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PubMed1997

Beneficial effect of lovastatin on sphincter of Oddi dyskinesia in hypercholesterolemia and hypertriglyceridemia.

This report describes an impaired sphincter of Oddi relaxation function in relation to hypercholesterolemia and hypertriglyceridemia. As indicated by repetitive amyl nitrite-augmented quantitative hepatobiliary scintgraphy, normalization of serum lipids by means of diet and a 3-month treatment period with 20 mg of lovastatin per day resulted in an improvement of sphincter of Oddi relaxation.

Aged↗
PubMed1998

Association between apolipoprotein A2 MspI polymorphism and hypertriglyceridemia in Koreans.

In view of the possible involvement of apolipoprotein A2 (apoA2) in lipoprotein metabolism, we investigated the association between genetic variation of the APOA2 gene and lipid levels in Korean subjects with hypertriglyceridemia. The MspI rare allele (M-) frequency in hypertriglyceridemic subjects was higher than that in normal control subjects, although the difference was not statistically significant. The M- allele frequency in a healthy population was higher in Koreans (0.27) than in Caucasian groups (0.10-0.21) studied previously. APOA2 polymorphism had an effect on plasma triglyceride levels in hypertriglyceridemic samples (p < 0.005). Triglyceride levels showed a gene dosage effect with the heterozygous genotype having an intermediate level between the two homozygous genotypes. However, the normal control group showed a lack of association with lipid traits. Thus the results suggest that, at least in Koreans, among hypertriglyceridemic subjects there is an association between APOA2 MspI genotypes and triglyceride levels.

Adult↗
PubMed1998

ApoA-I deficiency causes both hypertriglyceridemia and increased atherosclerosis in human apoB transgenic mice.

To study the role of low levels of high density lipoprotein (HDL) and apolipoprotein (apo) A-I in atherosclerosis risk, human apoB transgenic mice (HuBTg) were crossed with apoA-I-deficient (apoA-I-/-) mice. After a high fat challenge, total cholesterol levels increased drastically due to an increase in the non-HDL cholesterol as confirmed by FPLC analysis. In addition, total cholesterol levels in A-I-/- HuBTg mice were lower than the control HuBTg mice, due mainly to decreased HDL-C in A-I-/- HuBTg mice. Analysis of atherosclerosis in the proximal aorta in mice fed a high-fat Western-type diet for 27 weeks revealed a 200% greater lesion area in female apoA-I-/- HuBTg mice (49740+/-9751 microm2) compared to control HuBTg mice (23320+/-4981 microm2, P = 0.03). Lesion size (12380+/-3281 microm2) in male A-I-/- HuBTg mice was also about 200% greater than that in the control HuBTg mice (5849+/-1543 microm2), although not statistically significant. Very few and small lesions were observed in both apoA-I-/- HuBTg and control HuBTg animals fed a chow diet. Therefore, the adverse effect of low HDL on atherosclerosis in mice was only evident when LDL-cholesterol was markedly elevated by high-fat challenge. Male apoA-I-/- HuBTg mice exhibited hypertriglyceridemia when challenged with a high-fat diet. This correlated with both a reduction in lipoprotein lipase activity and a decrease in lipoprotein lipase activation by HDL. In summary, low high density lipoprotein levels due to apolipoprotein A-I deficiency exacerbated the development of atherosclerotic lesions in mice with elevated atherogenic lipoproteins. This mouse model mimics human conditions associated with low HDL levels and provides additional evidence for the anti-atherogenic role of apoA-I.

Animals↗
PubMed1997

[Risk factors for atherosclerosis in offspring of parents with primary hypertriglyceridemia].

High triglycerides and low fibrinolysis activity are considered as a significant predictors for atherosclerosis. The aim of our study was: 1-to compare these risk factors levels in children with positive family history of hypertriglyceridemia (HTG) with children from healthy families and 2-to assess the association between triglyceride and fibrinolysis activity in offspring (y) and parental risk factors (xl ... xn) for atherosclerosis. The study population consisted of: I Group 15 children 7-12 years old and their parents from HTG families and II Group 26 control children 5-12 years old from healthy families. Triglyceride (TG), total cholesterol, cholesterol esters, LDL-Ch, HDL-Ch, HDL2Ch, apolipoprotein AI and BII, fibrinogen plasma level were determined. Plasminogen activator inhibitor (PAI-1) and fibrinolysis activity and (ELT) were determined. We found significant differences in clinical examinations (higher blood pressure and ECG disturbances more frequently), HDL-Ch and HDL2-Ch plasma level was lower in children with positive family history than in control children. Multiple regression analysis of parental variables demonstrated, that children's TG and ELT are strongly determined by parental lipids and haemostasis parameters in children with positive family history of HTG.

Adult↗
PubMed1985

Hypertriglyceridemia: lipoprotein receptors and atherosclerosis.

We have shown first, that apoB mediates the binding of small VLDL Sf 20-60 and IDL, as well as LDL, to the LDL receptor. Second, apoE of an appropriate, accessible conformation is required for the binding of large VLDL to the LDL receptor; HTG-VLDL Sf greater than 60 but not normal VLDL Sf greater than 60 have this apoE population. Third, the same population of apoE that mediates binding of HTG-VLDL Sf greater than 60 to the LDL receptor modulates its binding to the beta-VLDL receptor, but it is not required for the latter interaction. Fourth, a domain of processed apoB or apoB-48 in association with a domain of the inaccessible apoE is required for binding to and uptake by the beta-VLDL receptor. Fifth, our observations suggest that the abnormal catabolism of VLDL that occurs in hypertriglyceridemia may be explained by the abnormal uptake of HTG-VLDL by either the LDL or the beta-VLDL receptor pathway. Finally, we suggest that plasma proteases may route apoB/E-containing lipoproteins to macrophages for disposal, and this results in foam cell formation.

Apolipoproteins B↗
PubMed1980

Relationship of alcoholic hypertriglyceridemia to stage of liver disease and dietary lipid.

To clarify contributions of alcoholic liver injury, dietary fat and acute ethanol intake to alcoholic hypertriglyceridemia, control subjects and alcoholics with fatty liver or cirrhosis were given a high fat meal with and without ethanol. The triglyceridemic response to the meal in patients with fatty liver (551.3 +/- 98.4 mg x hr/dl) was enhanced compared to controls (106.4 +/- 30.9) and characterized by increased fasting and postprandial pre-beta lipoproteins. The cirrhotics' response (262.5 +/- 34.9) was characterized by minimal fasting and postprandial pre-beta lipoproteins and increased postmeal chylomicrons. Ethanol added to the meal enhanced the lipemic response of controls, barely altered the response of patients with fatty liver, and decreased the response of cirrhotics. In an expanded group of alcoholic patients, the percentage of pre-beta lipoproteins determined by electrophoresis reflected the degree of liver injury. Therefore, major determinants of alcoholic triglyceridemia are stage of liver injury and dietary lipid; electrophoretic determination of pre-beta lipoproteins may indicate degree of alcoholic liver damage.

Dietary Fats↗
PubMed1985

Chylomicron-like particles in severe hypertriglyceridemia.

Plasma lipoproteins in a diabetic patient with severe hypertriglyceridemia and turbid, milky plasma were studied and compared with those found in three primary type V hyperlipoproteinemic and in three normal subjects after a fatty meal. All subjects had normal post-heparin lipolytic activity. Lipoprotein electrophoresis of the patient's plasma revealed no chylomicron band, and upon short-time ultracentrifugation the patient's supernatant showed most lipid staining in the pre-beta-lipoprotein region. This supernatant, which in type V hyperlipoproteinemia as well as in normal subjects after a fatty meal, contains a large proportion of apolipoprotein B-48 (of intestinal origin), was found in our patient to contain mostly apolipoprotein B-100 (of liver origin). Upon incubation of normal washed platelets with chylomicrons derived either from type V hyperlipoproteinemic or from normal subjects after a fatty meal, platelet aggregation was decreased, whereas the chylomicron-like particles from the patient increased platelet activity. It is, thus, suggested that the triglyceride-rich, cholesterol-poor lipoproteins are of liver and not of intestinal origin.

Adult↗
PubMed1986

Hypertriglyceridemia and carbohydrate intolerance: interrelations and therapeutic implications.

Atherosclerosis, the most frequent complication of diabetes, could be the result of hyperlipidemia, among other factors. Mounting evidence suggests that reducing the concentration of triglyceride-rich lipoprotein, which influences the production of the possibly atherogenic intermediate density lipoprotein (IDL), might diminish the circulating level of potentially atherogenic lipoproteins. Hypertriglyceridemia, even in the absence of obesity, is associated with insulin resistance. To compensate, pancreatic B cells respond to glucose challenge by producing hyperinsulinemia. If the B cells cannot respond adequately, carbohydrate intolerance ensues. Insulin-treated diabetics may also become hyperinsulinemic because routine insulin injection may not reflect physiologic need and because the insulin is administered peripherally rather than portally. Hyperinsulinemia increases the production of circulating triglyceride. It appears to do this in rats by causing the production of more triglyceride-rich lipoprotein particles rather than by increasing the triglyceride content of each particle. Further, at least in rats, the insulin-induced increase in triglyceride production requires the presence of supplementary dietary fructose. Hyperinsulinemia also increases the activity of adipose tissue lipoprotein lipase and the degradation of very low density lipoprotein (VLDL). The concentration of VLDL depends on balance of production and degradation. Accelerated VLDL degradation leads to an increase in IDL production. Because there is mounting evidence that IDL may be atherogenic, this cycle could accelerate atherogenesis. As such, it is reasonable to postulate that reducing the concentration of triglyceride-rich lipoproteins would break this cycle and would diminish the circulating level of potentially atherogenic lipoproteins.

Arteriosclerosis↗
PubMed1984

C-II anapolipoproteinemia and severe hypertriglyceridemia. Report of a rare case with absence of C-II apolipoprotein isoforms and review of the literature.

A new case of C-II anapolipoproteinemia (complete apolipoprotein C-II deficiency) as the cause of severe hypertriglyceridemia with chylomicronemia (type I lipoprotein phenotype) is described. The patient was a five-year-old boy living in Connecticut. He had splenomegaly, episodic abdominal pain, and bloody stools. Absence of apolipoprotein C-II (and its isoforms C-II1 and C-II2) was documented by a sensitive and specific radioimmunoassay, analytical isoelectric focusing, and in vitro lipolytic assay. Decreased levels of high- and low-density lipoprotein cholesterol and apolipoproteins A-I and A-II and increased levels of plasma triglycerides and apolipoprotein E were found. Post-heparin extra-hepatic lipoprotein lipase activity was within normal range. Incorporation of exogenous purified human apolipoprotein C-II to an incubation mixture of purified lipoprotein lipase and the patient's triglyceride-rich lipoproteins resulted in a dramatic increase in the catabolic rate of the defective triglyceride-rich lipoproteins. The absence of the isoforms of apolipoprotein C-II in this patient indicates that a common gene exists for the C-II isoproteins, which appear to be necessary for normal triglyceride transport in humans. A literature review of 23 reported cases indicates that xanthomas and hepatosplenomegaly are less common in C-II anapolipoproteinemia than in lipoprotein lipase deficiency, the other major etiologic cause of genetic chylomicronemia.

Adolescent↗
PubMed1987

Hypertriglyceridemia: a contraindication to the use of bile acid binding resins.

Bile acid binding resins are indicated for treatment of elevated plasma low-density lipoprotein cholesterol concentrations. In normoglyceridemic patients, plasma concentrations of low-density lipoprotein cholesterol and total cholesterol are closely linked, and for this reason resin treatment of elevated total cholesterol levels in these patients is rational and warranted. Hypertriglyceridemic patients may also have elevated total cholesterol concentrations, and several such patients have been treated with resin. However, resin therapy in these patients is hazardous, since the elevated cholesterol level mainly results from increased plasma concentrations of very-low-density lipoproteins or chylomicrons rather than low-density lipoproteins. In these patients, resin treatment has either no effect or an adverse effect on plasma triglyceride and cholesterol concentrations. The data presented show that fewer than 5 percent of patients whose total plasma triglyceride concentration exceeded 500 mg/dl had elevated low-density lipoprotein cholesterol concentrations, irrespective of total plasma cholesterol concentrations, and no patient whose plasma triglyceride concentration exceeded 1,000 mg/dl had elevated low-density lipoprotein cholesterol levels. Treatment with bile acid binding resins in hypercholesterolemic patients is contraindicated in the presence of hypertriglyceridemia.

Cholesterol↗
PubMed1985

Distribution of lipoprotein lipase and hepatic lipase between plasma and tissues: effect of hypertriglyceridemia.

Lipoprotein lipase and hepatic lipase were measured in rat plasma using specific antisera. Mean values for lipoprotein lipase in adult rats were 1.8-3.6 mU/ml, depending on sex and nutritional state. Values for hepatic lipase were about three times higher. Lipoprotein lipase activity in plasma of newborn rats was 2-4-times higher than in adults. In contrast, hepatic lipase activity was lower in newborn than in adult rats. Following functional hepatectomy there was a progressive increase in lipoprotein lipase activity in plasma, indicating that transport of the enzyme from peripheral tissues to the liver normally takes place. Lipoprotein lipase, but not hepatic lipase, increased in plasma after a fat meal. An even more marked increase, up to 30 mU/ml, was seen after intravenous injection of Intralipid. Plasma lipase activity decreased in parallel with clearing of the injected triacylglycerol. 125I-labeled lipoprotein lipase injected intravenously during the hyperlipemia disappeared somewhat slower from the circulation than in fasted rats, but the uptake was still primarily in the liver. Hyperlipemia, or injection of heparin, led to increased lipoprotein lipase activity in the liver. This was seen even when the animals had been pretreated with cycloheximide to inhibit synthesis of new enzyme protein. These results suggest that during hypertriglyceridemia lipoprotein lipase binds to circulating lipoproteins/lipid droplets which results in increased plasma levels of the enzyme and increased transport to the liver.

Adipose Tissue↗
PubMedDate not supplied

Effects of clofibrate treatment on arginine-induced insulin secretion in endogenous hypertriglyceridemia.

Arginine-induced insulin secretion was evaluated in 13 patients with endogenous hypertriglyceridemia (Fredrickson's Type IV) before and after a two-month period of Clofibrate therapy. Clofibrate reduced triglyceride, cholesterol and FFA levels by 68, 28 and 15% respectively and provoked a significant reduction in arginine-induced insulin secretion without modifying glucose response. Arginine-induced insulin secretion was also studied in 11 normal subjects during saline and intralipid infusions. Glucose and insulin basal values, and glucose and insulin response to arginine infusion were not influenced by Intralipid infusion in these controls. These results confirm that clofibrate reduces insulin secretion thereby contributing to decreased serum triglyceride levels.

Adult↗
PubMed1977

Treatment of hypertriglyceridemia with metformin. Effectiveness and analỳsis of results.

The triglyceride-lowering effect of metformin (N,N-dimethylbiguanide) was tested in a series of patients with stable hypertriglyceridemia (types IIB, III and IV) and with variable degrees of glucose intolerance. Metformin caused a 38% mean decrease of plasma triglycerides. A selective decrease of very low density lipoprotein cholesterol was observed without reciprocal increase of low density lipoproteins. Thirty patients completed the study. Eighteen, who showed a hypotriglyceridemic effect exceeding 30%, were considered as "Responders"; the other 12, where the effect was negligible, were considered as "Non-Responder". Analysis of the pre-and post-treatment glucose tolerance tests of Responders and Non-Responders showed that the former had, on the average, a normal glucose tolerance and insulin secretion, whereas the latter had an impaired glucose tolerance with increased insulin secretion. These parameters were only slightly modified by metformin. The conclusions of this study support the hypothesis that biguanides exert a triglyceride-lowering effect by decreasing lipoprotein secretion, independent of changes in glucose tolerance and/or insulin secretion.

Adult↗
PubMed1986

Role of alcohol, glucose intolerance and obesity in hypertriglyceridemia.

From a primary health screening 631 subjects with serum triglycerides greater than or equal to 4.0 mmol/l were investigated for underlying factors for hypertriglyceridemia. Obesity, glucose intolerance, or suspected high alcohol consumption were associated in 84.5% if the definitions were: Actual/ideal weight (A/I) greater than or equal to 1.2 (obesity), blood glucose in the fasting state or after 120 min of an oral glucose tolerance test (OGTT) greater than or equal to 7.0 mmol/l (glucose intolerance), and gammaglutamyltransferase (GGT) greater than or equal to 1.0 mu kat/l (suspected high alcohol consumption). Ninety-seven percent were associated if also those with positive alcohol anamnesis or with A/I 1.06-1.19, blood glucose after 120 min of an OGTT 6.5-6.99, or GGT 0.8-0.99 were included.

Adult↗
PubMed1988

Effects of acipimox on serum lipids, lipoproteins and lipolytic enzymes in hypertriglyceridemia.

Two separate studies were carried out with acipimox, a new antilipolytic agent with long-lasting activity. First, in a randomized, double-blind, cross-over study a dose of 750 mg/day of acipimox versus placebo was employed for 60 days in 11 patients with type IV hyperlipoproteinemia. Mean plasma triglyceride levels were reduced after acipimox compared to placebo (434 +/- 60 vs 777 +/- 224 mg/dl, P less than 0.01). Serum total cholesterol fell also significantly after acipimox compared to placebo. No significant alteration was observed in the HDL2/HDL3 ratio or in the concentration or composition of the HDL subfractions. Six patients with severe hypertriglyceridemia (2 type IV and 4 type V) and low lipoprotein lipase (LPL) activity took part in a second, open study, lasting for 9 months. Acipimox was given at a dose of 750 mg/day for the first 6 months and 1200 mg/day for the last period. The response of serum total and VLDL triglycerides was inconsistent. HDL cholesterol was significantly raised (+33.3%) after 9 months of treatment due to changes of HDL2 and HDL3 cholesterol, phospholipid and protein concentrations. LPL activity was markedly reduced in adipose tissue at 9 months. No significant changes occurred in postheparin plasma LPL activity. In contrast, hepatic lipase activity showed a reduction of about 25% from 6 months of treatment onwards.

Adult↗
PubMed1975

Adipocyte metabolism in endogenous hypertriglyceridemia.

In order to define specific metabolic abnormalities of adipose tissue metabolism in endogenous hypertriglyceridemia (EH) patients with this condition were compared with normolipidemic controls matched for body fat and fat cell size. In vitro the enlarged fat cells of EH were found to have an increased basal and noradrenaline-stimulated lipolysis in comparison with cells of the same size from normolipidemic controls. The insulin inhibition of noradrenaline-stimulated lipolysis was blunted. Lipoprotein lipase activity in these cells was clearly depressed. Basal triglyceride synthesis from labeled glucose was low in relation to plasma insulin. The reduction of insulin tolerance in vivo suggested that the depression of plasma glycerol and free fatty acid concentration was small in EH, suggesting that the more detailed findings in vitro were of relevance for in vivo conditions. It was suggested that the hyperinsulinemia and decreased glucose tolerance of EH may well be responsible for some of the aberrations of adipocyte metabolism in EH. The decreased responsiveness of lipolysis to insulin and the low lipoprotein lipase activity are, however, findings not typical for enlarged fat cells exposed chronically to insulin and might be characteristic for the fat cells of EH. It seems of importance to further define the factor(s) responsible for these metabolic aberrations, because the abnormalities of the acipocyte metabolism in EH may well offer a possible explanation to the pathogenesis of that condition.

Adipose Tissue↗
PubMed1975

Inhibition of lipoprotein lipase by uremic plasma, a possible cause of hypertriglyceridemia.

In an attempt to define pathogenesis of the previously described impaired triglyceride (TG) removal in uremia, the effects of the addition of normal and uremic plasma on the activity of lipoprotein lipase (LPL) from rat epididymal adipose tissue were examined. Six uremic patients on chronic dialysis and 13 normals were studied. Adding increments of normal and uremic plasma increased the LPL activity to maximal levels when 0.1 ml of plasma was added. Larger aliquots of uremic plasma produced marked inhibition of LPL activity. This inhibition was not observed with the normal plasma. When increasing amounts of uremic plasma were added to an incubation mixture already maximally activated by 0.1 ml of normal plasma, inhibition of LPL was again observed. This inhibition was still present in uremic plasma which had been dialysed against cold saline. The inhibitor was in the lipoprotein-free (d greater than 1.225) fraction of the plasma. The results indicate that uremic plasma has an LPL inhibitor which is probably a protein and may play a role in the pathogenesis of uremic hypertriglyceridemia.

Adipose Tissue↗