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PubMed2006

Isolated hypertriglyceridemia: an insulin-resistant state with or without low HDL cholesterol.

There are numerous reports on insulin resistance in subjects with hypertriglyceridemia but most of the studies involved obese or diabetic subjects. We were interested to study such events but in a population free from other confounders influencing insulin sensitivity (i.e., obesity, glucose intolerance and hypertension). From the population of a cross-sectional study we obtained 12 subjects with isolated hypertriglyceridemia and compared their insulin sensitivity with that of normolipidemic subjects in that study. Insulin sensitivity and secretory status were computed using homeostasis model assessment (HOMA) software. The insulin sensitivity of hypertriglyceridemic subjects was found to be lower than in normolipidemic subjects. For the hypertriglyceridemic subjects, insulin sensitivity (HOMA%S) was 60.07% (values adjusted for age, BMI, waist circumference, and cholesterol levels), which was substantially lower than that of normolipidemic subjects (150.03%; p<0.001). The insulin secretory status (HOMA%B) of the two groups was 248.17% and 124.63%, respectively, and significantly different (p<0.001). Relative insulin resistance, HOMA-IR, of the two groups was 4.90 and 1.54, respectively. We therefore concluded that in comparison with normolipidemic subjects, the insulin sensitivity of otherwise healthy non-obese hypertriglyceridemic subjects was lower, and that B cells had to work harder to compensate for the lowered insulin sensitivity.

Adult↗
PubMed1995

Hypertriglyceridemia caused by the autoantibody to lipases for plasma lipoproteins: a case report.

A 41-year-old female patient with muscle dystrophy, hepatosplenomegaly and tendinous xanthoma showed mild hypertriglyceridemia. The lipoprotein profile in blood showed increases in triglycerides in VLDL and LDL, and a marked decrease of cholesterol in HDL. Chylomicronemia was found, but was not severe. Both lipoprotein lipase and hepatic triglyceride lipase activities were reduced to a level that was only a few percent of the control. Immunoblotting study revealed that the IgG autoantibody in her serum was apparently reactable with hepatic triglyceride lipase and weakly with lipoprotein lipase. Hypertriglyceridemia in this patient is suggested to be due to the autoantibody to these lipases.

Adult↗
PubMed1995

Hypertriglyceridemia and fatty liver: clinical diagnosis of fatty liver and lipoprotein profiles in hypertriglyceridemic patients with fatty liver.

Fatty liver has prevailed by 14% in the healthy population of this country. The factors contributing genesis of fatty liver were gender (male), obesity, high alcohol consumption, glucose intolerance and hypertriglyceridemia. And hypertriglyceridemia seems to be the common underlying factor to all other causes. The mechanism for accumulation of triglycerides in the liver can be explained at least by increased HTGL activities and elevated apo A-II levels, a postulated co-factor of HTGL. An hypertriglyceridemic patients with fatty liver had the insulin resistance.

Adult↗
PubMedDate not supplied

Hypertriglyceridemia may cause a subclinical peripheral neuropathy.

Recently few patients with a painful neuropathy, attributed to extremely high triglyceride levels, were reported. In a prospective study, we evaluated 16 patients with marked hypertriglyceridemia without other causes of neuropathy, using nerve conduction and autonomic function tests. Six subjects (37%) showed mild signs of an asymptomatic motor and/or sensory and/or autonomic axonal polyneuropathy. The study demonstrates, that hypertriglyceridemia may be associated with a mild axonal polyneuropathy, usually subclinical, in significantly more patients than previously considered.

Action Potentials↗
PubMed2001

Tamoxifen-induced hypertriglyceridemia in association with diabetes mellitus.

Several pharmacological agents are associated with hyperlipidemia. Tamoxifen is an example of a drug-induced increase of serum triglyceride levels. However, there are only scarce reports on how inborn errors in lipid metabolism as well as secondary dyslipidemias, including diabetes mellitus, influence the hypertriglyceridemic effect of tamoxifen. Herein, we describe a case of a breast cancer patient receiving tamoxifen who presented with remarkable hypertriglyceridemia in the context of diabetes mellitus. We also provide a brief review of the relevant literature and discuss the mechanisms underlying the pathogenesis of hypertriglyceridemia related to tamoxifen.

Antineoplastic Agents, Hormonal↗
PubMed2001

Lipoprotein lipase gene polymorphism and lipid profile in patients with hypertriglyceridemia.

AIM: To assess lipid profile and the genotype distribution of lipoprotein lipase gene polymorphism at Pvu II polymorphic site within the intron between exons 6 and 7 in patients with hypertriglyceridemia. METHODS: Pvu II polymorphism was determined in 116 hypertriglyceridemic patients and 50 normolipidemic controls from Zagreb, Croatia. DNA was extracted from peripheral blood mononuclear cells. Polymerase chain reaction was used for amplification of 6th intron, which was then restricted with Pvu II-restriction endonuclease. Serum lipid and lipoprotein fractions were determined by standard enzymatic methods. Cholesterol concentrations in HDL subfractions, HDL2 and HDL3, were determined after precipitation with polyethyleneglycol. Apolipoproteins (apo) A-I and B were determined by immunonephelometry. RESULTS: Triglycerides showed a positive correlation with total cholesterol (r=0.222, 95% CI=0.041-0.389, p=0.017) and inverse correlation with HDL-cholesterol (r= -0.278, 95% CI= -0.449 to -0.088, p=0.005), especially with HDL3-cholesterol (r= -0.333, 95% CI= -0.497 to -0.147, p=0.001). The respective frequencies for genotypes /, +/, and +/+ were 22, 58, and 36 in the patient group, and 17, 17, and 16 in the control group. Serum triglycerides in the patient group, expressed as median in mmol/L, were 3.30 (range, 2.60-10.90), 3.60 (range, 2.50-21.50), and 3.99 (range, 2.50-15.56), respectively. Serum concentration of triglycerides differed significantly between the +/+ and / genotype (p=0.043). CONCLUSION: There is an association between genetic variation at the locus for lipoprotein lipase and high serum triglyceride levels. This might prove useful in the detection of individuals susceptible to the development of hypertriglyceridemia, as well as a marker in the analysis of this genetic defect in patient families.

Aged↗
PubMed2001

Lipoprotein lipase and apoE polymorphisms: relationship to hypertriglyceridemia during pregnancy.

Pregnancy is associated with increases in plasma total cholesterol (TC) and triglycerides (TG). Individuals with decreased LPL activity have a mild form of hypertriglyceridemia. Variations in the apolipoprotein E (apoE) gene have been associated with increases in plasma TG in addition to differences in plasma TC, LDL cholesterol (LDL-C), and HDL cholesterol (HDL-C). Because of the overproduction of TG-rich VLDL, normal pregnancy challenges the lipolytic capacity of LPL and the clearance of remnants particles. During pregnancy, LPL and apoE polymorphisms may contribute to hypertriglyceridemia. This study investigated the impact of three LPL polymorphisms and the apoE genotypes on lipid levels during pregnancy. Fasting plasma lipids were measured and analyses of the LPL and apoE polymorphisms were performed in 250 women in the third trimester of pregnancy. S447X carriers had lower TG (P = 0.003), and N291S carriers had lower HDL-C (P < 0.02) and higher fractional esterification rate of HDL (FER(HDL)) (P = 0.007), a measure of HDL particle size, than the noncarriers. The E2 allele was associated with lower TC, LDL-C, and FER(HDL) (P < 0.05) compared to the E3/E3 genotype. These findings support that LPL and apoE polymorphisms play an important role in lipid metabolism in pregnancy. The relationship of these polymorphisms to risk of coronary heart disease in women requires further study.

Adult↗
PubMed2001

Noninvolvement of hypertriglyceridemia and hyperleptinemia in blood pressure increases induced by dietary lard in rats.

We investigated whether hypertriglyceridemia and hyperleptinemia are involved in the development of increases in blood pressure induced by dietary lard. Rats received either chow alone or chow in which 50% of the energy content was from substituted lard. Each group was divided into two groups according to whether the diet included bezafibrate or not. In another series of experiments, rats were fed either chow alone or chow in which 50% of the energy content was from substituted lard, safflower oil, or sucrose. Systolic blood pressure (SBP) was measured every week during each 7-week feeding period. A steady-state plasma glucose method was used to determine insulin sensitivity after lard substitution with or without bezafibrate. After the 7-week feeding period, the plasma levels of glucose, immunoreactive insulin, triglyceride and leptin were measured. In rats fed with a high lard diet, SBP, plasma levels of immunoreactive insulin, triglyceride, leptin and steady-state plasma glucose concentrations significantly increased, compared with levels of these substances in controls. Bezafibrate treatment completely reversed these effects. In rats fed with a high safflower oil or a high sucrose diet, no significant change was seen in SBP and plasma immunoreactive insulin levels. However, the plasma triglyceride levels were increased by dietary lard or sucrose. Moreover, the plasma leptin level was also increased by dietary lard and safflower oil. Neither dietary hypertriglyceridemia nor hyperleptinemia were involved in the development of increases in blood pressure induced by dietary lard.

Adipose Tissue↗
PubMed2002

[Hypertriglyceridemia as a cause of atherosclerosis].

Many observational studies have investigated whether elevated levels of serum triglyceride are associated with increased risk of coronary heart disease. The results of these studies have been inconsistent. Recently, however, evidences are accumulating to suggest that hypertriglyceridemia is an independent risk factor for coronary heart disease. Elevated levels of serum triglyceride are associated with four pathogenic conditions which are considered to accelerate atherosclerosis. These are decreased serum HDL cholesterol levels, increased remnant lipoproteins, increased small dense LDLs, and increased thrombogenic conditions. The results of primary and secondary prevention studies support the concept that some types of hypertriglyceridemia will be the cause of atherosclerosis.

Coronary Artery Disease↗
PubMed1992

Diabetes mellitus, hypertriglyceridemia, and heart disease risk in women.

Coronary heart disease is the most common cause of death in men and women in developed countries. Three primary risk factors--high serum cholesterol concentration, hypertension, and cigarette smoking--are known to increase the risk in both men and women more or less equally, although the latter two risk factors are a somewhat greater risk to men. This paper reviews two additional risk factors whose impact may be greater in women: diabetes and hypertriglyceridemia. Understanding how diabetes and hypertriglyceridemia act differently in women may explain some of the sex differences in the risk of heart disease.

Adult↗
PubMed1992

[Composition and distribution of lipid and apolipoprotein in plasma lipoproteins of endogenous hypertriglyceridemia].

Lipids and apolipoproteins in plasma VLDL, IDL, LDL, HDL2 and HDL3 isolated by one-step density gradient ultracentrifugation from 7 subjects with endogenous hypertriglyceridemia (HTG) and 4 normalipemics were determined. HTG VLDL was enriched with cholesterol, and its triglyceride (TG), phospholipid (PL) and apo CII, CIII contents (mg/100 mg protein) were significantly higher than those in normal VLDL. ApoE content in HTG VLDL was prone to increasing, and apoB100 content had no apparent difference from that in normal VLDL. Compared with normal HDL2 and HDL3, the contents of total cholesterol (TC), apoAI, CII, and CIII in HTG HDL2, and apoCII, CIII in HTG HDL3 decreased. HTG HDL2 and HDL3 were rich in TG. By analysis of distribution of these lipids and apolipoproteins in various plasma lipoproteins, it was found that the abnormal composition of VLDL and HDL in HTG seemed to be a result of transport of TC, PL, and apoCII, CIII from HDL to VLDL. There was a significantly positive correlation between TC and apoAI, CII, CIII in HDL respectively, which indicated that apoCII and CIII were also associated with the alteration of HDL cholesterol. It is suggested that the elevated plasma VLDL-TG concentration in endogenous hypertriglyceridemia may induce abnormal redistribution of lipid and apolipoprotein among apoCII plasma lipoproteins, and and CIII may play an important role in these changes.

Apolipoprotein C-II↗
PubMed2003

[Effects of plasma very low density lipoprotein, low density lipoprotein and high density lipoprotein on platelet aggregation in endogenous hypertriglyceridemia].

OBJECTIVE: To study whether plasma very low density lipoprotein (VLDL), low density lipoprotein (LDL), high density lipoprotein (HDL) were oxidatively modified in endogenous hypertriglyceridemia (HTG) and to investigate the effects of HTG VLDL, LDL and HDL on platelet aggregation in vitro. METHODS: Blood samples were taken from 21 patients with endogenous triglyceridemia and 21 normal healthy subjects; these two groups were similar in respect to age and sex. Their plasma VLDL, LDL and HDL were isolated by density gradient ultracentrifugation method, and plasma triglycerides (TG), total cholesterol (TC), high density lipoprotein cholesterol (HDLC) were measured by enzyme method. The oxidative modification of LDL, VLDL and HDL was identified by agarose gel relative electrophoretic mobility (REM), absorbance at 234 nm (A234) and fluorescence of thiobarbituric acid reaction substances (TBARS). With the reaction system that consisted of mixed fresh normal plasma, platelet aggregation was induced by adenosine diphosphate (ADP), and the platelet maximal aggregation rate (MAR) was recorded on a 4-channel light aggregometer. RESULTS: The plasma TG, TBARS levels in HTG group were 1.6 and 0.4 times over those of the control group respectively (P < 0.01). The plasma HDLC in HTG group was 32% lower than those of the control group (P < 0.01). REM, A234 and TBARS of VLDL, LDL and HDL in HTG group were significantly higher than those in the control group (P < 0.01). MAR of VLDL, LDL and HDL in HTG group were significantly higher than those in the control group (P < 0.05). The correlation analysis indicated that REM, A234 and TBARS of LDL and HDL in HTG group were positively correlated with MAR (P < 0.01). CONCLUSION: The above data indicated that oxidative modification of plasma VLDL, LDL, HDL did occur in endogenous hypertriglyceridemia in vivo, and VLDL, LDL and HDL enhanced platelet aggregation in vitro.

Aged↗
PubMed1992

[Heparin increases platelet aggregation and inhibits fibrinolysis, especially in primary hypertriglyceridemia and after myocardial infarction].

The authors presented the effect of unfractionated heparin on platelet aggregation and fibrinolysis. The studies have been performed in the control group and with primary hypertriglyceridemia as well as in patients after myocardial infarction. Adrenaline and ADP induced platelet aggregation was examined in plasma rich platelets; fibrinolysis was estimated in euglobulin test. These parameters have been determined before and after (10, 20, 60, 240, 360 min.) intravenous injection of 50 units heparin per kg body weight. We have observed, that heparin increased also platelet aggregation and inhibited fibrinolytic activity in persons with primary hypertriglyceridemia particularly and after myocardial infarction. Correlation was found between investigated parameters and products of heparin lipolytic activity, especially with level of free fatty acids.

Adult↗
PubMed2004

[Tamoxifen-induced severe hypertriglyceridemia--report of 3 cases].

Tamoxifen, an anti-estrogen, has been used for a long time as an adjuvant therapy in cases of estrogen receptor positive breast cancer. Tamoxifen also demonstrates some weak estrogenic activity. A small increase in serum triglycerides is commonly found after tamoxifen administration. Herein we report 3 cases of sever hypertriglyceridemia due to tamoxifen. Case 1 recovered with tamoxifen withdrawal. Tamoxifen was replaced with toremifene in case 2. The level of triglyceride decreased significantly after the change of agent. Tamoxifen was discontinued and anastrozole administration was started in the third patient. Her triglyceride levels improved. Tamoxifen-induced severe hypertriglyceridemia seen in these patients was an effect of its estrogen action. Anastrozole has been used to treat postmenopausal metastatic breast cancer, and several clinical trials in the adjuvant setting are ongoing. Anastrozole does not affect lipid metabolism. Therefore, anstrozole might be safe for patiens with abnormal triglyceride profiles during tamoxifen treatment. We recommended that a periodic serum triglyceride check is needed for patients treated with tamoxifen.

Adult↗
PubMed2005

Hypertriglyceridemia and peripheral neuropathy in neurologically asymptomatic patients.

OBJECTIVES: In this study we intended to find a correlation between hypertriglyceridemia and peripheral neuropathy (PN) in patients with a high triglyceride level and no neurological complaints. METHODS: We recruited 24 patients (21 males and 3 females) having a triglyceride level above 300 mg/dl with no neurologic complaints and none of the other common causes of PN and they underwent an electroneurographic study. The distal motor or sensory latencies (DL), motor or sensory conduction velocities (CV), and motor or sensory amplitudes (AMP) were collected for the peroneal, posterior tibial, sural, median, and ulnar nerves and were considered abnormal if they fall above or below 2 standard deviations of reference values. RESULTS: Our results show that 70.8% of the patients had a significant delay in the DL of the sural nerves and 66.7% had a significant delay in the DL of the median sensory fibers. 54.2% of the patients had a significant decrease in the motor CV in the posterior tibial nerves and 33.3% had a significant decrease in the sensory CV in the sural nerves. The means of the DL and CV were significantly different from reference values in most of the nerves. Amplitudes were the least if at all affected. CONCLUSION: The pattern of the abnormalities affecting more the DL, the sensory nerves and the longer nerves of the lower extremities is suggestive of an early axonal polyneuropathy. We conclude that hypertriglyceridemia affects conduction parameters in peripheral nerves in a trend suggestive of early peripheral neuropathy.

Adult↗
PubMedDate not supplied

[Insulin therapy in patients with severe hypertriglyceridemia].

A series of seven patients with severe hypertriglyceridemia (triglyceride levels > 1000 mg/dL) is presented. Four of the patients were diabetics, two of them were in treatment with anti-retroviral drugs, and three of them presented acute pancreatitis. In all patients intravenous infusion of insulin was initiated at a rate of 0.05-2 U/kg/day. Two and a half days after this treatment, the serum triglyceride level remained lower than 400 mg/dL. There were no complications during the treatment. The long treatment included basal insulin, fibrates and avoidance of pharmacotherapy. Insulin therapy for diabetic and non-diabetic patients with severe hypertriglyceridemia is an effective and safe treatment.

Female↗
PubMed1991

Circulating interferon-alpha levels and hypertriglyceridemia in the acquired immunodeficiency syndrome.

PURPOSE: The metabolic disturbances seen during infection are thought to be due to cytokines, modulators of the immune response. The acquired immunodeficiency syndrome (AIDS) is characterized by a high prevalence of hypertriglyceridemia and at times depletion of body cell mass (wasting). Elevated circulating levels of cytokines have also been reported in AIDS. Therefore, we determined the relationship between circulating cytokine levels and lipid levels and between circulating cytokine levels and wasting in AIDS and human immunodeficiency virus (HIV) infection. PATIENTS AND METHODS: Serum samples from 45 patients with AIDS, 13 subjects with evidence of HIV infection by presence of antibody but without AIDS (HIV positive), and 17 seronegative control subjects who had previously undergone body composition analysis were analyzed for triglyceride, cholesterol, interferon, tumor necrosis factor (TNF), and interleukin-1 levels. Eleven subjects with AIDS or HIV infection had sequential measurements. Interferon was analyzed by bioassay with identification using specific antibodies. TNF and interleukin-1 were assayed by enzyme-linked immunosorbent assay. Lean body mass was assessed by total body potassium. RESULTS: Serum interferon-alpha levels were significantly elevated in patients with AIDS (p less than 0.001 compared to controls), with detectable levels in 84% of AIDS patients. Interferon-alpha was not detectable in serum from controls, while three of 13 HIV-positive subjects had detectable interferon-alpha levels. There was a significant correlation between interferon-alpha levels and serum triglyceride levels in AIDS and HIV-positive patients (R = 0.446, p less than 0.002). There was no relationship between interferon-alpha and serum cholesterol levels (R = -0.039, NS). In contrast only 11% of AIDS patients had detectable circulating TNF levels; the mean value for and the prevalence of detectable serum TNF levels were not significantly different from those of control subjects. Interleukin-1 was not detected in the circulation. There was no correlation between the presence of circulating TNF and serum triglycerides. There was no relationship between circulating interferon-alpha or TNF levels and the presence of wasting as measured by total body potassium. CONCLUSION: These studies suggest that interferon-alpha, which has previously been shown to modulate lipid metabolism in vivo and in vitro, may be responsible for the hypertriglyceridemia found in AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed1991

[Low-dose fish oil in primary hypertriglyceridemia. A randomized placebo-controlled study].

In a double-blind, randomized, placebo-controlled trial, we prospectively investigated the effects of two low doses of fish oil (10.5 and 5.25 g daily) in capsule form in patients with primary hypertriglyceridemia. During a 6 weeks' therapy with 10.5 g fish oil, serum triglycerides decreased by a mean of 38% from 578 +/- 167 to 358 +/- 66 mg/dl (p less than 0.05). With 5.25 g daily, triglyceride levels fell by 20% from 538 +/- 100 to 431 +/- 64 mg/dl (n.s.). With placebo, triglycerides increased by 8% from 835 +/- 176 to 900 +/- 228 mg/dl (n.s.). Total and HLD-cholesterol levels remained uninfluenced in all groups. Serum alkaline phosphatase decreased by a mean of 12% from 86 +/- 7 to 76 +/- 6 units/l in the patients treated with 10.5 g fish oil (p less than 0.01). Platelet aggregation after induction with collagen was slightly, but significantly inhibited in the patients treated with the higher dose of fish oil. Thus, in patients with primary hypertriglyceridemia, fish oil at a daily dose of 10.5, but not at 5.25 g, led to a significant reduction of serum triglyceride levels and to an inhibition of platelet aggregation.

Cholesterol↗