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PubMed1988

Triglycerides and apoproteins in toxemia of pregnancy.

In order to clarify the mechanism of hypertriglyceridemia caused by toxemia of pregnancy, apoprotein B, CII, CIII, and E in serum were determined by single radial immunodiffusion, and apoprotein CIII0, CII, CIII1 and CIII2 in very low density lipoprotein (VLDL) fractionated by ultracentrifugation were quantified by analytical isoelectric focusing. The increase in triglycerides in toxemia of pregnancy was estimated in VLDL and low density lipoprotein (LDL), mainly in VLDL. In contrast to the increase in triglycerides, apoprotein B and E, believed to interact with LDL receptors on cell membranes, remained unchanged from levels in normal pregnancy. The lack of correlation between triglycerides and these apoproteins may be related to the increase in triglyceride in VLDL. In toxemia of pregnancy, the relative amounts of apoprotein CII, an activator of lipoprotein lipase, and CIII, an inhibitor of lipoprotein lipase, in serum were similar to those in normal pregnancy, but those in VLDL decreased significantly. This finding suggests that the increase in triglyceride in VLDL was caused by inhibition of VLDL to LDL catabolism. These results suggest that one of the factors which causes hypertriglyceridemia in toxemia of pregnancy is impaired removal of triglyceride, in LDL fraction, but mainly in VLDL fraction.

Adult↗
PubMed1986

Ethanol inhibits triglyceride synthesis and secretion by human small intestinal mucosa.

We studied the effect of ethanol on human intestinal lipid absorption and on triglyceride synthesis and secretion. Human duodenojejunal biopsy specimens were incubated in a micellar lipid solution containing carbon 14-labeled oleate in the presence of ethanol 0.1%, 1.0%, and 5.0% (vol/vol). Tissue triglyceride synthesis was significantly decreased by 52.0% +/- 7.7%, 57.0% +/- 9.0%, and 81.3% +/- 4.0% (mean +/- SEM), respectively, when compared with triglyceride synthesis by control biopsy specimens incubated in the absence of ethanol. Tissue levels of oleate were increased in biopsy specimens incubated in the presence of ethanol by 90% +/- 30% and 115% +/- 5% for ethanol concentrations of 1.0% and 5.0% (vol/vol), respectively (P less than 0.02). At ethanol concentration of 0.01%, no change in tissue oleate or triglyceride levels was noted. The effect of 1.0% and 5.0% ethanol on triglyceride synthesis may reflect in large part their significant increase of the medium osmolarity. However, the osmolarity of the medium containing 0.1% ethanol was similar to that of the ethanol-free medium, and its effect is therefore probably specific. Duodenojejunal biopsy specimens were also preincubated for 30 minutes in a micellar lipid solution containing 14C-oleate, and subsequently were organ cultured in micellar-free medium in the presence or absence of ethanol 1.0% (vol/vol). During organ culture, the decrease in tissue oleate levels was similar in biopsy tissue cultured in the presence or absence of ethanol. However, in the presence of ethanol, triglyceride secretion to the organ culture medium was reduced by 49.9% +/- 11.1% (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Duodenum↗
PubMed1985

Apolipoprotein A-I synthesis in rat small intestine: regulation by dietary triglyceride and biliary lipid.

Techniques were developed to provide direct quantitation of apolipoprotein A-I (apoA-I) synthesis rates in rat small intestine. Following intralumenal administration of a pulse of [3H]leucine, newly synthesized enterocyte apoA-I was quantitated by specific immunoprecipitation and compared to [3H]leucine incorporation into total trichloroacetic acid-precipitable protein. ApoA-I synthesis rates (% total protein) were found to be significantly higher in jejunal enterocytes (1.84 +/- 0.20) compared to ileal enterocytes (0.91 +/- 0.25) from the same, fasting, animals, P less than 0.01. It was found that rats consuming regular (4.5% w/w fat) rodent chow had apoA-I synthesis rates, 30 to 240 min after receiving an intraduodenal bolus of 100 mg of triglyceride, that were indistinguishable from control animals receiving either saline or an isocaloric, but fat-free, enteral preparation. By contrast, animals consuming a fat-free chow for 8 days prior to study had a small but significant response to acute reintroduction of dietary triglyceride. Four hours after 100 mg of triglyceride was administered, jejunal apoA-I synthesis (% total protein) was 1.84 +/- 0.1 compared to 1.37 +/- 0.04 for animals exposed to an isocaloric, fat-free enteral preparation, P less than 0.01. External bile diversion for 48 hr, which effectively removed all lumenal sources of lipid, reduced apoA-I synthesis in jejunal enterocytes but produced no more depression than that found in sham-operated controls infused for 48 hr with dextrosesaline or control animals fasted for 30 hr. By contrast, apoA-I synthesis in ileal enterocytes was reduced significantly by external bile diversion (0.59 +/- 0.20) in comparison to sham-operated controls (1.19 +/- 0.32) P less than 0.01. Continuous infusion of 10 mM Na taurocholate for 48 hr or 10 mM Na taurocholate for 44 hr and 80 mg of micellar lipid for 4 hr produced results similar to those obtained by bile diversion alone (0.56 +/- 0.2 and 0.61 +/- 0.25, respectively) suggesting that bile salt deficiency alone was not responsible for the observed depression in ileal apoA-I synthesis. These results suggest that, under conditions of physiological dietary triglyceride intake, apoA-I synthesis in jejunal enterocytes is not actuely regulated by changes in triglyceride flux. After prolonged dietary triglyceride withdrawal, the reintroduction of fat produces a small, but significant, increase in jejunal apoA-I synthesis. The data further suggest that apoA-I synthesis in jejunal enterocytes is regulated in part by the availability of lumenal lipid, but that the presence of bile does not exert an additional level of control.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1985

Single-cuvet sequential determination of triglyceride and cholesterol.

I describe a sequential method for kinetic assay of serum triglyceride and cholesterol in a single cuvet. Triglyceride is assayed first, by an ultraviolet enzymic method with ATP and NADH as the driving reagents (Clin Chem 21:1627-1629, 1975); cholesterol is then assayed with use of cholesterol oxidase, peroxidase, and the Trinder reaction. Excess NADH left by the triglyceride assay is removed by adding either pyruvate or glycerol to the cholesterol reagent; the addition prevents interference of NADH with nascent H2O2, and does not affect the apparent Km of cholesterol oxidase or the pseudo-first-order reaction of the cholesterol assay. The method, tested in both a random-access analyzer (Hitachi 705) and a batch analyzer (Olli C/D), at three concentrations, gave the following within-run CVs:3.0, 1.6, 1.5% for cholesterol; 4.0, 4.2, 5.4% for triglyceride. The corresponding between-run CVs were 12.5, 9.0, 8.1% and 12.8, 11.1, 8.9%. The calibration was linear to at least 8.0 g/L for both cholesterol and triglyceride. Interference from bilirubin, hemoglobin, and certain drugs is almost negligible. Correlation studies with reference and routine methods showed r values ranging from 0.985 to 0.995 for cholesterol, 0.984 to 0.991 for triglyceride.

Autoanalysis↗
PubMed1972

Comparison of the triglyceride lipase of liver, adipose tissue, and postheparin plasma.

Heparin-released triglyceride lipase from three sources, adipose tissue, liver, and postheparin plasma, was compared. Heparin-released triglyceride lipase from liver differed in several major respects from that in adipose tissue. These differences included response to inhibitors and to high density lipoprotein in the incubation media. Heparin-released triglyceride lipase from liver, when compared with that from adipose tissue, was relatively inactive against lipoprotein substrates. The triglyceride lipase from postheparin plasma exhibited properties more like those of liver. These studies raise the possibility that triglyceride lipase in postheparin plasma may be heterogeneous and that levels of the enzyme in postheparin plasma may not accurately reflect the capacity for clearance of triglyceride from the plasma.

Adipose Tissue↗
PubMed1977

Decomposition of molecular types of triglycerides by lipoprotein lipase in man.

1. The lipoprotein triglycerides of human plasma can be separated by gas chromatography according to their carbon number into four main groups: C48, C50, C52 and C54. We studied the decomposition of molecular types of triglycerides by posttheparin lipoprotein lipase in vitro. 2. Decomposition of the molecular type C52 does not depend on its concentration. Decomposition of the molecular types C48, C50 and C54 is in a direct correlation to their concentration. 3. The above mechanism assures stability of the triglyceride profile of human plasma, which is species specific and is expressed by the figures: C48--9%, C50--20%, C52--43%, C54--20%, remainder 8%. 4. The plasma triglyceride profile can be altered by dietetic factors. After drinking cream, the triglyceride composition is: C48--12%, C50--22%, C52--37%, C54--14%, remainder 15%. Selective decomposition of molecular types of triglycerides ensures that the profile, after a given time, returns to the original state.

Dietary Fats↗
PubMed1984

Modulation by glycerol of hepatic glycero-3-phosphate concentration, ketogenesis, and output of triglyceride and glucose in perfused livers from hyperthyroid and euthyroid rats.

Decreased glycero-3-phosphate (glycero-3-P) concentration, decreased output of triglyceride and glucose, increased output of apolipoprotein A-I, and increased ketogenesis were observed with isolated perfused livers from triiodothyronine-treated rats in comparison to livers from euthyroid animals. Infusion of glycerol produced a concentration-dependent accumulation of glycero-3-P in perfused livers from hyperthyroid and euthyroid rats, which was considerably enhanced in the euthyroid group. The antiketogenic effect of glycerol in livers from triiodothyronine-treated rats was accompanied by increased output of glucose and triglyceride, while no change in the output of apolipoprotein A-I was observed. The reduction of ketogenesis (49%) in euthyroid livers by glycerol was not accompanied by increased triglyceride output, while with the largest amount of glycerol infused, decreased output of apolipoprotein A-I was seen. Output of triglycerides by livers from hyperthyroid rats correlated with hepatic concentration of glycero-3-P and was maximal at a glycero-3-P concentration (0.5 mumol/g), similar to that observed in livers from euthyroid rats in the absence of glycerol. Availability of glycero-3-P appears to be rate-limiting for synthesis and secretion of triglyceride by livers from hyperthyroid animals, whereas the glycero-3-P concentrations in euthyroid livers were sufficient to support maximal production of triglyceride limited only by the supply of free fatty acid.

Animals↗
PubMed1981

Estimation of very-low-density lipoprotein cholesterol from data on triglyceride concentration in plasma.

We examined the relationship in a large-living population between the concentration of triglycerides in plasma from fasting persons and the concentration of very-low-density lipoprotein cholesterol (VLDL-C) as determined after preparative ultracentrifugation. Data from individuals in the Framingham Heart Study who were free of coronary heart disease, did not have Fredrickson Type I, III, or V hyperlipoproteinemia, and whose plasma-triglyceride values were less than 4000 mg/L were considered in the analyses. A total of 4100 Framingham Offspring, ages 20-49 years, met these criteria, as did 2284 participants in the original Framingham Cohort, aged 50-79 years. We estimated a linear regression model with an intercept and slope coefficient, using VLDL-C (units, mg/L) as the dependent variable and triglycerides as the dependent variable. The intercept was approximately 30.0 mg/L, and the slope coefficient for triglycerides was about 0.20 when all age and sex groups were combined. However, when the analysis was performed by age group, the slope coefficient for triglycerides increased with each age group only for women. The model, in which a different intercept and slope is used for each age and sex group was statistically better than a previously developed simpler model. On the other hand, the older model, in which VLDL-C is easily estimated by multiplying the triglyceride value by 0.20, is reasonably accurate and is very simple to use. The generalizability of the model is discussed in the light of results from other population studies.

Adult↗
PubMed1982

Cholesterol, triglyceride and high-density lipoprotein cholesterol levels in non-insulin-dependent diabetes in the young.

Cholesterol, triglycerides and high-density lipoprotein (HDL) cholesterol levels were measured in Indian patients with non-insulin-dependent diabetes in the young (NIDDY). Both cholesterol and triglycerides were increased as compared with reference values. The HDL cholesterol levels were lower in cases of NIDDY. Aberrations in the lipid and lipoprotein levels were more pronounced in males. Significant correlations were found between the levels of cholesterol and glycosylated haemoglobin, and triglycerides and glycosylated haemoglobin; triglycerides and HDL cholesterol were inversely correlated. No correlation was found between triglycerides and obesity. NIDDY does not differ from the more common type of non-insulin-dependent diabetes in mature patients with regard to cholesterol, triglyceride and HDL cholesterol levels.

Adult↗
PubMed1982

Total cholesterol, high density lipoprotein-cholesterol and triglycerides after a standardized high-fat meal.

Total cholesterol, high density lipoprotein (HDL)-cholesterol and triglycerides were measured fasting and at 20, 40, 60, 120 and 180 min after a high-fat meal in 22 healthy subjects. Both HDL-cholesterol and total cholesterol fell during the first 20 min after the meal whereas the mean triglyceride level increased during the observation period. In 8 of the subjects the maximum triglyceride level was reached before the end of the observation period and their fasting HDL-cholesterol level was significantly higher than in the rest of the subjects. The higher the fasting HDL-cholesterol concentration, the more rapidly the triglyceride levels returned towards initial values. The study supports the concept that the degradation rate of triglyceride-rich particles is dependent on the HDL-cholesterol level. It also suggests the use of non-fasting triglyceride values in addition to HDL-cholesterol as independent predictors in longitudinal studies for CHD.

Adolescent↗
PubMed1978

Effects of cholestyramine and chenodeoxycholic acid on the metabolism of endogenous triglyceride in hyperlipoproteinemia.

Previous studies conducted under basal conditions have suggested a linkage between the formation of plasma triglyceride and the degradation of cholesterol to bile acids. To further examine this relationship, plasma endogenous triglyceride kinetics were determined using [(3)H]glycerol in 26 hyperlipidemic subjects before and during stimulated (cholestyramine treatment) and inhibited (chenodeoxycholic acid treatment) bile acid synthesis. All patients with hyperlipoproteinemia (HLP) type II (n = 9) treated with cholestyramine (12 g daily for 2-4 months) displayed increased apparent biosynthesis (12.8 +/- 1.5 vs. 9.7 +/- 1.2 micro mol kg(-1)hr(-1), mean +/- SEM, P < 0.005) and an elevated apparent fractional turnover rate (0.230 +/- 0.017 vs. 0.176 +/- 0.014 hr(-1), P < 0.001) as determined over a 10-hr period, in spite of essentially unchanged plasma triglyceride concentrations. No consistent effect of this therapy was encountered in the five patients studied with type IV HLP. Chenodeoxycholic acid feeding (1.9 mmol daily for 3-4 months) resulted in a reduced apparent synthesis of plasma triglycerides both in type IIa (n = 5, 7.9 +/- 0.5 vs. 13.1 +/- 1.2 micro mol kg(-1)hr(-1), P < 0.01) and type IV HLP (n = 7, 15.5 +/- 1.8 vs. 23.6 +/- 3.7 micro mol kg(-1)hr(-1), P < 0.02). Furthermore, a 20-25% reduction of the apparent fractional turnover rate was seen, and the plasma concentration of triglycerides was reduced by about 15%. It is concluded that the present experimental conditions that primarily influence cholesterol and bile acid biosynthesis also affect the metabolism of plasma triglycerides-and presumably that of very low density lipoprotein-in a regulatory manner. Hypothetically, this may be achieved via a hepatic pool of newly synthesized cholesterol.

Adult↗
PubMed1980

[Triglyceride synthesis and oleic acid catabolism by hepatic microsomes and mitochondria in clofibrate or procetofen-treated rats].

Several studies have explained the influence of clofibrate on lipid metabolism, and the depressive effect of this drug on blood triglyceride and cholesterol levels is now well-known. Inhibition of triglyceride formation in the liver, and thus a reduced release of newly synthesized triglycerides coupled with increased fatty acid catabolism, might partially explain the lipid-lowering effect of clofibrate. These in vitro studies were designed to determine the effects of a new normolipemic product, procetofen, on hepatic microsomal synthesis of triglycerides and mitochondrial catabolism of oleic acid. These subcellular particles were isolated from normal rats or those treated for 8 days with clofibrate (250 mg/kg/day) or procetofen (100 mg/kg/day). Microsomal triglyceride synthesis from 3H oleate was not significantly changed in the clofibrate-treated group, while it decreased by 25 p. 100 in the procetofen-treated group. In the mitochondrial system, 14CO2 production from 10-14C oleate was small and unaffected by either drug. Therefore, the radioactivity of acid-soluble products was enhanced by 40 or 130 p. 100 when mitochondria were isolated from the livers of rats treated with clofibrate or procetofen, respectively. These data support the hypothesis that the plasma lipid-lowering effect of procetofen in vivo could be explained by increased hepatic fatty acid degradation which probably induced a reduction of triglyceride synthesis.

Animals↗
PubMed1995

[Cholesterol, HDL-cholesterol, triglycerides and beta-lipoprotein in diabetic pregnancy].

UNLABELLED: Follow up studies regarding lipid metabolism in diabetic pregnancy are important in maternal and fetal morbidity. OBJECTIVE: With this background it is particularly opportune to consider the difference of cholesterol, triglycerides and HDL-cholesterol of diabetics and nondiabetics in pregnancy. In addition the correlation of lipids to the glycosylated hemoglobin (HbA1), White groups and other clinical parameters is of interest. Attention is given to the comparison of insulin dependent diabetics (IDDM) and gestational diabetes (GDM) in the 3rd trimester. PATIENTS: A diabetic group of 84 patients (IDDM, GDM) was used for the prospective study over a two years period. The lipid metabolism was estimated preconceptionally, during pregnancy and on 7th day after delivery. 36 pregnant healthy women served as controls. The information obtained from each patient was entered into an SPSS data base. Statistical analysis were done by Mann-Whitney U and Kruskall-Wallis test and by means of Pearson's correlation coefficient to correlate with age, parity, body mass index, creatinin, albumiuria, HbA1, blood pressure. RESULTS: There were no any correlations between lipid parameters cholesterol, triglycerides, HDL-C, beta-lipoprotein and HbA1 as well as White groups (Pearson's coefficient). The triglyceride levels were significant lower in diabetic pregnants compared with healthy controls (p = 0.0095; Wilcoxon Test); diabetes: mean = 1,831 mmol/l; min 0.35; max 5.99 and control group mean = 2,133 mmol/l; min 0.36; max 4.70. Cholesterol levels were higher in the 3rd trimester of GDM patients than values of IDDM's (p = 0.0017; Wilcoxon Test). The longitudinal study during diabetic pregnancy resulted in significantly progressive increase in cholesterol and triglyceride levels (p = 0.0035 bzw. p = 0.0099; Kruskal-Wallis Test). CONCLUSIONS: Significant lower triglyceride levels had been found in diabetic pregnants than in healthy controls. There was no any correlation between lipid parameters cholesterol, triglycerides, HDL-cholesterol, beta-lipoprotein on the one side and HbA1 and White groups on the other side. Increased cholesterol levels were noted in the 3rd trimester of pregnancy in the gestational diabetes in comparison of insulin dependent pregnant diabetics.

Adolescent↗
PubMed1977

Cholesterol and triglyceride concentrations in serum/plasma pairs.

Serum/plasma pairs of samples from 506 subjects were analyzed for cholesterol and triglycerides (triacylglycerols). In the 1 to 5 g/liter range for both cholesterol and triglycerides, values for serum averaged about 3% higher than the corresponding plasma values. We derived equations for the best-fitting lines relating the gram per liter concentrations of cholesterol and of triglycerides in serum and plasma: [Serum cholesterol] = 1.036[plasma cholesterol] -- 1.380[Serum triglyceride] = 1.031[plasma triglyceride] -- 0.37 No clinical significance is attribuled to the observed serum plasma differences, but they may be of importance when cholesterol and triglyceride values from different clinical trials or epidemiological studies are being compared.

Cholesterol↗
PubMed1993

Discordant results for determinations of triglycerides in pig sera.

We recently determined triglyceride concentrations in pig sera by three fully enzymatic methods (Kodak Ektachem 700, Hitachi 707, and Abbott EPx) and obtained significantly lower values than those obtained with chemical or enzymatic methods based on chemical hydrolysis. All methods used involve microbial lipases for liberating glycerol from glycerides and glycerol phosphate dehydrogenases or oxidases for subsequent oxidation. The methods were validated against reference methods by using fresh human sera and survey materials. The discordant results were not from matrix sample-method interaction but from incomplete hydrolysis of pig serum triglycerides by the lipolytic enzymes. When serum triglycerides from 10 pigs showing the highest biases were hydrolyzed by microbial lipases and the reaction mixture was subjected to thin-layer and gas-liquid chromatography, the predominant end products were palmitoyl monoglyceride and a mixture of free fatty acids with the following composition (fatty acid as percent of total +/- SD): 16:0, 7.8 +/- 2; 18:0, 5.4 +/- 2.2; 18:1, 53 +/- 12; 18:2, 31 +/- 4.6; and 18:3, 2.5 +/- 1. Assuming that the lipases exhibit the usual specificity toward the 1 and 3 positions of the triglyceride, the data suggest that, in pig, triglycerides 18:1 and 18:2 occupy the 1 and 3 positions and 16:0 (palmitic acid) predominantly occupies the 2 position. Triglycerides of this structure may not be well hydrolyzed by the typical lipolytic enzymes in clinical assays.

Animals↗
PubMed1993

Docosahexaenoic acid shows no triglyceride-lowering effects but increases the peroxisomal fatty acid oxidation in liver of rats.

The effect of docosahexaenoic acid (DHA) on mitochondrial and peroxisomal fatty acid oxidation and on key enzymes in triglyceride metabolism was investigated in the liver of rats fed a standard diet, a cholesterol diet, and a pelleted chow diet. Unexpectedly, in all three rat models repeated administration of highly purified DHA (92% pure) at different doses and times, at a dose of 1000 mg/day per kg body weight, resulted in no significant decrease of hepatic and plasma concentration of triglycerides. The serum concentrations of cholesterol and phospholipids showed an increase in a time-dependent manner in rats fed the pelleted chow diet. The hepatic concentration of cholesterol was increased in rats fed the cholesterol diet and pelleted chow diet after administration of DHA compared to palmitic acid. In all rat models, treatment with DHA tended to increase the peroxisomal beta-oxidation. This was accompanied with a significant increase (1.5-fold) of fatty acyl-CoA oxidase activity. The mitochondrial fatty acid oxidation system and carnitine palmitoyl-transferase activity, however, were almost unchanged. Moreover, palmitoyl-CoA synthetase activity was increased, whereas the palmitoyl-CoA hydrolase activity was decreased. Neither microsomal phosphatidate phosphohydrolase activity nor cytosolic phosphatidate phosphohydrolase activity was affected by DHA feeding in the three rat models. Acyl-CoA:1,2-diacylglycerol acyltransferase activity was also unaffected. In contrast to docosahexanoic acid feeding, eicosapentaenoic acid (EPA) administration possessed a hypotriglyceridemic effect and resulted in an increase of mitochondrial and peroxisomal oxidation of fatty acids. Carnitine palmitoyltransferase activity was also stimulated. Phosphatidate phosphohydrolase activity was unaffected whereas diacylglycerol acyltransferase activity was increased by EPA treatment compared with palmitic acid feeding. The results indicate that docosahexaenoic acid, in contrast to eicosapentaenoic acid, does not inhibit the synthesis and secretion of triglycerides in the liver. In addition, the results emphasize the importance that stimulation of peroxisomal beta-oxidation by these n-3 fatty acids is not sufficient to decrease the serum levels of triglycerides. In addition, increased mitochondrial beta-oxidation of fatty acids and thereby decreased availability of nonesterified fatty acids may be a mechanism by which EPA inhibits triglyceride, and subsequently very low density lipoprotein-triglyceride, production. Whether DHA and EPA possess different metabolic properties should be considered.

Animals↗
PubMed1995

[Role of cholesterol esters in triglyceride transport].

Biosynthesis of cholesterol esters in the blood flow and their function are determined by the fact that these compounds are the sole endogenously synthesized molecules whose hydrophobicity is higher than that of triglycerides transferred by the blood. Within the structure of intermediate density lipoproteins, cholesterol esters substitute for triglycerides during association of apoprotein B-100 with the C-terminal lipid-binding domain. Substitution of the liquid-crystalline phase of triglycerides for the corresponding phase of cholesterol esters results in a significant alteration of the apoprotein B-100 conformation and the formation of low density lipoproteins. Within the structure of low density lipoproteins, the N-terminal domain (apoprotein B-100 ligand) acquires an active conformation and an ability to interact with cell membrane receptors, thereby facilitating their absorption of low density lipoproteins. Cholesterol synthesis in the blood is an independent step in triglyceride transport. Inhibition of cholesterol ester synthesis into high density lipoproteins and their conversion into intermediate density lipoproteins is unaccompanied by the acquisition by apoprotein B-100 of a final conformation or by the formation of low density lipoproteins. Remnants of intermediate density lipoproteins having an intermediate conformation of apoprotein B-100 and the inactive position of the domain ligand are accumulated in the blood. This results in the development of IIb type hyperlipoproteinemia. Resumption of conversion of cholesterol esters from high density lipoproteins into intermediate density lipoprotein remnants normalizes the triglyceride transport. The final conformation of apoprotein B-100 can be modelled by substituting triglycerides in intermediate density lipoprotein remnants for another substance whose hydrophobicity is similar to that of cholesterol esters (dolichol, probucol).(ABSTRACT TRUNCATED AT 250 WORDS)

Anticholesteremic Agents↗
PubMed1996

Chylomicron metabolism in rats: lipolysis, recirculation of triglyceride-derived fatty acids in plasma FFA, and fate of core lipids as analyzed by compartmental modelling.

Chylomicrons labeled in vivo with [14C]oleic acid (primarily in triglycerides (TG), providing a tracer for lipolysis) and [3H]retinol (primarily in ester form, providing a tracer for the corelipids) were injected into rats. Disappearance of the two labels from plasma and appearance of label in plasma free fatty acids (FFA) were analyzed by compartmental modelling. Both core and TG label distributed into an apparent volume 10-15% larger than the blood volume. Part of this probably represents margination to endothelial-binding-lipolysis sites. An open two-compartmental model for plasma FFA was derived from experiments where unesterified oleic acid complexed to albumin was injected. Applying this model revealed that most of the oleic acid from chylomicron triglycerides mixes with the FFA. The disappearance of chylomicron core label required a model in which the label transfers into a second compartment before it leaves the blood. The rate constant for the transformation was high and predicted that, on average, chylomicron spent less than 2 min in the first compartment. The rate out from the second compartment predicted that about 60% of the core label left blood while, on average, chylomicron retained more than half of its triglyceride molecules, i.e., after rather limited lipolysis. The mechanism by which the core label leaves blood is not clear. Modelling showed that under the assumption that the process is shared by chylomicron triglycerides, about half of them go out by this pathway. Comparing fed and fasted rats, the main differences were in the turnover of FFA and in the extent to which chylomicron TG label reappeared in the FFA. This study indicates that a large fraction of the triglycerides in chylomicrons leave plasma together with the core lipids and that most of the fatty acids from chylomicron triglycerides mix into the same metabolic compartments as do plasma free fatty acids.

Animals↗