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PubMed1986

Output of triglyceride from the sebaceous gland and to the skin surface of cattle.

Radiolabelled fatty acids, when injected intradermally into cattle skin, were largely incorporated into the triglyceride and phospholipid fractions of the sebaceous gland lipids. Linoleic acid was incorporated into the triglycerides to a greater extent than oleic or palmitic acids, whereas the phospholipids had a greater affinity for palmitic acid. The peak uptake of linoleic acid into the glandular triglyceride fraction was at about 61 hours compared with 52 hours and three hours for oleic and palmitic acids. Radioactively 14C labelled triglycerides appeared on the skin surface within one day of intradermal injection of 14C linoleic acid. At an ambient temperature of 20 degrees C, a single output-peak occurred at nine days while at 35 degrees C two peaks at four and eight to nine days were observed. From the data an estimate of 6.5 days for the mean storage time of sebum triglycerides in the hair follicle canal at 20 degrees C has been made.

Animals↗
PubMed1986

Conversion of human plasma high density lipoprotein-2 to high density lipoprotein-3. Roles of neutral lipid exchange and triglyceride lipases.

Cholesterol esters accumulating in human plasma high density lipoproteins (HDL) are important in conversion of HDL3 to larger HDL2. We studied whether mechanisms of removal of cholesterol esters from HDL might be important in a reverse direction, i.e. conversion of HDL2 to HDL3. Native HDL2 or HDL3 is incubated with very low density lipoproteins (VLDL) and lipoprotein-poor plasma (d greater than 1.21 g/ml) at 37 degrees C. After incubation, "modified" (M) VLDL, and HDL2 or HDL3 are reisolated by ultracentrifugation. In modified M-HDL2 or M-HDL3, triglyceride becomes the major core lipid as the triglyceride/cholesterol ester weight ratio increases 8-10-fold relative to native HDL. With only small changes in protein/phospholipid ratios in M-HDLs, the large decrease in cholesterol ester/protein ratios suggest net cholesterol ester loss from HDL. Quantitative recovery analyses prove that the cholesterol esters lost from HDL are transferred to M-VLDL, which is now richer in cholesterol ester and poorer in triglyceride. These substantial exchanges of HDL lipids are not associated by significant transfer of HDL apoproteins but are dependent on neutral lipid transfer factors present in human lipoprotein-poor plasma (d greater than 1.21 g/ml). Similar results are obtained when purified core lipid transfer protein replaces d greater than 1.21 g/ml plasma in these incubations. After depletion of cholesterol ester from HDL, most but not all, exchanged triglyceride can be removed by lipolysis with either hepatic or lipoprotein lipase, resulting in a post-lipolysis HDL2 with an increased triglyceride content relative to normal HDL. With successive incubations with VLDL, and core lipid transfer factors, HDL2 loses more than two-thirds of its cholesterol esters. After lipolysis of acquired triglyceride, HDL2 is remodeled, in both composition and flotation parameters, toward HDL3.

Apoproteins↗
PubMed1985

Hydroxyurea interferes negatively with triglyceride measurement by a glycerol oxidase method.

Measured triglyceride concentrations were extremely low (less than 100 mg/L) in the serum of some patients who were receiving hydroxyurea for myeloproliferative diseases. The assay being used to quantify triglycerides was a "cascaded" enzymatic method involving (a) lipase, to generate glycerol from triglycerides; (b) glycerol oxidase, to convert glycerol to glyceraldehyde, with generation of hydrogen peroxide; and (c) peroxidase, which acts on the hydrogen peroxide with subsequent coupled generation of a red-violet quinone (reagent system used in the Technicon RA-1000). Hydroxyurea added to serum samples appeared to inhibit the action of glycerol oxidase, with a stoichiometric relation to the concentration of substrate (a decrease of roughly 2.4 mmol/L in measured triglyceride per 1 mmol of hydroxyurea per liter). A different enzymatic assay for triglycerides, which involves glycerol kinase (Beckman Instruments) did not show this effect of hydroxyurea.

Autoanalysis↗
PubMed1985

[Extent of coronary sclerosis in relation to lipoprotein lipase activity and plasma triglyceride levels].

Coronary artery disease (CAD) is closely connected with an increased concentration of cholesterol and a decreased concentration of high-density lipoprotein cholesterol (HDL-chol) in human plasma. No general agreement exists about the atherogenic potential of increased plasma triglycerides. Although both a negative correlation between plasma triglycerides and post heparin lipoprotein lipase (LPL) and a positive correlation between the plasma concentration of HDL-chol and LPL-activity are well documented, only a few studies have investigated the relationship between CAD and LPL. Therefore, 109 male patients with angiographically assessed CAD were investigated with respect to plasma lipids, post heparin LPL, and plasma testosterone and estradiol, which are both known to influence LPL-activity. Many well known results were confirmed. The extent of CAD, assessed by coronary angiography as coronary score (CS), was significantly positively correlated to plasma cholesterol, plasma triglycerides, plasma phospholipids, plasma low-density lipoprotein cholesterol (LDL-chol) and age. CS was significantly negatively correlated to LPL-activity and to the plasma concentration of HDL-chol. LPL itself was significantly negatively correlated to plasma cholesterol, plasma triglycerides and phospholipids, and significantly positively correlated to HDL-chol and plasma testosterone. The most surprising result of this study was the significant correlation between CS and LPL (r = -0.4624; p less than 0.001), a correlation which could explain the increased plasma triglycerides and decreased plasma HDL-chol.

Adult↗
PubMed1985

"Ex vivo" influence of fatty acids from plasma cholesterol and triglycerides on the fatty acid pattern of platelets.

We have studied "ex vivo", in 92 normal subjects, the influence of fatty acids (FA) that esterify plasma cholesterol and triglycerides on the fatty acid composition of phospholipids, triglycerides and free fatty acid fractions in platelets. High and significant correlations (p less than 0.001) were found for some of the platelet phospholipid FA and the same FA that esterify plasma cholesterol [18:1 (r = 0.56); 18:2 (r = 0.71) and 20:5 (r = 0.42)] and plasma triglycerides [18:1 (r = 0.57) and 18:2 (r = 0.66)]. Some significant correlations were also found between some of the platelet triglyceride FA and the same FA that esterify plasma phospholipids [18:1 (r = 0.58)], triglycerides [18:1 (r = 0.51), 18:2 (r = 0.52)] cholesterol [18:1 (r = 0.44)] and plasma free fatty acids [18:1 (r = 0.39); 18:2 (r = 0.40)]. By evaluating these results in conjunction with those of an earlier study, it can be concluded that "in vivo" the FA from different plasma lipid fractions and especially those esterifying the plasma cholesterol and phospholipid fractions, can influence the FA composition of platelet phospholipids in normal subjects. In trying to interpret the role played by plasma lipids in platelet lipids, it may be of interest to take into account the interrelationships found in this study.

Adult↗
PubMed1979

Risk factors for myocardial infarction in the Stockholm prospective study. A 14-year follow-up focussing on the role of plasma triglycerides and cholesterol.

A 14-year follow-up of the Stockholm prospective study is reported. A number of 130 new myocardial infarctions (MI) were found in a prospective group of men (n = 3189) and another 46, i.e. a total of 176 MI, in the total group (n = 3486). Different types of multivariate statistical analyses show that age, blood pressure, smoking, fasting plasma concentrations of cholesterol and triglycerides, ESR and Hb were independent risk factors for MI, while the weight/height index was not. Elevated BP became an important risk factor only after the age of 50. When only age, BP, smoking and the two plasma lipids were entered into the logistic multivariate analysis, plasma triglycerides were more important as a risk factor than cholesterol. Quintile analysis showed that the rate of new MIs increased more with increasing triglyceride than increasing cholesterol levels. In the prospective group, the average rate of new MIs for men below 60 years was 32 per 1000. In the bottom and top quintile these rates were 16 and 65 for plasma triglycerides and 27 and 47 for cholesterol. When the men were divided into 4 groups with regard to both plasma lipids, the rate of new MIs increased successively from group to group along this chain: both lipids normal, only cholesterol high, only triglycerides high and both plasma lipids high.

Adult↗
PubMed1970

Accumulation and release of triglycerides by rat liver following partial hepatectomy.

Regenerating liver accumulates lipid for about 20 hr following partial hepatectomy. During this time incorporation of intravenously administered palmitate-9, 10-(3)H into beta-lipoprotein increased. 13 hr after partial hepatectomy, there was no change in the level of serum beta-lipoproteins, but the specific activities of the triglycerides in the liver and beta-lipoproteins were significantly diminished. Extension of these studies to the isolated perfused liver system demonstrated that 13 hr after partial hepatectomy the regenerating liver is capable of secreting greater quantities of the lipid, but not the protein, moiety of the beta-lipoproteins in comparison with liver taken immediately from a partially hepatectomized animal, although there was no difference between the weights of the livers. However following addition of palmitate-(3)H and (14)C-labeled amino acids to the perfusate, the specific activity of the hepatic and beta-lipoprotein triglycerides of the liver excised 13 hr after partial hepatectomy was diminished, but that of the protein was not affected. Prelabeling of the accumulated triglyceride with palmitate-1-(14)C in vivo revealed that the proportions of the accumulated triglyceride secreted as beta-lipoproteins by perfused livers excised immediately and 13 hr after partial hepatectomy were identical. It is concluded that regenerating liver rapidly acquires the ability to mobilize triglycerides at a rate equal to that of the much larger normal liver, so that it can handle all free fatty acids presented to it.

Amino Acids↗
PubMed1977

Hepatic triglyceride accumulation and the ethanol physical withdrawal syndrome in mice.

Physical dependence on ethanol was induced in TO strain mice by chronic administration of ethanol by inhalation. The severity of the behavioral syndrome of withdrawal from ethanol was quantified by a subjective scoring method. During the chronic administration of ethanol, triglycerides accumulated in livers of male or female mice with a time course similar to that of the induction of physical dependence. When ethanol was withdrawn from adult or weaning dependent mice, a relationship was observed between the decline of triglyceride concentrations in liver and the duration of the ethanol withdrawal syndrome. The addition of DL-carnitine (7% w/w) to diet during the administration of ethanol markedly inhibited the accumulation of triglycerides, and significantly reduced the intensity of the ethanol withdrawal syndrome. Administration of carbon tetrachloride ((1.3 ml/kg i.p.), however, although augmenting hepatic triglyceride accumulation, had no significant effect on the withdrawal syndrome. The results are interpreted as suggesting either that ethanol-induced liver dysfunction plays a part in dependence, or, more likely, that triglyceride accumulation reflects an ethanol-induced metabolic disorder which is itself related to the induction of dependence.

Alcoholism↗
PubMed1977

Increased activity of vitamin K-dependent clotting factors in human hyperlipoproteinaemia - association with cholesterol and triglyceride levels.

Levels of blood coagulation factors, cholesterol and triglyceride were measured in human plasma. Prothrombin was significantly elevated in type IIa hyperlipidaemia; prothrombin and factors VII, IX and X in type IIb; and prothrombin and factors VII and IX in type V. Multiple regression analysis showed significant correlation between the levels of these plasma lipids and the vitamin K-dependent clotting factors (prothrombin, factors VII, IX and X). Higher cholesterol levels were associated with higher levels of prothrombin and factor X while higher triglyceride levels were associated with higher levels of these as well as factors VII and IX. Prothrombin showed a significant cholesterol-triglyceride interaction in that higher cholesterol levels were associated with higher prothrombin levels at all levels of triglyceride, with the most marked effects in subjects with higher triglyceride levels. Higher prothrombin levels were noted in subjects with high or moderately elevated (but not low) cholesterol levels. Ultracentrifugation of plasma in a density of 1.21 showed activity for prothrombin and factors VII and X only in the lipoprotein-free subnatant fraction. Thus, a true increase in clotting factor protein was probably present. The significance of the correlation between levels of vitamin K-dependent clotting factors and plasma lipids remains to be determined.

Adult↗
PubMed1967

Molecular weight distributions of milk fat triglycerides from seven species.

The triglyceride compositions of the milk fats of man, dog, guinea pig, cow, sheep, goat, and horse were compared by gas-liquid chromatography of the intact triglycerides and of the butyl esters of the component fatty acids. The milk fats of man, dog, and guinea pig, which were largely made up of long-chain fatty acids, showed a common pattern with major contributions made by the glycerides with 48-54 acyl carbon atoms. The milk fats of cow, sheep, and goat, which were rich in short-chain acids, showed significant proportions of triglycerides with 28-54 acyl carbon atoms. Horse milk, which contains large amounts of medium-chain fatty acids, gave a characteristic triglyceride pattern in the 26-54 carbon atoms range. The experimentally determined distributions of the molecular weights of the triglycerides of all milk fats deviated significantly from the distributions predicted by random association of the fatty acids from a single pool. The data suggest that in all species the milk fat may be formed by a partial resynthesis of preformed glycerides.

Animals↗
PubMed1984

Elevated plasma triglyceride levels are associated with human protoporphyria.

Six patients with protoporphyria had mildly elevated triglyceride levels (200 to 300 mg/dl) on serum chemistry screening panels. Measurement of fasting plasma lipid profiles indicated that triglyceride levels were mildly elevated in 22 patients with protoporphyria compared with the values of a age- and sex-matched population of the Lipid Research Clinics prevalence study (p = 0.021). The effect of ingestion of the retinoid precursor beta-carotene on plasma triglyceride levels was assessed in 13 of these patients, both during carotene therapy and during therapy-free intervals. There was no significant increase in plasma triglyceride levels during administration of carotene; eight of 13 patients had lower levels during therapy. There was no significant correlation between plasma triglyceride levels at p less than or equal to 0.05 and serum carotene or blood protoporphyrin levels. Our results indicate that mild hypertriglyceridemia occurs with increased frequency in patients with protoporphyria, but not as a direct result of beta-carotene therapy.

Adolescent↗
PubMed1982

The clearance and placental transfer of free fatty acids and triglycerides in the pregnant guinea-pig.

Bolus injections of [14C]palmitic acid and endogenously prepared very low density lipoprotein (VLDL) were given to 12 guinea-pigs in late gestation in whom the fetal side of the placenta was perfused in situ. Disappearance of [14C] palmitate in the mother was rapid, with a half life of 2.4 min. The [14C] palmitic acid which crossed the placenta into the perfusate disappeared in parallel with the maternal label but with a delay time of 1.6 min. Following injection of [14C] labelled very low density lipoprotein maternal plasma [14C] triglyceride declined rapidly (half life of 0.7 to 9.8 min) and gave rise to [14C] free fatty acids in the plasma. These fatty acids disappeared at a slower rate (half life of 13.5 min) than found following [14C]palmitate bolus. No [14C] triglyceride appeared to cross the placenta, but triglyceride derived free fatty acids did with a delay time of 9.4 min. In experiments performed after 55 days gestation quantities of [14C] free fatty acids were higher in the perfusate than in maternal plasma implying hydrolysis of triglyceride within the placenta. It is concluded that maternal triglyceride may make a considerable contribution to fetal lipids which increases with gestational age.

Animals↗
PubMed1980

Effect of controlled alcohol feeding on triglycerides in patients with outpatient 'alcohol hypertriglyceridemia'.

Hypertriglyceridemia in alcohol-consuming out-patients that abates after the discontinuation of alcohol is assumed to be caused by alcohol. It is unclear, however, whether this hypertriglyceridemia is the consequence of the energy-content of alcohol or of a specific stimulation of triglycericde production. To evaluate this question triglyceride levels and removal rate were studied before and after isocaloric replacement of food with alcohol under metabolic ward conditions. In paired studies, triglyceride concentrations and removal rate were decreased with alcohol in four out of six patients on a mixed diet and three out of four on a fat-free diet. The plasma triglyceride levels and removal rates increased in the other three patients. Since the changes in level and removal rate were concordant, alcohol probably affects production more than removal. In conclusion, alcohol can be shown to have a specific hypertriglyceridemic effect in only three out of ten patients with 'alcohol hypertriglyceridemia'. Isocaloric substitution of alcohol for food does lead to a decrease in triglyceride level in seven out of ten patients, who respond with a drop in triglycerides to ethanol withdrawal as out-patients.

Adult↗
PubMed1995

Quantification of apolipoproteins B-100, B-48, and E in human triglyceride-rich lipoproteins.

We have developed a procedure to quantify apolipoprotein (apo) B-100, apoB-48, and apoE in human triglyceride-rich lipoproteins. This procedure permits delipidation of small amounts of triglyceride-rich lipoproteins without appreciable losses, and quantification of these apolipoproteins in samples containing as little as 10 micrograms of protein. Delipidated triglyceride-rich lipoproteins are subjected to sodium dodecyl sulfate polyacrylamide slab gel electrophoresis, and the mass of apolipoproteins is estimated after densitometric scanning and volume integration of Coomassie blue-stained bands. The chromogenicities of apoB-100 and apoB-48 are virtually identical, and twofold lower than that of apoE. The standard curve for each apolipoprotein follows a power function over a wide protein range, permitting quantification of as little as 0.2 microgram of apoB-48 and as much as 30 micrograms of apoB-100 from a single application of triglyceride-rich lipoproteins to the gels. This method is suitable for routine use in studies of the intestinal and hepatic contributions to triglyceride-rich lipoproteins and their responses to postprandial lipemia.

Apolipoprotein B-100↗
PubMed1995

[The prognostic value of plasma triglycerides in human immunodeficiency virus infection].

BACKGROUND: Infection with the human immunodeficiency virus (HIV) is associated with an increased prevalence of hypertriglyceridemia, which is more common in advanced stages of disease. Nevertheless, the role of hypertriglyceridemia as a predictive marker of progression of disease and/or mortality is not fully elucidated. METHODS: One-hundred nineteen patients with HIV infection attended at our Outpatient Clinic or hospitalized in our Service were retrospectively studied. At the beginning of the study and every six months a complete medical history and physical examination were obtained, with a complete blood count, serum biochemistry, total lymphocytes and CD4 subpopulations, cholesterol, triglycerides and IgA. With comparative purposes cholesterol and triglyceride values were also determined in a control group of healthy subjects with the same age and gender. The relationship between triglyceride levels and the other clinical and analytical parameters was evaluated by means of the Pearson linear correlation. The risk for developing clinical disease and survival were studied by the method proposed by Kaplan and Meier. RESULTS: The mean age of patients was 27 +/- 6 years and the male/female ratio was 86/33. Eighty-three percent (99) of patients consumed drugs parenterally. Compared with the control group, patients with HIV infection had hypertriglyceridemia (159 +/- 80 mg/dl vs 79 +/- 53 mg/dl) and hypocholesterolemia (143 +/- 41 mg/dl vs 174 +/- 36 mg/dl) (p < 0.05). There was a positive correlation between triglycerides and IgA levels (p < 0.01) and a negative correlation with serum albumin (p < 0.05). A higher risk towards progression of disease was not observed among patients with hypertriglyceridemia (TG > 143 mg/dl) in non-AIDS infected patients, nor mortality in the overall group. CONCLUSIONS: HIV infected patients have a higher prevalence of hypertriglyceridemia and hypocholesterolemia. Plasma triglycerides were not useful as a prognostic factor for the development of disease nor as mortality risk.

Adult↗
PubMed1995

Palmitic acid and linoleic acid metabolism in Caco-2 cells: different triglyceride synthesis and lipoprotein secretion.

Polarized monolayers of intestinal Caco-2 cells were used to study the effects of saturated palmitic acid (16:0) and polyunsaturated linoleic acid (18:2) on triglyceride synthesis and lipoprotein secretion. Monolayers were incubated for 24 h, at the apical or lumenal side, with palmitic acid (16:0) or linoleic acid (18:2) in physiological concentrations. Incubation with 1.0 mM 16:0 or 18:2 resulted in differences in the composition and amount of secreted lipoproteins. Radiolabeled lipids in the lipoproteins secreted during incubation with 18:2 were found in the chylomicron/VLDL (very low density lipoprotein) density whereas with 16:0 the secreted lipoproteins were in the intermediate density/low density lipoprotein (IDL/LDL) density range. More triglyceride was secreted into the (basolateral) medium during incubation with 1.0 mM 18:2 (41 +/- 12% of total triglyceride synthesized) than with 1.0 mM 16:0 (18 +/- 3% of total). The biochemical findings correlate with conspicuous morphological changes in the cells in the presence of 16:0, but not 18:2. Increasing concentrations of 16:0 (0.1-1.0 mM) caused gradual accumulation of intracellular membrane. Microvilli became strongly reduced in number. With 1.0 mM palmitic acid we found an increased incorporation of [1-14C]palmitic acid into phosphatidic acid (14.8% of total incorporation into phospholipid with 16:0 vs. < 0.5% with 18:2) and diacylglycerol (12.5% with 16:0 vs. < 0.5% with 18:2) and diacylglycerol (12.5% with 16:0 vs. 0.5% with 18:2) and the amount of intracellular phospholipid doubled. The morphological changes were completely reversed after 24 h with 1.0 mM 18:2. We conclude from our results that, compared to 18:2, 16:0 is not efficiently incorporated into triglycerides. 16:0 is incorporated into cellular phospholipids in a greater proportion than 18:2, causing accumulation of intracellular phospholipid and the precursors phosphatidic acid and diacylglycerol. Different processing of 18:2 and 16:0 by Caco-2 cells resulted in profound differences in triglyceride synthesis and lipoprotein composition and secretion.

Carbon Radioisotopes↗
PubMed1976

Plasma post-heparin lipolytic activity and triglyceride clearance in uremic and hemodialysis patients and renal allograft recipients.

In order to study mechanisms in the pathogenesis of hypertriglyceridemia in uremia, maintenance hemodialysis, and post-renal transplantation, plasma post-heparin lipolytic acitivity was measured and the kinetics of triglyceride removal were determined during infusions of triglyceride in patients from each of these groups and in healthy control subjects. In addition, plasma lipolytic activity was measured both during the course of a single hemodialysis treatment and in response to daily hemodialysis over a five-day period. The mean serum triglyceride level was significantly elevated and the mean plasma post-heparin lipolytic activity significantly reduced in all three groups. Post-heparin lipolytic activity in transplant recipients with a normal serum creatinine concentration was not significantly different from that in control subjects. Those transplant recipients with mildly impaired graft function had levels of post-heparin lipolytic activity comparable to those in patients with end-stage renal failure. Triglyceride clearance was significantly reduced in both the transplant recipients and in the uremic patients. During a single hemodialysis treatment with systemic heparinization plasma lipolytic activity decreased after the first hour. With daily hemodialysis, predialysis post-heparin lipolytic activity progressively declined after the second day. It is concluded that reduced post-heparin lipolytic activity and decreased triglyceride clearance contribute to the hypertriglyceridemia seen not only in uremic patients and in patients on maintenance hemodialysis but also in renal allograft recipients. Diminished lipolytic activity in hemodialysis patients may be in part due to heparin-induced depletion.

Adolescent↗
PubMed1994

Fatty acids as determinants of triglyceride and cholesteryl ester synthesis by isolated hepatocytes: kinetics as a function of various fatty acids.

Triglyceride synthesis by hepatocytes is currently thought to be the rate-limiting step for lipoprotein formation. In order to determine whether triglyceride and cholesteryl ester syntheses in hepatocytes are sensitive to physiological fluctuations of serum fatty acids, the fatty acid dependence of these pathways was examined. Uptake of various fatty acids and incorporation into triglyceride and cholesteryl esters were studied in isolated rat hepatocytes. Rates were determined under conditions of linear incorporation and related to the concentrations of total and unbound fatty acid in a mixture of fatty acids and albumin. The findings were: pathways for triglyceride and cholesteryl ester synthesis saturated at unbound fatty acid concentrations (or fatty acid albumin ratios) within the range of serum values and thus would be acutely modulated by fluctuations in serum fatty acids. Addition of cholesterol to the medium increased cellular cholesterol, but did not alter rates of cholesterol esterification, suggesting that endogenous cholesterol synthesis provided the needed substrate. Oleate, palmitate, and linoleate were comparable in their saturation kinetics and ability to support triglyceride and cholesteryl ester synthesis. Consequently, their binding affinity for serum albumin would determine their lipid-incorporation rates. On this basis, in humans, oleate would yield the lowest rates as it has the lowest unbound fatty acid at each fatty acid-albumin ratio. Stearate, in contrast to the other fatty acids, was poorly esterified into neutral lipids by hepatocytes. Poor hepatic metabolism of stearate most likely explains previous findings of a hypocholesteremic effect of diets high in stearate as compared to other saturated fatty acids.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗