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PubMed1993

Genetic markers in the apo AI-CIII-AIV gene cluster for combined hyperlipidemia, hypertriglyceridemia, and predisposition to atherosclerosis.

The aim of the present study was to search for genetic determinants of combined hyperlipidemia and hypertriglyceridemia, and to evaluate whether such determinants might be associated with predisposition to atherosclerosis. Four DNA polymorphisms in the apo AI-CIII-AIV gene cluster (G to A mutation at position -75 basepairs in the apo AI promoter, XmnI, PstI and SstI) were studied in relation to combined hyperlipidemia, hypertriglyceridemia, lipoprotein levels, atherosclerosis and age in 221 Danish men. The frequency of the rare allele of the XmnI polymorphism, the X+ allele, was higher in individuals below 55 years of age with combined hyperlipidemia than in individuals with normal lipid levels (0.31 vs. 0.14; P = 0.05). The rare allele of the SstI polymorphism, the S+ allele, was more frequent in hypertriglyceridemic individuals compared with normotriglyceridemic individuals (0.16 vs. 0.09; P < 0.05) and on analysis of variance the combined S-S+ and S+S+ genotypes were also associated with the highest triglyceride levels. Furthermore, the frequency of the S+ allele decreased significantly as a function of age in nonatherosclerotic subjects (from 0.15 to 0.10 to 0.02 in 48-, 63- and 85-year-olds, respectively; 48- versus 85-year-olds, P = 0.03). These results suggest that genetic variation in the apo AI-CIII-AIV gene complex is associated with combined hyperlipidemia and hypertriglyceridemia and may have an impact on longevity and/or predisposition to atherosclerosis.

Aged↗
PubMed1990

Effect of triiodothyronine on triglyceride synthesis in human fibroblasts in different types of hypertriglyceridemia.

Fibroblasts from 12 normotriglyceridemic subjects and 30 hypertriglyceridemic patients and family members were used to investigate triglyceride synthesis and the influence of triiodothyronine on it. The monolayers were incubated for 72 hours with and without the thyroid hormone, followed by incorporation studies of radiolabeled acetic acid or palmitic acid into the cellular triglyceride fraction. Triiodothyronine had no influence on triglyceride synthesis of normal cell lines and of cells derived from patients with secondary hypertriglyceridemia, whereas fibroblasts from endogenous type IV patients showed higher rates of triglyceride synthesis under identical conditions. Values for type IV were in the range of 134% to 466% of the hormone-free control incubations. In cultures derived from patients with familial combined hyperlipidemia, no stimulation by triiodothyronine was observed: values were in the range of 64% to 144% of the hormone-free controls. Three out of four lines with type V gave "normal" values and are supposed to represent secondary hypertriglyceridemia, whereas one line may express endogenous type IV. The evidence obtained in vitro with cultured cells indicates different metabolic defects in endogenous type IV and familial combined hyperlipidemia; it also shows the biochemically heterogenous nature of the disease "hypertriglyceridemia."

Acetates↗
PubMed1991

Apolipoprotein E allele frequencies in non-insulin-dependent diabetes mellitus with hypertriglyceridemia (type IIb, III, IV, and V hyperlipoproteinemia).

We examined apolipoprotein E (apo E) allele frequencies in non-insulin-dependent diabetes mellitus (NIDDM) patients with normolipidemia or various types of hypertriglyceridemia to elucidate the association of the apo E alleles with hypertriglyceridemia in NIDDM. NIDDM patients with normolipidemia (N = 134) or hypertriglyceridemia [type IIb hyperlipoproteinemia (HLP) (N = 42), III HLP (N = 7), IV HLP (N = 96), and V HLP (N = 8)] were randomly selected from our Diabetic Clinics. Apo E phenotypes (genotypes) were determined by our rapid flat-gel isoelectric focusing method. The frequency of the epsilon 4 allele was significantly higher in the type IIb (20.2%, P less than .01) and V (25.0%, P less than .05) HLP patients than in the normolipidemic patients (8.9%), whereas the frequency of the epsilon 3 allele was significantly (P less than .025) lower in the type IIb HLP patients (78.6%) than in the normolipidemic patients (89.2%). The frequency of the epsilon 2 allele was significantly higher in the type III (64.3%, P less than .001) and IV (5.2%, P less than .05) HLP patients than in the normolipidemic patients (1.9%), whereas the frequency of the epsilon 3 allele was significantly lower in the type III (28.6%, P less than .001) and IV (82.8%, P less than .05) HLP patients than in the normolipidemic patients. Thus, it has proven that the epsilon 2 allele is related to type III and IV HLP in NIDDM, whereas the epsilon 4 allele is related to type IIb and V HLP in NIDDM.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Hypertriglyceridemia in patients with psoriasis treated with cyclosporine.

Eight patients received cyclosporine at doses of 2.0 to 7.5 mg/kg/day. Seven of these patients had increased fasting plasma triglyceride levels with cyclosporine therapy compared with pretreatment values, which peaked after 1 month of therapy. Four patients experienced elevations in fasting triglycerides, over the upper limits for age- and sex-matched controls, which were at least two times higher than their baseline values. It was striking that all four of these patients had previously had hypertriglyceridemia while using etretinate and three of these patients had preexisting hypertriglyceridemia before both etretinate and cyclosporine therapy. Triglyceride elevation did not correlate with cyclosporine levels. Thus cyclosporine, similar to etretinate, unmasks a latent tendency for mild to moderate hypertriglyceridemia. Fasting triglyceride levels should be monitored during cyclosporine therapy, especially after 1 to 2 months of use, and in patients with preexisting increased triglycerides and/or a history of etretinate use.

Adult↗
PubMed2004

Endothelial cell adhesion molecules in healthy adults during acute hyperhomocysteinemia and mild hypertriglyceridemia.

OBJECTIVE: Hyperhomocysteinemia and hypertriglyceridemia are independently associated with atherosclerotic disease. The process of atherogenesis involves inflammation and endothelial dysfunction. We tested whether concurrent acute hyperhomocysteinemia and mild hypertriglyceridemia increase the concentrations of circulatory cellular adhesion molecules in healthy subjects. STUDY DESIGN AND METHODS: Twelve healthy volunteers aged 37.5 years (range, 25-51) participated in the present study. The concentrations of plasma total homocysteine (p-tHcy), serum triglycerides, circulatory cellular adhesion molecules (CAMs), and concentrations of nitrate were measured at 0 (fasting), 2, 4, and 6 h after loading with (1) methionine, (2) fat, (3) methionine + fat, and (4) water (control). Wash out period between each loading was >or=1 week. RESULTS: Percent relative changes from baseline in the concentrations of p-tHcy, 2, 4, and 6 h after methionine and methionine + fat were significantly different from after water and fat loading. Changes in the concentrations of serum triglycerides 2 h after fat loading were significantly different from water loading, whereas methionine + fat loading caused a significant difference after 2, 4, and 6 h. We detected a synergistic increase in the triglyceride area response to methionine + fat loading. We detected also a significant difference in percent relative changes in the concentrations of P-selectin (PSEL) (P = 0.02), E-selectin (ESEL) (P = 0.003), and vascular cell adhesion molecule-1 (VCAM-1) (P = 0.005) 6 h after methionine + fat loading as compared to water loading. There was an additive increase in the PSEL area response to methionine + fat loading. Furthermore, area response to VCAM was greater to methionine loading than water loading (P = 0.01). A decrease in the concentration of NO(3) was more pronounced after methionine + fat loading and a significantly decreased area response of nitrate to methionine + fat loading was detected than to area response to water loading (P = 0.002). CONCLUSION: Inflammatory activation of the endothelium takes place during concurrent transient hyperhomocysteinemia and mild hypertriglyceridemia.

Acute Disease↗
PubMed2004

A comparison of the effectiveness of soy protein isolate and fish oil for reducing the severity of retinoid-induced hypertriglyceridemia.

The effectiveness of soy protein isolate (SPI) to reduce the severity of retinoid-induced hypertriglyceridemia has been demonstrated in the rat, but not in human subjects. Because fish oil has been demonstrated to be effective at lowering serum triglyceride concentration in human subjects undergoing retinoid therapy, a study was conducted to compare the ability of SPI with that of fish oil to reduce the severity of retinoid-induced hypertriglyceridemia in the rat. Male Fischer 344 rats, n=8/group, were fed one of four isonitrogenous, isoenergetic diets, consisting of a control diet containing 24% casein +20% corn oil (C), and three 13-cis retinoic acid (13cRA)-supplemented diets containing 24% casein +20% corn oil (R), 24% SPI +20% corn oil (SR), and 24% casein +15% fish oil and 5% corn oil (FR). There was no effect of diet on food intake or final body weight. Serum triglyceride concentration for group R was higher (P<0.001) than for groups C, SR, and FR (7.20 vs. 2.50, 2.84, and 2.02 mmol/L, respectively); values for groups SR and FR did not differ for this parameter. The serum concentration of 13cRA for group R did not differ from that for groups SR and FR. Thus, SPI was as effective as fish oil in reducing the severity of retinoid-induced hypertriglyceridemia in an animal model, suggesting that it may be effective for this purpose in human subjects.

Animals↗
PubMed2004

Fenofibrate prevents obesity and hypertriglyceridemia in low-density lipoprotein receptor-null mice.

Our previous study demonstrated that fenofibrate improves both lipid metabolism and obesity, in part through hepatic peroxisome proliferator-activated receptor alpha (PPARalpha) activation, in female ovariectomized, but not in sham-operated, low-density lipoprotein receptor-null (LDLR-null) mice. The aim of this study was to determine whether fenofibrate prevents obesity and hypertriglyceridemia in male LDLR-null mice. Mice fed a high-fat diet for 8 weeks exhibited increases in body and white adipose tissue (WAT) weights and developed severe hypertriglyceridemia compared with mice fed a low-fat control diet. However, these effects were effectively prevented by fenofibrate. Mice given a fenofibrate-supplemented high-fat diet showed significantly reduced body weight, WAT weight, and serum triglycerides versus high-fat diet-fed animals. Triton WR1339 study showed that fenofibrate-induced reduction in circulating triglycerides was due to the decreased secretion of triglycerides from the liver. Moreover, the administration of fenofibrate not only resulted in liver hypertrophy and reduction in hepatic lipid accumulation, but also regulated the transcriptional expression of PPARalpha target genes, such as hepatic acyl-coenzyme A (CoA) oxidase and apolipoprotein C-III (apoC-III). Therefore, our results suggest that alterations in hepatic PPARalpha action by fenofibrate seem to suppress diet-induced obesity and severe hypertriglyceridemia caused by LDLR deficiency in male mice.

Acyl-CoA Oxidase↗
PubMed2006

Thr54 allele carriers of the Ala54Thr variant of FABP2 gene have associations with metabolic syndrome and hypertriglyceridemia in urban South Indians.

The intestinal fatty acid-binding protein gene is proposed as a candidate gene for diabetes because the protein it codes is involved in fatty acid absorption and metabolism. This study investigates the association of the Ala54Thr variant of the intestinal fatty acid-binding protein gene on type 2 diabetes mellitus and other related metabolic traits in Asian Indians. Ala54Thr polymorphism was genotyped by using polymerase chain reaction-restriction fragment length polymorphism in unrelated 773 type 2 diabetic and 899 normal glucose-tolerant (NGT) subjects, randomly chosen from the Chennai Urban Rural Epidemiology Study, an ongoing population-based study in South India. The Ala54Thr polymorphism was not associated with type 2 diabetes mellitus or obesity. However, genotype-phenotype study revealed that the NGT subjects carrying the Thr54 allele had significantly higher 2-hour plasma glucose (P = .007), glycated hemoglobin (P = .004), 2-hour insulin (P = .027), and fasting low-density lipoprotein cholesterol (P = .032) levels compared with those with the Ala54 allele. Normal glucose-tolerant subjects with Ala54Thr and Thr54Thr genotypes had significantly higher fasting serum triglyceride levels (P = .003) compared with those with Ala54Ala. The subjects were stratified into those with hypertriglyceridemia (serum triglyceride levels >or=150 mg/dL) and those without. The odds ratio for hypertriglyceridemia for the individuals carrying the Ala54Thr genotype was 1.491 (95% confidence interval [CI], 1.22-1.83, P < .0001), and for those carrying the Thr54Thr genotype, it was 1.888 (95% CI, 1.34-2.67; P < .0001). Subjects were also stratified into those with metabolic syndrome (MS) and those without, according to modified Adult Treatment Panel III guidelines. The odds ratio (adjusted for age and sex) for MS for the individuals carrying the Ala54Thr genotype was 1.240 (95% CI, 1.02-1.51; P = .03), whereas for those carrying the Thr54Thr genotype, it was 1.812 (95% CI, 1.28-2.57; P = .001). Carriers of the Thr54 allele have associations with MS and hypertriglyceridemia in this urban South Indian population.

Adult↗
PubMed2006

Characterization of hypertriglyceridemia-induced erectile dysfunction.

OBJECTIVES: To characterize the effects of experimental hypertriglyceridemia on erectile function. METHODS: The daily water intake of 40 sexually mature male rats (groups II to V) was supplemented for 12 weeks with 10% fructose solution to induce hypertriglyceridemia. In addition, animals from three groups (III, IV, and V) were given through daily oral gavage metformin (group III), fenofibrate (group IV), and fish oil (group V) to estimate their therapeutic effects on fructose-induced metabolic alterations. Another group (I) of 10 rats served as controls. At 12 weeks, changes in sexual behavior and cavernous pressure response to nerve stimulation were correlated with serum triglyceride levels and response to preventive measures. RESULTS: After administration of 10% fructose, triglyceride levels increased fourfold to 1.79 +/- 0.31 mmol/L (mean +/- standard deviation) (group II). Coinciding with this elevation was a significant impairment of the copulatory pattern, with prolongation of mount (3.70 +/- 3.44 minutes), intromission (7.09 +/- 4.49 minutes), and ejaculatory latencies and reduced intracavernous pressure (27.56 +/- 2.04 mm Hg) response to nerve electrical stimulation. Whereas similar significant impairment was seen in group III, the other two groups (IV and V) showed beneficial effects of triglyceride reduction on these parameters. CONCLUSIONS: Our results provide the first evidence for an impact of triglycerides on erectile function. This detrimental effect is likely to be due to functional vascular and neuronal deficits related to hypertriglyceridemia.

Animals↗
PubMed1997

Usefulness of hypertriglyceridemia in predicting myocardial infarction late after coronary artery bypass operation.

We prospectively followed 446 consecutive patients who had coronary bypass operations 15 years earlier. Serum levels of cholesterol and triglycerides were measured before and 5 years after bypass, and we established the relation between these lipid levels and the incidence of myocardial infarction (MI) and cardiac mortality during 15 years of follow-up. Follow-up was complete in 99.8% of the patients and averaged 15.4 years for the survivors. Multivariate Cox proportional-hazards analysis revealed that patients with preoperative hypertriglyceridemia (> or = 2.0 mmol/L [176 mg/dl]) had a 2.1 times increased risk for MI during follow-up (p = 0.04). Hypertriglyceridemic patients 5 years after surgery had a 2.2 times increased risk for MI during the subsequent follow-up period, although this difference was not statistically significant (p = 0.09). The only significant risk factor for MI 5 years after surgery was smoking. Hypercholesterolemia (> or = 6.5 mmol/L [254 mg/dl]) both before and 5 years after surgery was not a risk factor for MI during follow-up. Cardiac mortality was not significantly related to either hypercholesterolemia or hypertriglyceridemia. Independent predictors for cardiac mortality were poor left ventricular function, diabetes mellitus, incomplete revascularization, and the use of sequential bypass grafts. These data provide evidence that hypertriglyceridemia, both before and 5 years after surgery, have predictive value for the incidence of MI during long-term follow-up after venous coronary bypass surgery.

Adult↗
PubMed1999

Chronic selective hypertriglyceridemia impairs endothelium-dependent vasodilatation in rats.

OBJECTIVE/METHODS: In order to investigate whether selective hypertriglyceridemia impairs endothelium-dependent vasodilatation in the rat hindlimb, rats were selectively bred to establish two strains, one with a pronounced hypertriglyceridemia (HT) and the other with normal plasma levels of triglycerides (LT). RESULTS: Carotid arteries and aortae removed from 3, 6, 9 and 12 month old LT- and HT-rats exhibited a normal morphology. However, marked morphological differences were observed between vessels from 18-20 month old HT- and LT-rats. The endothelium-dependent vasodilator acetylcholine (2 to 50 micrograms/kg), administered into the iliac artery, elicited a concentration-dependent increase in hindlimb blood flow which was not different in 3, 6 and 9 month old LT- or HT-rats but was impaired in 12 and 18-20 month old HT-rats. In contrast the endothelium-independent vasodilator sodium nitroprusside enhanced blood flow in both strains to a similar extent. Neither administration of the nitric oxide (NO) synthase (NOS) substrate, L-arginine, nor the NOS inhibitor NGnitro-L-arginine, affected the responsiveness to endothelium-dependent vasodilators in 12 month old HT-rats. These attenuated responses could not be attributed to a decrease in endothelial NOS expression as Western blot analysis revealed identical levels of this enzyme in the aortae and carotid arteries from LT- and HT-rats. Determination of superoxide anion (O2-) formation however, demonstrated a markedly elevated production of O2- in aortae from HT-rats. CONCLUSION: We conclude that chronic selective hypertriglyceridemia, an independent risk factor in the development and progression of atherosclerosis, leads to an endothelial dysfunction which is associated with an increased vascular O2- production and a subsequent decrease in bioavailable NO.

Acetylcholine↗
PubMed2001

Apolipoprotein E1 Baden (Arg(180)-->Cys). A new apolipoprotein E variant associated with hypertriglyceridemia.

Apolipoprotein (apo) E mediates the removal of chylomicron and very low density lipoprotein remnants from plasma. It is polymorphic in sequence and the products of the three common alleles (epsilon 2, epsilon 3, epsilon 4) differ from one another in their binding to lipoprotein receptors. ApoE2 is defective in binding and homozygosity for apoE2 is associated with type III hyperlipoproteinemia (HLP). Other rare isoforms of apoE have been found to be associated either with dominant type III HLP or with the development of hypertriglyceridemia. We identified a 42 year-old hypertriglyceridemic woman with an apoE phenotype 3/1. Restriction isotyping using AflIII/HaeII resulted in an apparent apoE genotype 3/2, suggesting that the mutation occurred in an epsilon 2 allele. DNA sequence analysis revealed a C-->T point mutation at the first position of the codon for amino acid residue 180 of the mature apoE. This predicted a change Arg(180)-->Cys. The mutation altered a recognition site for the endonuclease HaeII, which allowed us rapidly to screen for this mutation. In relatives of the proband, apoE1 Baden was consistently associated with hypertriglyceridemia. Similar to other apoE variants linked to hypertriglyceridemia, the Arg(180)-->Cys mutation is located within the lipid binding domain of apoE. We therefore suggest that apoE1 Baden may cause hypertrigylceridemia, possibly by inhibiting the hydrolysis of triglycerides associated with very low density lipoproteins.

Adult↗
PubMed2001

Severe hypertriglyceridemia with plasma inhibitory factor(s) on lipoprotein lipase activity in a patient with a common Ser(447)-Ter LPL mutation.

Severe hypertriglyceridemia is a major risk for acute pancreatitis. So far, several mutations on the lipoprotein lipase (LPL) gene causing type I hyperlipidemia have been identified. However, the common mutation Ser(447)-Ter has been recently proposed to have a lowering effect on serum triglyceride concentrations in the general population. In this study, we analyzed blood from a patient suffering from severe hypertriglyceridemia and pancreatitis with the mutation on the lipoprotein lipase gene, Ser(447)-Ter. The patient's plasma showed inhibitory effects on the LPL activities from normal subjects. The bottom fraction separated by ultracentrifugation revealed enhanced effects as an inhibitory factor. The inhibitory effect observed in the bottom fraction was dose-dependent, stable at treatment of 65 degrees C for 30 min, and decreased significantly after being dialyzed using membranes with a cut-off molecular weight of 3500 or 6000 Da. The inhibitory effect was significantly higher when the post-heparin plasma was used from the patient or a subject with the same LPL mutation as an LPL source, compared to that from normal subjects. These results suggest that the patient has inhibitory factors in his plasma. Such inhibitory factors might cause severe hypertriglyceridemia in a case with the common mutation, which has been proposed to show the lowing effect on serum triglyceride concentrations in the general population.

Acute Disease↗
PubMed2002

A family-based study of hyperinsulinemia and hypertriglyceridemia in heterozygous lipoprotein lipase deficiency.

CASE REPORT: A case is presented of predisposing a patient's father with obligate heterozygous lipoprotein lipase (LPL) deficiency to mild hypertriglyceridemia in Japanese I-family members (n=8) with patient DI, who was a compound heterozygote for a novel missense mutation of G154V (GG(716)C-->GTC/Gly(154) Val) in exon 5 and a novel splice mutation (Int8/5'-dss/t(+2)c; a T-to-C transition in the invariant GT at position +2 of the 5' donor splice site (dss)) in intron 8 of the LPL gene. RESULTS: The patient's father and paternal grandmother were heterozygotes for the Int8/5'-dss/t(+2)c allele, while the patient's mother and maternal grandmother were heterozygotes for the G154V allele. These four heterozygous carriers with one defective LPL allele showed 45-57% of the mean LPL activity and mass in the post-heparin plasma (PHP) observed in normal individuals. Among the four heterozygous carriers, the patient's father, who was <40 years old, nonobese and hyperinsulinemia, manifested mild hypertriglyceridemia (type IV hyperlipoproteinemia). The remaining three healthy heterozygous carriers (two were >40 years old and the other was <40 years old) were all normolipidemic state. CONCLUSION: In this family, hyperinsulinemia as a marker of insulin resistance may be a strong determinant of hypertriglyceridemia in the carrier with heterozygous LPL deficiency.

Adult↗
PubMed2001

Effect of raloxifene on serum triglycerides in postmenopausal women: influence of predisposing factors for hypertriglyceridemia.

BACKGROUND: Estrogen increases serum triglyceride (TG) levels and induces hypertriglyceridemia in susceptible women. The effect of raloxifene (RLX), a selective estrogen-receptor modulator, on serum TG has not been studied in detail. OBJECTIVE: The purpose of this study was to examine the effect of RLX on serum TG levels in postmenopausal women with and without osteoporosis, including those with predisposing factors for hypertriglyceridemia. METHODS: Fasting serum TG levels were assessed over 36 months in 2738 osteoporotic postmenopausal women (mean age, 67 years) assigned to placebo or RLX (60 or 120 mg/d) in an osteoporosis treatment trial and over 24 months in 1318 postmenopausal women without osteoporosis (mean age, 54 years) assigned to placebo or RLX (60 or 150 mg/d) in 3 osteoporosis prevention trials. RESULTS: In the osteoporosis treatment trial, the median serum TG concentration decreased in all groups, but significantly more in the placebo group (placebo, -3.4%; RLX 60 mg/d, -1.4%; RLX 120 mg/d, -1.3%; P = 0.002). In the osteoporosis prevention trials, the percentage change in median serum TG concentration was not significantly different among treatments (P = 0.22). Among women with varying degrees of hypertriglyceridemia at baseline (>2.82, >3.39, and >4.51 mmol/L), the median serum TG level at the end of the study decreased from baseline in all groups, with no significant differences among treatments (P > or = 0.13). The effect of RLX on serum TG level was not influenced by age, smoking status, use of alcohol, or presence of diabetes (P > or = 0.10 for all interactions). Among women in the highest tertile of body mass index (>26.4 kg/m2), RLX increased serum TG levels significantly compared with placebo (placebo, -3%; RLX 60 mg/d, 6%: RLX 120 mg/d, 4%; P < 0.05); the absolute increase from baseline with RLX in this subgroup was 0.05 mmol/L (4.4 mg/dL). CONCLUSIONS: RLX did not increase serum TG in postmenopausal women overall or among women with elevated TG levels or evidence of diabetes at baseline. TG levels increased slightly but statistically significantly in women in the upper tertile of body mass index who were treated with RLX.

Adult↗
PubMed2003

Postprandial hypertriglyceridemia-induced endothelial dysfunction in healthy subjects is independent of lipid oxidation.

BACKGROUND: To analyze the effects of postprandial hypertriglyceridemia with or without antioxidant supplementation-on endothelial function as related to lipid oxidation in healthy young subjects. METHODS AND RESULTS: Ten healthy male subjects (mean age: 26 years) were examined three times in fasting state (10 hours) following a high-fat meal, a low-fat meal, or a high-fat meal with additional antioxidant vitamin E (800 IU), respectively. Serum triglycerides significantly increased 2 and 4 hours after eating the high-fat meal with or without additional vitamin E. Endothelium-dependent, flow-mediated brachial artery vasodilations (FMD; percentage change in diameter) changed from 13.3+/-1.1% to 6.6+/-1.1% (p<0.05), 7.1+/-0.6% (p<0.05), or 13.2+/-0.8% at 2, 4, or 6 hours after eating a high-fat meal. However, there were no changes of FMD observed following either a low-fat meal or a high-fat meal with additional vitamin E. The flow-dependent vasodilation inversely correlated to postprandial hypertriglyceridemia (r=-0.54, p<0.05). Serum malondialdehydes (MDA; lipid oxidation products) did not significantly change following ingestion of any of the 3 types of meal. CONCLUSIONS: This study suggests that postprandial hypertriglyceridemia-induced endothelial dysfunction is not associated with lipid oxidation and that the protective effects of vitamin E on endothelial function may be due to some alternative, as of yet unknown, mechanism.

Adult↗
PubMed1997

Acipimox attenuates hypertriglyceridemia in dyslipidemic noninsulin dependent diabetes mellitus patients without perturbation of insulin sensitivity and glycemic control.

Hyperlipidemia, hypertriglyceridemia in particular, is a common feature in patients with noninsulin dependent diabetes mellitus (NIDDM) and may associate with insulin insensitivity. Acipimox, being widely prescribed for treating hypertriglyceridemia, is also used in NIDDM patients for their dyslipidemia. In the present study, we evaluated the effect of acipimox in Chinese NIDDM patients with hypertriglyceridemia. A total of 16 patients enrolled in a double-blind, randomized, placebo-controlled and two-period crossover study. After an 8 week run-in period, patients were randomly assigned into two groups receiving either acipimox (250 mg, twice daily) or placebo treatment. A total of 12 weeks later, these two groups switched their treatment for an additional 12 weeks. Blood samples were collected at the end of the run-in period and then at 4-week intervals in the whole study for lipid profile. A modified insulin suppression test was performed at the ends of the run-in period, 12-week and 24-week treatment to assess changes in insulin sensitivity. Our results showed that acipimox significantly lowered serum total triglyceride while compared to those by placebo. However, no difference was observed in serum non-esterified fatty acid, low-density lipoprotein cholesterol, total cholesterol (TC), high density lipoprotein-cholesterol (HDL-C) and HDL-C/ TC ratio between the two groups. Furthermore, glycemic indices and insulin sensitivity were similar during the base-line, placebo or acipimox periods. Taken together, our data suggest that acipimox significantly lowered TG without perturbation of insulin sensitivity in hypertriglyceridemic NIDDM patients.

Adult↗
PubMed2006

Hypertriglyceridemia-associated acute pancreatitis with chylous ascites in pregnancy.

Both cholesterol and triglyceride levels in serum increase progressively during pregnancy. Hypertriglyceridemia is a well-recognized cause of acute pancreatitis, while pancreatitis-associated chylous ascites has rarely been reported. We report a 28-year-old female with coexistence of hypertriglyceridemia, acute pancreatitis, and chylous ascites during pregnancy. After emergency cesarean section, she was treated with nil per os, intravenous hydration, antibiotics, and analgesics as required. Due to the development of positive peritonitis 5 days later, an exploratory laparotomy was performed. Surgical interventions included pancreatic necrosectomy, right hemicolectomy and ileostomy, cholecystostomy, gastrostomy, and feeding jejunostomy. Postoperative treatment included antibiotics, total parenteral nutrition, and then low-fat diet with medium-chain triglyceride supplementation. She was discharged on the 43rd day after surgery and was free of symptoms during 6 months of follow-up. Ileocolostomy was performed 6 months after discharge. Fasting lipid profile should be regularly monitored during pregnancy due to the association of hypertriglyceridemia with development of acute pancreatitis in the mother.

Acute Disease↗