subjects with combined familial hyperlipidemia (CFH), with normal glucose tolerance, relating the observed changes with plasma triglycerides and lipoprotein phenotype. MATERIALS AND METHODS: The study was conducted with 21 subjects (16 males and 5 females; mean age: 45.9 +/- 9.1 years), diagnosed of CFH after the clinical and analytical study of patients and their first degree relatives (9 with phenotype IIa, 8 IIb, and 4 IV) and 21 healthy control subjects, of similar age, sex and body weight. In both groups, lipids, plasma lipoproteins, glucose, basal plasma insulin, and insulin after and oral glucose overload (OGO) were quantitated. RESULTS: Diastolic blood pressure was higher (p < 0.01) in CFH group compared with controls (means: 132/80 vs 123/71 mmHg, respectively). TC, TG and Apo B were also higher in the CFH group. With OGO significantly higher serum insulin levels were observed at 0, 30, 60, 90 and 120 minutes in CFH subjects compared with control group. Basal serum insulin and the area under the curve of insulin secretion after OGO was higher in subjects with triglycerides (45,579 +/- 13,056 in controls, 61,385 +/- 22,254 in CFH IIa, 70,645 +/- 17,271 IIb and 124,884 +/- 36,944 in CFH IV. Insulin secretion correlated significantly (p < 0.01) with plasma triglycerides. As conclusion, hyperinsulinism is a finding in CFH non obese subjects and with normal glucose tolerance, and has an increasing frequency in subjects with high triglycerides levels.

Adult↗
PubMed1998

[How I study hypertriglyceridemia].

The strategy for the diagnosis of hypertriglyceridaemia comprises three successive steps. First, the physician should confirm the biological abnormality by at least one additional blood sample taken after an overnight fast; recent data, however, suggest that postprandial hypertriglyceridaemia may also represent a cardiovascular risk factor. Second, the phenotype of hypertriglyceridaemia should be considered as either isolated high triglyceride levels or hypertriglyceridaemia combined with hypercholesterolemia may be present; the combination of hypertriglyceridaemia with a low HDL cholesterol concentration or its association with the metabolic or insulin resistance syndrome should also be investigated. Third, all should be done in order to find the etiology of the hypertriglyceridaemia (by determining its genetic or nutritional origin, by excluding possible underlying pathologies, by looking for drugs able to increase serum triglyceride levels). These various steps should help the physician to take the final decision of treating one particular patient as well as to chose the most appropriate, nutritional or pharmacological, treatment.

Cholesterol, HDL↗
PubMed1998

Relationship of HDL and coronary heart disease to a common amino acid polymorphism in the cholesteryl ester transfer protein in men with and without hypertriglyceridemia.

Plasma triglyceride (TG) levels are inversely related to HDL-cholesterol levels and subjects with high TG and low HDL cholesterol have increased coronary heart disease (CHD) risk. Plasma cholesteryl ester transfer protein (CETP) transfers cholesteryl esters from HDL to TG-rich lipoproteins. In this study we determined the relationship between a common CETP amino acid polymorphism (I405V) and CETP and HDL levels and CHD prevalence in 576 men of Japanese ancestry in the Honolulu Heart Program cohort. This conservative substitution was associated with altered plasma CETP concentration (1.95 +/- 0.54, 1.91 +/- 0.57, and 1.77 +/- 0.57 microg/ml for the II, IV and VV genotypes, respectively). The distribution of plasma CETP concentrations among the VV, but not II, men appeared bimodal (P < 0.01), suggesting the presence of a functionally significant CETP gene mutation(s) in a subset of V alleles. HDL-C levels were higher in VV than IV for II men (55.4 +/- 17.4, 51.3 +/- 16.6, 51.1 +/- 17.0 mg/dl, P < 0.04). However, the increase in HDL was only significant in VV men with plasma TG > 165 mg/dl. Although CHD prevalence was not significantly different among the three genotypes in this population, in the subpopulation with high plasma TG, CHD prevalence appeared higher among VV than IV or II subjects (38% vs. 27% vs. 18%, P < 0.05 for an interaction of genotype and plasma TG levels). In fresh plasma from a separate group of normolipidemic subjects, the V/I polymorphism was not associated with any change in plasma CETP specific activity. The data suggest that a widespread and common CETP gene mutation(s) in linkage disequilibrium with 405V causes low CETP. Among hypertriglyceridemic men this is associated with higher HDL and possibly with increased CHD.

Amino Acids↗