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PubMed1975

Lipid metabolism in pregnancy. II. Postheparin lipolytic acitivity and hypertriglyceridemia in the pregnant rat.

Plasma postheparin lipolytic activity (PHLA) has been measured in rat pregnancy to qualitatively assess mechanisms of triglyceride removal from the circulation. This assessment can be made if the larger plasma volume of pregnancy is considered. A supramaximal dose of heparin avoids dilution of the heparin stimulus to PHLA release. Dilution of the released PHLA is corrected using measurements of plasma volume. In addition, no evidence of circulating inhibitors is present, and timing of PHLA appearance is unaffected by pregnancy. Prior studies of postheparin lipolytic activity in human pregnancy have not taken the effect of plasma volume into account and must therefore be reconsidered in light of the present results. We observed a biphasic pattern in PHLA over the course of gestation. Levels were increased in midgestation (day 12), declined to normal by day 19, and fell rapidly to one-half of control by day 21. Assuming a functional role for the triglyceride lipases represented in PHLA, the data suggest the following hypothesis: triglyceride removal is increased or normal for the greater part of gestation and is decreased only at term. If this hypothesis proves true, the hypertriglyceridemia of pregnancy should be due largely to overproduction, with decreased removal contributing only near term.

Adipose Tissue↗
PubMed1977

Effects of short-term clofibrate administration on glucose tolerance and insulin secretion in patients with chemical diabetes or hypertriglyceridemia.

The effect of 1-wk administration of clofibrate on plasma glucose and insulin (IRI) before and during oral glucose tolerance tests (OGTT), as well as on serum lipids, uric acid, growth hormone (GH), and cortisol, were evaluated in 18 nondiabetic patients with hypertriglyceridemia and in 28 patients with chemical diabetes. Fasting plasma glucose, OGTT-glucose, and IRI areas were significantly decreased in both groups of patients, though the effects on glucose metabolism were much more marked in diabetics; 30-min IRI relative increase was unchanged; fasting plasma IRI was reduced in diabetics only. Glucose utilization during insulin tolerance tests carried out in 6 diabetics was significantly enhanced after treatment. Serum triglycerides (TG) and cholesterol (Chol) were significantly decreased in both groups of patients, as were serum free fatty acids and uric acid in diabetics; plasma GH and cortisol did not change. Significant correlations were found in diabetics between the postclofibrate decrease in OGTT-glucose area and the following: pretreatment values of serum Chol (r + 0.42, p less than 0.05) and of 30-min IRI absolute and relative increase (r + 0.44 and + 0.38, respectively, p less than 0.05); postclofibrate decreases in serum TG (r + 0.40, p less than 0.05), in fasting plasma glucose (r + 0.73, p less than 0.001), and in OGTT-IRI area (r + 0.57, p less than 0.01). These data suggest that the improvement in glucose metabolism observed during short-term clofibrate administration may be due to increased insulin sensitivity.

Adolescent↗
PubMed1980

Hyperinsulinemia in fructose-induced hypertriglyceridemia in the rat.

Rats were fed diets containing (as percent of calories) 66% glucose or fructose, 22% casein, and 12% lard, for 1 wk. The effects of these diets on plasma triglyceride, glucose, and insulin concentrations were compared to those of control rats eating regular rat chow. Plasma triglyceride levels increased from a mean (+/- SE) control level of 85 +/- 7 to 142 +/- 9 (p less than 0.001) and 380 +/- 38 (p less than 0.001) mg/dl in dextrose- and fructose-fed rats, respectively. Plasma insulin concentrations demonstrated a similar increase, rising from a mean (+/- SE) control value of 29 +/- 4 microunits/ml to 55 +/- 10 microunits/ml in dextrose-fed rats and 85 +/- 12 microunits/ml in rats eating the fructose diet. Plasma glucose concentrations of the three groups were comparable. These results indicate that fructose-induced hypertriglyceridemia is associated with significant hyperinsulinemia.

Animals↗
PubMed1981

Prevention of age-related hypertriglyceridemia by caloric restriction and exercise training in the rat.

Plasma triglyceride concentrations were determined in three experimental groups of rats as they grew from 1 1/2-12 mo of age. One group was kept sedentary and allowed food ad lib (control), the second group was allowed to eat and exercise in a running wheel ad lib, and the third calorically-restricted in order to maintain weight equal to that of the exercising rats. The exercise-trained and calorically-restricted rats gained less weight than did the control rats, and the age-related rise in plasma triglyceride concentration in control rats was totally abolished in the other two groups. In addition, exercise training and caloric restriction inhibited the increase in plasma insulin concentrations noted to occur with age in the control rats. These data indicate that there are two effective ways to prevent the development of hypertriglyceridemia that occurs with age in otherwise normal rats.

Aging↗
PubMed1981

Inhibition of carbohydrate-induced hypertriglyceridemia by a disaccharidase inhibitor.

The ability of an inhibitor of intestinal alpha-glucosiadase activity to prevent sucrose-induced hypertriglyceridemia was studied in nonobese rats. The results indicated that plasma triglyceride levels were approximately twice as high in untreated rats, and the reduction in plasma triglyceride levels of drug-treated rats was associated with lowered very low density lipoprotein-triglyceride secretion rates and plasma insulin levels. Since these changes could be produced with an amount of glucosidase inhibitor which did not prevent normal rate of weight gain, the possibility arises that this approach may be useful in the treatment of various hypertriglyceridemic states in man. Finally, the observation that the fall in plasma TG concentration was associated with a fall in plasma insulin concentration provides further evidence for the existence of a causal relationship between the two variables.

Acarbose↗
PubMed1984

Chylomicron and very low-density lipoprotein apolipoprotein B metabolism: mechanism of the response to stanozolol in a patient with severe hypertriglyceridemia.

Studies of simultaneous autologous 131I-chylomicron (Sf greater than 400) and 125I-very low density lipoprotein (VLDL) (Sf 20 to 400) apolipoprotein B (apo B) were performed both before (triglyceride level c 1500 mg/dL) and during treatment with stanozolol, a 17 alpha-methyl anabolic androgenic steroid (triglyceride level c 750 mg/dL) in a 74-year-old woman with a past history of recurrent chylomicronemic pancreatitis. Both before and during stanozolol treatment chylomicron apo B disappeared rapidly and directly, little appearing in VLDL and virtually none in intermediate (IDL) or low density lipoproteins (LDL). Multicompartmental analysis indicated that the great majority of chylomicron apo B was removed via an extremely rapid compartment (estimated fractional catabolic rate [FCR], 5.0/h), accounting for 66% before and 88% during stanozolol treatment. The remaining 131I-apo B decayed biphasically, with total Sf greater than 400 residence times of 8.6 hours before and 3.7 hours during stanozolol treatment. Hence, despite a moderately depressed adipose tissue lipoprotein lipase activity, the subject's hypertriglyceridemia did not appear to proceed solely from retarded chylomicron removal, nor was the dramatic decrease in triglyceride in response to stanozolol a function only of the acceleration of such removal. VLDL apo B kinetics were analyzed by a multicompartmental model featuring a rapid, stepwise delipidation chain which proceeds either rapidly to IDL and LDL or to a slowly turning over compartment within VLDL. While VLDL. apo B synthesis remained essentially constant, the major effect of stanozolol was a substantial reduction in the fraction of VLDL apo B diverted to this slowly turning over compartment, which decreased from 5.0% before to 1.2% during treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1985

Effect of exercise training on glucose tolerance, in vivo insulin sensitivity, lipid and lipoprotein concentrations in middle-aged men with mild hypertriglyceridemia.

The effects of 9 weeks of aerobic exercise training with maintenance of stable body weight upon insulin sensitivity and upon glucose, lipid, and lipoprotein concentrations were studied in 10 middle-aged men with mild hypertriglyceridemia. Following training, mean maximum oxygen consumption improved from 33.5 +/- 1.9 to 39.3 +/- 1.9 mL/kg/min (means +/- SEM), (P less than 0.01). Glucose concentrations, both fasting and during oral glucose tolerance testing, remained stable but both fasting insulin concentrations and insulin responses to oral glucose decreased (P less than 0.1 and less than 0.01, respectively). In vivo insulin sensitivity improved 25 +/- 6.1% (P less than 0.01) following training. Exercise training resulted in decreases in fasting serum triglyceride concentrations from 203 +/- 12.6 to 126 +/- 9.0 mg/dL (P less than 0.01), primarily as a result of the reduction in VLDL-triglycerides (P less than 0.01). The magnitude in percentage decrease of VLDL-triglycerides was found to be significantly correlated (r = 0.71, P less than 0.05) with the magnitude in percent increase in max VO2. Serum cholesterol levels declined from 211 +/- 8.9 to 193 +/- 11.9 mg/dL (P less than 0.01), and the ratio of HDL-cholesterol to total cholesterol was improved. This study demonstrates that exercise training at a level of intensity feasible for many middle-aged men has beneficial effects on several factors that have been associated with an increased risk of cardiovascular disease.

Adult↗
PubMed1985

Postprandial distribution of apolipoproteins C-II and C-III in normal subjects and patients with mild hypertriglyceridemia: comparison of meals containing corn oil and medium-chain triglyceride oil.

Five healthy male subjects and five patients with mild hypertriglyceridemia were studied following the administration of 800-kcal liquid meals containing 40% of energy from fat, 40% from carbohydrate, and 20% from protein. On the first day of the study, the fat source was corn oil (long-chain triglyceride), whereas medium-chain triglyceride (MCT) oil was used the second day. Meals were infused into the duodenum using a peristaltic pump. Plasma samples, obtained at hourly intervals for 8 hours, were analyzed for glucose, cholesterol, triglyceride, and apolipoproteins C-II and C-III. The distribution of apoC-II and apoC-III between ultracentrifugally-separated triglyceride-rich lipoproteins (TRL) and high-density lipoproteins (HDL) was also evaluated. The patient group had significantly elevated fasting levels of triglyceride, apoC-II and apoC-III, as well as much greater lipemic response to the meal containing corn oil. In both groups, TRL apoC-II and apoC-III levels were positively correlated with the triglyceride level as it increased following the corn oil meal. These correlations were also observed in the normal subjects when the MCT oil meal was administered, even though changes in plasma triglycerides were minimal. In normal subjects, whole plasma levels of apoC-II and apoC-III decreased significantly following the meal containing corn oil, whereas no net changes occurred following the MCT oil meal. In hypertriglyceridemic subjects, small decreases in plasma apoC-II and apoC-III levels occurred after both meals, although the changes in apoC-II were not statistically significant. The tendency for decreased plasma apoC levels following alimentary lipemia confirms previous reports, and provides further data to support the concept that some apoC is cleared from plasma in association with TRL remnants. The finding that mildly hypertriglyceridemic subjects responded similarly to both conventional fat and MCT may indicate that their rates of remnant clearance were similar following the two meals.

Adult↗
PubMed1986

Endogenous hypertriglyceridemia in a nonobese rat model: plasma lipoproteins and dietary sensitivity.

Sprague-Dawley male rats from the Ivanovas-Sieve colony (IVA-SIV) show higher plasma triglyceride levels compared to the standard Charles River (CR) rats. The triglyceride enrichment occurs primarily in the very-low-density lipoproteins (VLDL), otherwise of a normal % composition, suggesting that the number of particles is increased, rather than their triglyceride (TG) content. High-density lipoprotein (HDL) particles, corresponding to HDL1, appear to be increased in the IVA-SIV rats, as confirmed by rate-zonal ultracentrifugation. The apoprotein composition of isolated lipoproteins (apo B content and isoelectric focusing pattern), does not differ in the two strains. The IVA-SIV rats are remarkably more TG inducible, compared to the standard CR. This can be shown with fructose loading and with a cholesterol-cholic acid diet. The plasma TG increase, after Triton administration, indicative of the VLDL-TG production, is fourfold higher in the IVA-SIV, compared to the CR rats. These findings provide evidence for some similarities between the IVA-SIV rat and human endogenous hypertriglyceridemia, and suggest an increased TG biosynthesis in this model.

Animals↗
PubMed1992

Treatment of primary chylomicronemia due to familial hypertriglyceridemia by omega-3 fatty acids.

Primary familial forms of chylomicronemia can lead to acute life-threatening complications, especially acute pancreatitis. The main aim of therapy is to avoid this so-called chylomicronemia syndrome. In 12 patients with primary chylomicronemia due to familial hypertriglyceridemia, the addition of 2.16 g omega-3 fatty acids over 4 weeks and 4.32 g for 8 weeks resulted in a decrease of serum triglyceride levels from 1,624 +/- 333 to 894 +/- 241 mg/dL after 12 weeks. Cholesterol and triglyceride levels in the chylomicron fraction were reduced concomitantly, the apolipoprotein B-100/B-48 ratio increased, very--low-density lipoprotein (VLDL) triglycerides, VLDL cholesterol, and total cholesterol levels decreased, and low-density lipoprotein (LDL) cholesterol showed a tendency to increase, but this finding did not reach significance. High-density lipoprotein (HDL) cholesterol levels remained unchanged, as did the levels of apolipoproteins A-I, A-II, and E, and lipoprotein(a). Apolipoprotein B levels decreased significantly. The decrease of triglyceride levels to still-elevated concentrations was accompanied by a substantial decrease in plasma and whole-blood viscosity and erythrocyte aggregation, which reached normal values. As in chylomicronemia, complications usually occur at triglyceride levels higher than 1,500 mg/dL; patients can still profit from treatment with omega-3 fatty acids, even though triglyceride levels are still substantially elevated. No clinically relevant side effects occurred, with the exception of the manifestation of diabetes mellitus in one patient, which could be reversed after discontinuation of treatment.

Adult↗
PubMed1993

Hypoalphalipoproteinemia: postprandial response of subjects with preprandial normotriglyceridemia and hypertriglyceridemia to various diets.

The effect of a single oral fat meal (60 g fat/m2 body surface area) enriched in either saturated (SFA) or polyunsaturated ([PUFA] omega-6 or omega-3) fatty acids on postprandial lipoprotein levels was studied in four men with primary hypoalphalipoproteinemia (HP) and in four age- and sex-matched controls. Vitamin A was included in the meal to label intestinally derived triglyceride-rich particles (TRP) with retinyl palmitate (RP). The HP subjects were either mildly hypertriglyceridemic (group A) or normotriglyceridemic (group B) and were phenotyped for post-heparin lipoprotein lipase (LPL) and hepatic triglyceride lipase (HTGL) activities and apolipoprotein (apo) E isoforms. Postprandial total plasma triglyceride (TG), high-density lipoprotein (HDL) cholesterol, and RP and TG concentrations in the chylomicron (Sf > 1,000) and nonchylomicron (Sf > 1,000) fractions were evaluated for 24 hours after the meal. At each time point, HDL composition and size and apolipoprotein distributions were also measured. Following the SFA meal, HP subjects had maximal plasma TG levels at 8 hours (4 hours in controls) with a slow return to baseline levels at 12 to 24 hours (8 to 12 hours for controls). In contrast, after the omega-6 meal plasma TG levels decreased in group A subjects, while group B subjects and controls showed only a small increase. The results after the omega-6 meal were intermediate between the SFA and the omega-3 meal. When compared with group B, subjects in group A showed higher levels of RP-associated TRP, slower clearance rates, 30% to 50% lower fasting LPL activity, and 1.5-fold to twofold higher fasting plasma apo C-III levels. The major preprandial HDL subclass in HP subjects was HDL3, which showed a relative decrease in cholesterol esters (CE) and an increase in TG levels following the SFA meal. After the omega-3 meal, HDL of group A subjects showed a decrease in TG, a reciprocal increase in CE, and either no changes or minor changes in phospholipid (PL) and free-cholesterol (FC) levels. The results show that HP subjects with mild preprandial hypertriglyceridemia respond to a single fat meal differently than subjects with normotriglyceridemia, and that this difference is the result of HP in addition to other factors such as low LPL and HTGL activities, high plasma apo C-III levels, and apo E2 phenotype.

Adult↗
PubMed1986

Increased in vitro platelet aggregation in hypertriglyceridemias.

Platelet aggregation induced by ADP and collagen was monitored in 25 patients with increased serum levels of triglycerides (7 HLPs type IIb, 14 type IV, 4 type V patients) and compared with a group of 10 normolipidaemic control persons. Platelet aggregation was studied simultaneously in platelet rich plasma (PRP) by both turbidometric and impedance technique and also in whole blood (WB) by the impedance method. Whereas platelet aggregation testing by turbidometry was limited by the optical density of the plasma samples in hypertriglyceridemia, the aggregation process could easily be registered in PRP and WB using the impedance method. Threshold aggregatory concentrations with both agonists were significantly lower for all three groups of HLP.

Adenosine Diphosphate↗
PubMed1986

Physical training and plasma intermediate density lipoprotein cholesterol levels in men with hypertriglyceridemia.

Plasma lipoprotein lipid levels including IDL cholesterol concentration, physical fitness parameters, and anthropometric data were measured in 10 men with primary hypertriglyceridemia during a 12 week program of moderate physical training. Reduced pulse rate at submaximal workload and increased work performed on the treadmill indicated that the men had increased their physical fitness during the training period. Body weight (-4.9%) and total skinfold thickness (-15.6%) fell during the training program. A characteristic fall (-23%) in plasma triglyceride levels was seen over the first 8 weeks training. Plasma IDL cholesterol concentration fell (-18%) after 2 weeks training but then rose after 8 weeks to levels which tended to be higher than baseline values. Our data suggest that regular physical exercise is more likely to raise levels of the "proatherogenic" IDL than to lower them in hypertriglyceridemic patients.

Adult↗
PubMed2006

A novel substitution at the translation initiator codon (ATG-->ATC) of the lipoprotein lipase gene is mainly responsible for lipoprotein lipase deficiency in a patient with severe hypertriglyceridemia and recurrent pancreatitis.

A patient with severe hypertriglyceridemia and recurrent pancreatitis was found to have significantly decreased lipoprotein lipase (LPL) activity and normal apolipoprotein C-II concentration in post-heparin plasma. DNA analysis of the LPL gene revealed two mutations, one of which was a novel homozygous G-->C substitution, resulting in the conversion of a translation initiation codon methionine to isoleucine (LPL-1). The second was the previously reported heterozygous substitution of glutamic acid at residue 242 with lysine (LPL-242). In vitro expression of both mutations separately or in combination demonstrated that LPL-1 had approximately 3% protein mass and 2% activity, whereas LPL-242 had undetectable activity but normal mass. The combined mutation LPL-1-242 exhibited similar changes as for LPL-1, with markedly reduced mass, and for LPL-242, with undetectable activity. These results suggest that the homozygous initiator codon mutation rather than the heterozygous LPL-242 alteration was mainly responsible for the patient phenotypes.

Adolescent↗
PubMed1997

Cholesterol metabolism in familial hypertriglyceridemia: effects of obesity versus triglyceride level.

Excessive production of cholesterol has been associated with type IV hyperlipidemia, but the influence of the confounding variable of obesity has been difficult to ascertain. Moreover, cholesterol metabolism has not been systematically evaluated in patients with familial hypertriglyceridemia (FHT), one of the two major subsets of type IV patients. We used isotope dilution to measure cholesterol production, pools, and kinetic constants in 8 hypertriglyceridemic subjects, 6 of whom could be confidently classified as FHT. These were compared with measurements in 9 control subjects matched for sex, age, serum cholesterol, and body mass index (BMI). By t test, hypertriglyceridemic subjects did not differ from controls with respect to cholesterol production, size of readily or slowly miscible pools, or kinetic transfer coefficients. Results were the same whether controls were compared with all hypertriglyceridemic patients or only the 6 with definite FHT. By analysis of covariance (ANCOVA), serum triglyceride level was not a significant determinant of any parameter of cholesterol metabolism. However, BMI was a highly significant determinant of cholesterol production (p = 0.0001) and size of both readily and slowly miscible pools (p = 0.001 to 0.008). These data suggest that FHT per se is not associated with abnormalities of cholesterol metabolism but that an apparent association could result from the confounding variable of obesity.

Adult↗
PubMed1988

Fish oil supplementation results in decreased hypertriglyceridemia in patients with psoriasis undergoing etretinate or acitretin therapy.

Although retinoid derivatives are an effective treatment for severe psoriasis, they result in systemic toxicity, including hyperlipidemia. In an attempt to reverse this retinoid-related hyperlipidemia in patients with psoriasis, a prospective 4-week pilot study of fish oil supplementation was carried out in 25 patients with psoriasis vulgaris receiving etretinate (Ro-10-9359) or acitretin (Ro 10-1670). Daily fish oil supplements containing 3 gm of omega-3 fatty acids (1.8 gm of eicosapentaenoic acid 20:5 omega 3, and 1.2 gm of docosahexaenoic acid 22:6 omega 3) were found to be effective in reducing hypertriglyceridemia, with a significant mean reduction from 215.6 +/- 92.5 to 156.9 +/- 58.5 mg/dl (-27%) when compared with controls (203.6 +/- 46.9 to 204.1 +/- 54.3 mg/dl). High-density lipoprotein cholesterol levels increased from 41.4 +/- 10.5 to 46.1 +/- 10.8 mg/dl (+11%), and the ratio of total cholesterol to high-density lipoprotein cholesterol decreased from 6.6 +/- 1.9 to 5.9 +/- 1.7 (-11%). It is concluded that fish oil supplementation may prove a valuable adjunct to ameliorate the lipid changes secondary to retinoids.

Acitretin↗