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PubMed1997

Thrombophilia in Patients with Hypertriglyceridemia.

Objectives: To investigate a possible relationship between hypertriglyceridemia and the coagulation system, a Cardiovascular Risk Factor Two-township Study was conducted in Taiwan. Design: A case-control study. This longitudinal, prospective study focused on the evolution of cardiovascular disease risk factors with emphasis on haemostatic factors. Subjects: Hypertriglyceridemic subjects (triglyceride <2.26 mmoll+1, n = 327) and age-matched normal controls from a population screening program. Main outcome measures: Haemostatic parameters measured in this study included prothrombin time (PT), activated partial thromboplastin time (aPTT), fibrinogen, factors VIIc and VIIIc, and antithrombin-III and plasminogen levels. Results: In our male hypertriglyceridemic subjects, aPTT was not significantly reduced, while significant elevations of factor VIIIc, factor VIIc, and plasminogen and antithrombin-III levels were noted. In the female hypertriglyceridemic subjects, the elevation of factor VIIc, factor VIIIc, and plasminogen and antithrombin-III levels was highly-significant, whereas aPTT was not significantly reduced. Unexpectedly, the levels of the established coronary risk factor, fibrinogen, did not show a statistically different change. Similar to previous data, our hypertriglyceridemic subjects also presented with hyperinsulinemia, glucose intolerance, upper body obesity, and elevated blood pressure. Conclusions: Despite the fact that in population studies, triglycerides do not consistently appear to be an independent risk factor for coronary heart disease, our data suggest that a pronounced increase in triglycerides warrants aggressive therapy, because this increase may be associated with a hypercoagulable state. This phenomenon contributes another perspective to the study of higher cardiovascular mortality in hypertriglyceridemic subjects.

Journal Article↗

PubMed2000

Platelet function in patients with familial hypertriglyceridemia: evidence that platelet reactivity is modulated by apolipoprotein E content of very-low-density lipoprotein particles.

We evaluated platelet function in patients with familial hypertriglyceridemia (FHTG). Compared with healthy gender-matched controls, platelets from patients showed lower aggregation (P < .01) and thromboxane formation (P < .01) in response to collagen. Very-low-density lipoprotein (VLDL) particles obtained from the patients inhibited collagen-induced aggregation, whereas VLDL particles from controls had opposite effects. The VLDL-induced effect was regulated by its apolipoprotein E (apoE) content. Indeed, apoE-VLDL-rich fractions caused antiaggregative effects, whereas apoE-VLDL-poor fractions produced a strong proaggregative response. Since we have recently demonstrated that VLDL particles may regulate the activity of platelet low-density lipoprotein (LDL) receptor by a phenomenon of downregulation and desensitization, in this study, we have investigated the effect of prolonged exposure to circulating VLDL levels on the activity of platelet LDL receptor by a double-blind controlled study with gemfibrozil (600 mg twice daily) in 18 subjects with FHTG. Platelets from patients exhibited fewer platelet LDL receptors and 125I-LDL binding was saturable at a lower protein concentration. After 6 months, gemfibrozil therapy versus placebo had a marked lipid-lowering effect, significantly decreased triglycerides (61%), VLDL cholesterol (72%), apoB (28%), and apoE (55%), and increased high-density lipoprotein (44%) and apoA-I (18%). Furthermore, gemfibrozil affected the apoprotein composition of VLDL: total protein increased by 28%, the molar ratio of apoE to apoB decreased 64%, and apoE content decreased 55%. However, no differences in phospholipid, triglyceride, or total cholesterol were detected. Moreover, platelet function was markedly altered by gemfibrozil therapy. Collagen-induced aggregation and thromboxane formation were significantly enhanced (P < .01). The initial antiaggregative pattern of VLDL particles was changed to a significant proaggregative effect (P < .01), and the number of LDL binding sites was markedly upregulated (P < .001). Both receptor upregulation and the change in the aggregative effect of VLDL particles were associated with the reduction of apoE content in VLDL particles (P < .05). The overall results indicate that in the regulation of platelet reactivity in hypertriglyceridemic patients, apoE content of VLDL particles and their interaction with the platelet LDL receptor are involved.

Adult↗

PubMed2001

Impaired glucose tolerance without hypertriglyceridemia does not enhance postprandial lipemia.

Postprandial lipemia has been thought to be one of risk factors for coronary heart disease, and enhances in potential patients for atherosclerotic disease. Patients with impaired glucose tolerance (IGT) often show hypertriglyceride, which is caused by enhanced portprandial lipemia. Therefore, postprandial lipemia in patients with IGT and without hypertriglyceridemia has not been cleared. We have examined the levels of plasma triglyceride and chylomicron remnants after a high fat meal load (1250 kcal, 40% fat and 420 mg cholesterol) in 13 normotriglyceridemic subjects with IGT and 10 controls with normal glucose tolerance (NGT). Chylomicron remnants were evaluated as remnant-like particles (RLP) that were not bound to an immunoaffinity gel mixture containing apo A-I and apo B-100 monoclonal antibody. RLP cholesterol levels 4 hours after the fat load were significantly lower in IGT subjects than in NGT subjects. Increase of RLP cholesterol after the fat meal load only significantly correlated with increase of insulin during the first 30 min after a 75 g oral glucose tolerance test, but not fasting lipid, insulinogenic index and HOMA-R (homeostasis model) in all subjects. These results suggest that postprandial response does not enhance in IGT subjects, and may associate with early-phase insulin secretion and without insulin resistance in normotriglyceridemic men with IGT or NGT.

Antibodies, Monoclonal↗

PubMed1988

Lipoprotein-mediated cellular mechanisms for atherogenesis in hypertriglyceridemia.

Structurally and functionally abnormal VLDL exist in hypertriglyceridemic humans. These large abnormal VLDL, in contrast to large normal VLDL, interact with cell surface receptors. One large VLDL particle carries far more total cholesterol than one LDL particle. Receptor-mediated uptake of abnormal VLDL is injurious to endothelial cells and converts macrophages into foam cells in vitro. These observations lead to the hypothesis that if similar phenomena occur in vivo, abnormal VLDL, which have prolonged residence times and increased opportunity to interact with arterial cells, are atherogenic by promoting endothelial injury and initiating foam cell formation. Since premature atherosclerosis is associated with some forms of hypertriglyceridemia and foam cells accumulate in certain hypertriglyceridemic subjects, similar events may indeed occur in vivo.

Arteriosclerosis↗

PubMed1984

Inhibition of carbohydrate-induced hypertriglyceridemia by metformin.

The ability of metformin to prevent carbohydrate-induced hypertriglyceridemia was studied in fructose fed rats. The results indicated that plasma triglycerides were approximately 50% reduced in the drug treated rats and the reduction was associated with lowered very low density lipoprotein-triglyceride secretion rates and plasma insulin levels. Since the drug does not affect the fructose intestinal absorption, it did not prevent normal rate of weight gain. These results provide further evidence for the existence of a causal relationship between plasma TG concentration and plasma insulin concentration; metformin is able to modify both these variables likely affecting primarily the ambient insulin level.

Animals↗

PubMed1982

Plasma apolipoprotein E levels in hypertriglyceridemia.

A specific, precise and sensitive double-antibody radioimmunoassay for the measurement of human apolipoprotein E (apo E) was developed. Antibody specific to apo E was raised in a rabbit. This antibody did not crossreact with plasma low density lipoproteins (d = 1.030-1.063) and apo-proteins such as pao CII, CIII, AI and AII. Mean plasma level with SD of apo E in 29 normalipidemic subjects was 9.5 +/- 1.8 mg/100 ml. Plasma apo E concentrations in 25 hypertriglyceridemic patients with plasma triglyceride concentrations ranging from 169 to 1190/mg/100 ml correlated positively with plasma triglyceride concentrations (r = 0.84, p less than 0.001). Among subjects with hypertriglyceridemia, there was a negative correlation between the apo E per mg triglyceride ratio and plasma triglyceride concentrations (r = 0.49, p less than 0.02). Plasma apo E levels did not show any correlation with plasma cholesterol concentrations. These results indicate that plasma apo E is closely associated with plasma triglyceride levels, which suggests a possible connection of this apoprotein with the metabolism of plasma triglyceride.

Adult↗

PubMed1978

Hypertriglyceridemia associated with deficiency of apolipoprotein C-II.

A 59-year-old man with severe hypertriglyceridemia and no post-heparin lipolytic activity was studied because of a marked fall in plasma triglyceride concentrations after a blood transfusion. An apolipoprotein activator (apolipoprotein C-II) for lipoprotein lipase could not be detected by polyacrylamide-gel electrophoresis of apoproteins, immunodiffusion of the plasma against anti-apolipoprotein CII or activation assays for lipoprotein lipase. Furthermore, the patient's triglyceride-rich lipoproteins would not serve as substrate for lipoprotein lipase. The patient had latent post-heparin lipolytic activity, which appeared after the addition of apolipoprotein CII to the post-heparin plasma. After a transfusion of 1 unit of plasma from a normal subject the patient's plasma triglycerides fell, within one day, from 1000 to 250 mg per deciliter and remained below preinfusion concentrations for six days. We conclude that this patient's hyperlipoproteinemia resulted from a deficiency of apolipoprotein C-II.

Animals↗

PubMed1979

Increase in lipoprotein lipase during clofibrate treatment of hypertriglyceridemia in patients on hemodialysis.

In 11 hypertriglyceridemic patients on hemodialysis, clofibrate (1 to 1.50 g per week) reduced plasma triglyceride (-40 +/- 20%, P less than 0.001), very-low-density-lipoprotein triglyceride (-44 +/- 20%, P less than 0.001) and very-low-density lipoprotein cholesterol (-39 +/- 25%, P less than 0.01), and it increased high-density-lipoprotein cholesterol (82 +/- 106%, P less than 0.005). Low pretreatment lipoprotein-lipase activity in adipose-tissue specimens and postheparin plasma increased to normal with clofibrate, whereas low hepatic triglyceride lipase activity did not change. The reduced very-low-density-lipoprotein triglyceride correlated with the increased lipoprotein-lipase activity in adipose tissue (rs = 0.792, P less than 0.02, n = 8) and postheparin plasma (rs = 0.851, P less than 0.02, n = 8), whereas increased high-density-lipoprotein cholesterol correlated with changes in this activity in adipose tissue (rs = 0.696, P less than 0.06) and post-heparin plasma (rs = 0.679, P less than 0.10). There was no correlation between changes in hepatic triglyceride lipase activity and plasma lipids during treatment. Reduced lipoprotein-lipase activity may cause hypertriglyceridemia and decreased high-density-lipoprotein cholesterol in patients on hemodialysis; clofibrate may correct these abnormalities by increasing lipoprotein-lipase activity to normal.

Adipose Tissue↗

PubMed1985

Reduction of plasma lipids, lipoproteins, and apoproteins by dietary fish oils in patients with hypertriglyceridemia.

Dietary fish oils, which are rich in omega-3 fatty acids, have been reported to reduce plasma lipid levels in normolipidemic subjects. We examined the effects of fish oil in 20 hypertriglyceridemic patients: 10 with Type IIb hyperlipidemia and 10 with Type V. These patients were put on three diets differing primarily in fatty acid composition and fat content. The control diet contained a fatty acid mixture typical of a low-fat therapeutic diet (ratio of polyunsaturated to saturated fat, 1.4), the fish-oil diet contained omega-3 fatty acids, and the vegetable-oil diet was rich in the omega-6 fatty acid, linoleic acid. Each diet was followed for four weeks. In the Type IIb group, the fish-oil diet led to decreases in both plasma cholesterol (-27 per cent) and triglyceride (-64 per cent), as compared with the control diet. Very-low-density lipoproteins (VLDLs) were also reduced markedly. The vegetable-oil diet had much less effect. With fish oil, the Type V group had marked decreases in total cholesterol and triglyceride levels (-45 and -79 per cent, respectively). VLDL levels were dramatically lowered, as were apoprotein E levels. The vegetable-oil diet (unlike the fish-oil diet) produced a rapid and significant rise in plasma triglyceride levels. We conclude that fish oils and fish may be useful components of diets for the treatment of hypertriglyceridemia.

Adult↗

PubMed1986

A crossover trial of high and low sucrose-carbohydrate diets in type II diabetics with hypertriglyceridemia.

Earlier work shows that hyperlipemic type II diabetics tolerate wide ranges of sucrose and carbohydrate intake without effects on glycemic control, but a rise of fasting serum triglycerides sometimes occurs. To address further the issue of individual susceptibility to carbohydrate, the current study was designed to use each patient as his own control when given diets widely varying in sucrose content. After a stabilization period in the hospital on a normal sucrose content diet, each subject was given either a very low sucrose (less than 3 gm/day)-low carbohydrate (38 +/- 2%) diet or a high sucrose (220 gm)-high carbohydrate (63 +/- 3%) diet for 4 weeks. On a separate admission the opposite diet was assessed, again after an initial normal sucrose content diet. No consistent differences occurred in serum glucose levels or in 24-hr urinary glycosuria. High sucrose-carbohydrate intake raised fasting hypertriglyceridemia after 2 weeks but less thereafter. Severe sucrose-carbohydrate restriction did not significantly decrease fasting serum triglycerides; postprandial triglycerides changed in a trend opposite to fasting levels. No differences occurred in fasting serum insulin or serum cholesterol levels, but postprandial insulin levels were higher in high sucrose-carbohydrate diets. A diet with low sucrose and low total carbohydrate appears to offer no improvement in glycemic control over at least 70-fold higher dietary sucrose levels. However, high sucrose and carbohydrate diets increase fasting triglyceride levels in hypertriglyceridemic type II diabetics.

Adult↗

PubMed1986

Recombinant gamma interferon induces hypertriglyceridemia and inhibits post-heparin lipase activity in cancer patients.

Animals suffering from malignancy or chronic infection develop characteristic metabolic abnormalities, including a well-defined hypertriglyceridemic state. These abnormalities have been attributed to release of one or more mediators from activated macrophages. We report that cancer patients receiving RIFN-gamma, a potent macrophage activator, at doses of greater than or equal to 0.25 mg/m2/d i.m. show marked increases in triglyceride but not in cholesterol levels (pretreatment triglyceride level of 180 +/- 190 mg/dl [mean +/- SD] vs. a day-14 level of 370 +/- 242 mg/dl, n = 23, p less than 0.001 by the paired t test). This hypertriglyceridemia was characterized by an increase in very low-density lipoproteins and a decrease in plasma post-heparin lipase activity, consistent with defective triglyceride clearance (mean pretreatment lipase level of 2.1 mumol/ml/h vs. a day-14 level of 1.2 mumol/ml/h, n = 6, p = 0.02 by the paired t test). rIFN-gamma did not directly inhibit lipoprotein lipase enzymatic activity in vitro. Other possible mechanisms of action, such as suppression of lipase by an rIFN-gamma-induced mediator released from activated macrophages, or a direct effect of interferon on lipase biosynthesis, require further investigation. Our observations provide evidence that factors produced by the immune system can regulate lipid metabolism in man.

Adult↗

PubMed1976

Hypertriglyceridemia produced by endotoxin: role of impaired triglyceride disposal mechanisms.

The role of Salmonella typhimurium endotoxin in producing hypertriglyceridemia was investigated in 70 male rhesus monkeys. Dose-response studies were performed with 0.3-9.0 mg of endotoxin/kg injected intravenously; free fatty acids and triglycerides were measured during the subsequent 8 hr. The effect of endotoxin on lipid disposal mechanisms was assessed by both intravenous lipid-loading tests and total plasma lipolytic activity after administration of heparin. The possible interference of endotoxin with lipid-clearing enzymes was also explored. Smaller doses of endotoxin (0.3 and 0.9 mg/kg) produced significant increments in free fatty acids within 2-5 hr of administration, with minimal trilgyceride increments. Larger doses of endotoxin (2.8-9.0 mg/kg) failed to produce significant elevations in free fatty acids but did result in significant triglyceride increases 2-6 hr after administration. Within 4 hr after administration of 7 mg of endotoxin/kg, both tests showed impaired disposal of lipids. However, once lipid-clearing enzymes were activated, endotoxin did not reduce lipolytic activity in vitro. These results support the contention that endotoxin significantly elevates serum triglyceride concentrations and leads to impaired lipid disposal mechanisms by interfering with the activation of lipid-clearing enzymes.

Animals↗

PubMed1975

Association between a low adipose tissue content of polyunsaturated fatty acids and both glucose intolerance and hypertriglyceridemia in apparently healthy men.

The fatty acid spectrum of adipose tissue (AT) lipids has been determined in 43 apparently healthy men with different levels of plasma triglycerides (TG) and different degrees of glucose tolerance (GT). Compared to men with normal plasma TG levels those with hypertriglyceridemia (HTG) had a similar percentage of linoleic acid (18:2) but lower amount of fatty acids, tentatively identified as linolenic (18:3) and arachidonic (20:4) acid. Men with HTG also had lower k-values for the i.v. GT. The content of 18:3 and 20:4 was positively correlated to the k-value of the GT and negatively to plasma TG. These correlations were independent of each other. As usual there was a negative correlation between plasma TG levels and the k-value, which however disappeared after partial correlation analysis when 18:3 was kept constant. Apparently a low content of 18:3 in AT is common both in HTG and glucose intolerance (GI) and might partly explain the often seen association between these two metabolic abnormalities. Since the content of 18:2 was normal it is suggested that the low amount of 18:3 and 20:4 was caused by metabolic rather than dietary factors. The possibility that a low content of 18:3 and 20:4 might play a role in the pathogenesis of GI and HTG is discussed.

Adipose Tissue↗

PubMed2001

Perspectives: A Practical Approach to the Dietary Treatment of Hypertriglyceridemia.

Reducing high plasma triglyceride (TG) levels is an important step in the treatment and prevention of coronary artery disease. The rise in plasma TGs seen after subjects consume low-fat, high-carbohydrate diets for a period of time may be due to the simple form of carbohydrate provided and/or prevention of weight loss in these studies. Ad libitum low-fat, high-carbohydrate intake often results in weight loss and decreases in plasma TGs. Replacing dietary carbohydrate with monounsaturated fat lowers serum TG levels and maintains serum high-density lipoprotein levels but fails to result in weight loss. Low-fat, high-complex carbohydrate intake reduces incidence rates of coronary artery disease. On the basis of the evidence, a low-fat, high-complex carbohydrate diet combined with limited alcohol and sugar intake is recommended for the treatment of hypertriglyceridemia. (c)2001 CHF, Inc.

Journal Article↗

PubMed1976

Neonatal hypertriglyceridemia: a new index of antepartum-intrapartum fetal stress?

The 95th percentile value of cord serum triglyceride concentration in 82 consecutively live born infants was found to be 0.79 mmol/l. This level was arbitrarily used to define neonatal hypertriglyceridemia. A comparison between 78 normotriglyceridemic and 61 hypertriglyceridemic newborn infants showed a significant association between elevated cord serum triglyceride concentration and insufficiency of the placenta, fetal bradycardia, meconium-stained amniotic fluid and one-minute Apgar score less than or equal to 7. A significantly (p less than 0.001) greater number of infants with one or several of these four factors, indicating antepartum and/or intrapartum fetal stress were found to be hypertriglyceridemic at birth. This finding suggests that estimation of cord serum triglyceride which is easy and inexpensive might be of value for a more complete evaluation of the newborn infant, and can serve as a supplement to the Apgar Score system.

Cholesterol↗

PubMedDate not supplied

Asymptomatic massive hypertriglyceridemia in an octogenarian.

OBJECTIVE: To report the case of an 85-year-old man with asymptomatic massive hypertriglyceridemia (MHTG). CLINICAL PRESENTATION AND INTERVENTION: Our case was a non-smoker, healthy 85-year-old Caucasian male, with no excessive alcohol intake and no evidence of an excessive sedentary lifestyle, body mass index = 23.2 kg/m(2), BP = 125/85 mm Hg and plasma triglyceride (TG) >1,000 mg/dl. The MHTG was an incidental finding at the age of 70. He had no cardiovascular disease, xanthomas, xanthelasmas or keratic precipitate. During the last 15 years, his average TG plasma levels showed a significant variability independent of specific diet treatment and fibrate therapy. Liver ultrasound examination excluded hepatomegaly and fatty degeneration. Carotid artery ultrasound showed only intimal thickening in both carotid bifurcations. CONCLUSION: In this patient, MHTG had been silent for many years, with no evidence of coronary heart disease and liver fatty degeneration, both typical complications present in MHTG subjects with low high-density lipoprotein. Hence, this case must be considered as a rarity.

Aged↗

PubMed1991

Effect of dietary treatment on the lipid, lipoprotein and fatty acid compositions in type IV familial hypertriglyceridemia.

The effects of a 2-month dietary treatment (1,625 +/- 177 kcal, 40 +/- 2.3% carbohydrate, 35 +/- 3.7% fat, 25 +/- 2% protein, polyunsaturated/saturated fat ratio = 1.02 +/- 0.06) on the overall composition of serum lipids, lipoproteins and the fatty acid composition of cholesterol esters and phospholipids in very low (VLDL), intermediate (IDL), low (LDL) and high (HDL) density lipoprotein in 5 patients with primary familial hypertriglyceridemia type IV were assessed. The data were compared with those for 9 normolipidemic subjects. Treatment decreased serum triglycerides (-52%) and total cholesterol (-12%) due to decrease in free cholesterol (-30%). It produced a significant decrease in all the constituents of VLDL (-58%), but the VLDL remained significantly higher after treatment than those of control subjects. The diet caused a decrease in triglycerides (-16%, -29% and -33%, respectively), and an increase in cholesterol in IDL, LDL and HDL. The IDL level in the treated patients remained significantly higher than in the controls. The LDL cholesterol/HDL cholesterol ratio was unchanged after treatment. The fatty acid compositions of the patients before treatment and the controls were not significantly different. The diet caused a decrease in palmitoleic and oleic acids in the cholesterol ester fraction and an increase in linoleic acid, but this was significant only in VLDL and HDL. The diet decreased the eicosapentaenoic acid but the drop was only significant in IDL and LDL. There was also a decrease in linolenic acid, only significant in IDL. The diet induced only minor changes in the phospholipid fractions. We concluded that a single nutritional regimen can effectively decrease the serum lipids and normalize the lipoprotein composition of type IV hypertriglyceridemic patients.

Adult↗

PubMed1994

Conjoint high triglycerides and low HDL cholesterol across generations. Analysis of proband hypertriglyceridemia and lipid/lipoprotein disorders in first-degree family members.

BACKGROUND: To discern whether hypertriglyceridemia (hyper-TG, TG > 95th percentile) and hypoalphalipoporteinemia (hypoalpha, high-density lipoprotein [HDL-C] < or = 10th percentile) are jointly transmitted in families, we studied 385 probands with marked elevations in TG or cholesterol levels (TG or cholesterol > 99th percentile in a previous visit) and their 2072-first-degree relatives in the Lipid Research Clinics' Family Study. Repeat TG measurement, with exclusion criterion of TG < or = 95th percentile, resulted in 162 probands with hyper-TG. METHODS AND RESULTS: When the proband demonstrated the conjoint trait (CT; ie, TG > 95th percentile, HDL-C < or = 10th percentile, n = 82), an average of 10.6% of first-degree relatives conjointly expressed hyper-TG and hypoalpha in contrast to only 4.1% of first-degree relatives of a proband who expressed high TG levels with normal HDL-C levels (TG > 95th percentile, HDL-C > 10th percentile, n = 80). Hyper-TG was expressed in 24.2% of first-degree relatives of probands with CT. However, hyper-TG was expressed in only 14.4% of first-degree degree relatives of probands with hyper-TG alone. CT probands and their family members tended to have more reported cardiac events and symptoms (P = .02 and .09, respectively) than those subjects associated with hyper-TG alone. CONCLUSIONS: The differences in HDL-C-TG abnormalities between families related to hyper-TG probands with or without hypoalpha indicate that bottom decile HDL-C is not simply secondary to hyper-TG. A familial interaction is suggested between HDL-C and TG levels consistent with the transmission of hyper-TG and hypoalpha among first-degree relatives. Among subjects and their families with hyper-TG, those who in addition have low HDL-C demonstrate a tendency for more coronary artery disease than do those with normal HDL-C levels.

Adult↗