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Results for “Esterification”

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At least 19 recordsLinked to original sources

PubMed1977

Stimulation of cholesterol esterification in rhesus monkey arterial smooth muscle cells.

The influence of homologous high density lipoprotein (HDL) and low density lipoprotein (LDL) and of whole hypercholesterolemic serum on the esterification of oleic acid and cholesterol was studied in rhesus monkey arterial smooth muscle cells. Whole hypercholesterolemic serum and isolated LDL stimulated cholesterol esterification as much as 10-fold using either cholesterol-1,2-3H or oleate-1-14C as substrate. At the same concentrations of cholesterol, HDL stimulated cholesterol esterification to a lesser extent, to a maximum of 3-fold. Associated with the stimulation of cholesterol esterification by LDL or whole hypercholesterolemic serum was a greater than 10-fold increase in the cholesteryl ester content of the arterial smooth muscle cells. Esterification to cholesterol reached a maximum after 8-12 hours of culture with either hypercholesterolemic serum or LDL. The stimulation of esterification was specific for esterification to cholesterol because there was little change in incorporation of fatty acid into triglycerides and phospholipids. These studies provide further evidence that a major consequence of the interaction of plasma LDL with the cellular elements of the arterial wall is a stimulation of cholesterol esterification. These studies, coupled with the observation that cholesteryl esters, more than any other single component, increase in the atherosclerotic artery, suggest an important role of a stimulation in cholesterol esterification in the pathogenesis of atherosclerosis.

Animals↗

PubMed1991

Regulation of retinol uptake and esterification in MCF-7 and HepG2 cells by exogenous fatty acids.

The influence of extracellular fatty acids on the uptake and esterification of [3H]retinol bound to human retinol-binding protein (RBP), to RBP-transthyretin (TTR), or in dispersed form by the human hepatoma, HepG2, and human mammary epithelial carcinoma, MCF-7, cell lines was studied. The esterification of [3H]retinol was significantly increased in cells incubated with myristic, palmitic, stearic oleic, or linoleic acid-albumin complexes and was observed for all forms of [3H]retinol. Enhancement of [3H]retinol uptake was also observed in cells incubated with these fatty acids, but this increase was relatively small for the dispersed form as compared to that observed for [3H]retinol bound to RBP or RBP-TTR. Comparing equal concentrations of the [3H]retinol donors, cell uptake and esterification was greatest from the dispersed form and least from that bound to RBP-TTR. After preincubation of cells with oleate, uptake and esterification of [3H]retinol was increased but not to the extent observed when oleate and [3H]retinol donor were co-incubated. Incubation of cells with oleate resulted in rapid and correlated increases in the rates of [3H]retinol uptake and esterification which persisted until the steady state for [3H]retinol uptake was achieved. Beyond this time, net esterification of [3H]retinol continued in the presence of oleate. This kinetic pattern was observed for all [3H]retinol donors. These effects on [3H]retinol uptake and esterification were dose-dependent as the oleate to albumin ratio was varied from 0.5 to 3.0 and were observed across a physiological concentration range of RBP-3H-retinol. The data indicate that: 1) the fatty acid status of cells is a determinant of retinol uptake and esterification; and 2) the form of retinol presentation to cells is not qualitatively important for these processes.

Animals↗

PubMed1979

Development of fatty acid esterification mechanisms in rat small intestine.

Fatty acid esterification was measured in fetal jejunal and ileal isografts implanted under the kidney capsules of adult host rats and compared to the age-controlled intestine grown in situ. Studies were conducted on the 21st, 35th, 49th, and 63rd postconceptional days, corresponding to prenatal, suckling, weaning, and weaned rats. Substantial fatty acid esterification activity was found in prenatal jejunum but not in ileum. A proximal-distal gradient of fatty acid esterification was observed in all groups grown in situ, but not in isografts. The monoglyceride pathway (MG-P) accounted for about one-third of total fatty acid esterification (TFAE) in jejunum grown in situ and remained constant through the study. In the ileum, MG-P was the major esterification pathway during the first 4 postnatal weeks, but decreased progressively after weaning to become insignificant in adult rats. TFAE fell in the jejunal isografts, whereas it increased in the ileum. MG-P remained as the major pathway in the implanted jejunum and ileum. Our studies suggest that luminal contents are probably the most important modulator for the development and maintenance of intestinal fatty acid esterification, and "fetal programming" manifested by changes in fatty acid esterification mechanisms in the isografts is less important.

Animals↗

PubMed1992

Cultured fibroblasts from patients with Niemann-Pick disease type C and type D exhibit distinct defects in cholesterol esterification.

The Niemann-Pick group of diseases can be broadly classified into two types based on clinical and biochemical characteristics. Type I is characterized by a primary deficiency of lysosomal sphingomyelinase while Type II may have a defect in the regulation of intracellular cholesterol metabolism. We have studied cholesterol esterification in cultured fibroblasts from patients with two phenotypes of Type II disease: an Acadian population of southwestern Nova Scotia (Canada) with a form of the disease known as Niemann-Pick type D (NPD) and a group of panethnic origin with Niemann-Pick type C (NPC). Addition of whole serum to normal fibroblasts grown initially in lipoprotein-deficient serum caused a rapid (within 6 h) increase in cholesterol esterification, reaching maximum values at around 24 h, while NPC fibroblasts showed little increase (less than 10% of normal). In contrast, cholesterol esterification in NPD fibroblasts increased slowly during the first 6-12 h and reached 50% of normal values by 24 h. 25-Hydroxycholesterol, a non-lipoprotein stimulator of cholesterol esterification, caused a similar stimulation of cholesterol esterification in NPC, NPD and normal cells. This was inhibited by addition of serum in mutant but not in normal cells. Within 24 h of serum addition, free cholesterol accumulated in all cell types with NPC greater than NPD greater than normal. These observations indicate that (a) regulation of cholesterol esterification in response to serum lipoproteins (but not 25-hydroxycholesterol) is abnormal in both NPC and NPD fibroblasts, and (b) the biochemical phenotypes of fibroblasts from NPC and NPD patients are distinct.

Cells, Cultured↗

PubMed1979

Small intestinal mucosal fatty acid uptake and esterification in infants and children.

Oleic acid uptake and esterification in intact intestinal mucosa were studied in 14 infants and children with chronic non-specific diarrhea, but histologically normal small intestinal mucosal biopsies, using an in vitro technique. The uptake rate was 5.876 +/- 1.942 nmol fatty acid/mg Nigrogen/minute and the esterification rate was 4.060 +/- 1.010 nmol fatty acid/mg Nitrogen/minute, comparable to previous adult esterification studies. No effect of age on either esterification or uptake was present. Mucosal injury resulted in significant reductions in esterification (p less than 0.001) and uptake (p less than 0.05) compared to controls. Bile acid deficiencies led to reductions in mucosal esterification (p less than 0.05) but not uptake.

Bile Acids and Salts↗

PubMed1975

Effects of administration of hypolipidemic agent, 2,2'''- [ (1-methyl-4, 4-diphenylbutylidene) bis (p-phenyleneoxy)] bistriethylamine oxalate (SQ 10,591) upon cholesterol esterification by aorta, adrenal, and testes of cholesterol-fed rabbits].

Administration of 2,2'''-([1-methyl-4, 4-diphenylbutylidene] bis(p-phenyl-eneoxy]) bistriethylamine oxalate (SQ 10,591) at 20 mg/Kg daily for 5 days to cholesterol-fed rabbits resulted in no change in aortic microsomal cholesterol esterification with a palmitoyl coenzyme A substrate or of aortic mitochondrial cholesterol esterification with a palmitate substrate. Esterification by both reactions in the adrenal was much higher than in either aorta or testes. Adrenal and testicular mitochondrial esterification and testicular microsomal esterification were inhibited significantly after SQ 10,591 administration. In vitro addition of 0.0001 M SQ 10,591 significantly inhibited both microsomal and mitochondrial cholesterol esterification in aorta, adrenal, and testes.

Adrenal Glands↗

PubMed1976

The esterification of exogenous fatty acids by adipose tissue of hypertriglyceridaemic subjects with or without diabetes mellitus.

1. The esterification of exogenous palmitate to diglyceride and triglyceride in adipocytes was studied in obese and diabetic patients with and without hypertriglyceridaemia. The rate of esterification correlated significantly with the triglyceride content of adipocytes. 2. In diabetic patients with hypertriglyceridaemia, the rate of esterification to triglyceride was significantly greater than in diabetic patients with normotriglyceridaemia. This difference could not be attributed to differences in glucose tolerance or to the degree of obesity. 3. Fasting plasma insulin levels were greater in the hypertriglyceridaemic group than in the normotriglyceridaemic group. The difference in esterification rates could have been due to differences in adipocyte size. 4. The esterification of fatty acid in adipose tissue of diabetic patients was lower than in non-diabetic subjects and this difference could not be accounted for by differences in adipocyte size or differences in the intracellular pools of fatty acid in adipose tissue. 5. The role of esterification of exogenous fatty acids in adipose tissue as a possible determinant of the uptake of glyceride fatty acids from plasma is discussed.

Adipose Tissue↗

PubMed1977

Plasma cholesterol esterification in hypertriglyceridaemia.

Plasma cholesterol esterification was assessed in hypertriglyceridaemic patients and normal subjects by two in vitro methods, one using autologous substrate and one using exogenous substrate. There was a significant negative correlation between cholesterol esterification rate and the plasma triglyceride concentration when this was assessed with autologous substrate or with substrate from a hypertriglyceridaemic donor. The percentage of esterified cholesterol in plasma and the esterification rate were always reduced when the plasma triglyceride concentration exceeded 7 mmol/1 and the rate of esterification rose significantly with appropriate triglyceride-lowering therapy in such patients. Evidence is presented that the impaired cholesterol esterification observed in severe hypertriglyceridaemia is secondary to a reduced concentration of substrate high density lipoprotein cholesterol, as well as to an excess of large triglyceride-rich lipoproteins.

Adult↗

PubMed1978

Effect of sugar and monoglyceride on fatty acid esterification.

The effect of hexose and monoolein on fatty acid esterification was studied in everted rings of rat jejunum. By use of [3H]oleic acid and [U-14C]glucose, esterification via both phosphatidic acid and monoglyceride pathways was quantified. Our results showed that 1) metabolizable sugars stimulate fatty acids esterification regardless of their mode of transport; 2) in the presence of glucose alone, in vitro fatty acid esterification is mediated entirely by the phosphatidic acid pathway; 3) glucose stimulates both esterification pathways in the presence of monoolein; 4) monoolein stimulates only the monoglyceride pathway and has no effect on the phosphatidic acid pathway; and 5) the rate-limiting factor in the presence of monoolein alone is the formation of acyl-CoA, whereas in the presence of glucose alone, the rate-limiting factor is the formation of alpha-glycerophosphate.

Acyl Coenzyme A↗

PubMed1975

Substrate specificity of lecithin:cholesterol acyltransferase. Esterification of desmosterol, b-sitosterol, and cholecalciferol in human plasma.

Desmosterol and beta-sitosterol were esterified when incubated with normal human plasma. The initial rate of demosterol esterification was 1.7 times faster, and that of beta-sitosterol 0.4 times slower, than the esterification rate of cholesterol. These ratios were found to be almost the same when plasma from different normal individuals was tested. Plasma from a patient with familial lecithin:cholesterol acyltransferase deficiency did not esterify any of the sterols. The esterification of desmosterol and beta-sitosterol was considerably slower in normal plasma in which in vitro cholesterol esterification previously had taken place. The different esterification rates could not be explained by a different affinity of the plasma lipoproteins for the sterols tested. Cholecalciferol added to normal plasma did not become esterified.

Acyltransferases↗

PubMed1977

In vitro cholesterol esterification in human serum.

We report a simple, convenient, and reproducible method, involving the use of radiolabeled cholesterol dispersed in Tween 20 as a tracer and endogenous lipoproteins as a substrate, for measuring the rate of serum cholesterol esterification in vitro. The reaction of lecithin acyltransferase (EC 2.3.1.43) was enhanced by the presence of Tween 20, which probably accelerates the exchange between radiolabeled cholesterol and endogenous lipoprotein cholesterol. In sera from 65 normal subjects, the in vitro cholesterol esterification rate was significantly correlated (r=0.47,P=0.001) with age. The mean rate of esterification of 31 subjects 30 years old or younger was significantly lower than that of 34 subjects 31 to 64 years of age. We found no significant difference in the rate of esterification between men and women. The rate of cholesterol esterification (nmol/ml per h) was significantly correlated with the concentration of endogenous free cholesterol in serum, but the fractional rate (the percentage of radiolabeled cholesterol esterified per hour) was inversely proportional to the endogenous free cholesterol. The fatty acid composition of the cholesteryl esters formed by the acyltransferase reaction may provide an index in recognizing some specific disorder.

Adolescent↗

PubMed1992

Esterification of fatty acids by bovine intramuscular and subcutaneous adipose tissues.

Exogenous fatty acid esterification in intramuscular and subcutaneous adipose tissues from 72-hr fasted or ad libitum fed Angus cattle was investigated. Intramuscular (interfascicular) and subcutaneous adipose tissue snips were obtained from the longissimus dorsi muscle and were incubated with radioisotopically labeled fatty acids (palmitate, stearate, oleate, linoleate or linolenate) at three different concentrations (0.3 mM, 0.6 mM and 2.0 mM) to assess rates of fatty acid incorporation into glycerolipids. Rates of fatty acid esterification in vitro increased with fatty acid concentration in both intramuscular and subcutaneous adipose tissues. For all of the fatty acids investigated, triglycerides were the predominant products (60-85%). Subcutaneous adipose tissue had larger adipocytes and more actively (P less than 0.05) esterified fatty acids, with the exception of palmitate, than intramuscular adipose tissue. The rate of palmitate esterification was not different between tissues, although intramuscular adipose tissue esterified a greater proportion (P less than 0.10) of palmitate as triglyceride (85%) than did subcutaneous adipose tissue (75%). Relative rates of incorporation of fatty acids into lipids in intramuscular and subcutaneous adipose tissues were: palmitate greater than linolenate greater than linoleate greater than stearate. In general, 72-hr fasting did not significantly reduce the rates of fatty acid incorporation in bovine adipose tissues. Results of this study revealed that:i) rates of exogenous fatty acid incorporation into adipose tissue lipids were dependent on the medium fatty acid concentration and adipose tissue depot; and ii) the relative esterification rates of the various fatty acids in vitro did not necessarily reflect the proportion of these fatty acids in bovine adipose tissues.

Adipose Tissue↗

PubMed1992

Modulation of sphingomyelinase-induced cholesterol esterification in fibroblasts, CaCo2 cells, macrophages and smooth muscle cells.

The present study has focused on three questions concerning the effect of sphingomyelinase on release of free cholesterol from the plasma membrane and its intracellular translocation: (i) Can one change the direction of the flow of cholesterol? (ii) Can one modulate the flow? (iii) May such a mechanism be relevant in atherogenesis? (i) The results obtained show that even in the presence of potent nonlipoprotein cholesterol acceptors in the medium, the intracellular flow of cholesterol is not reduced as measured by cholesterol esterification. Moreover, in sphingomyelinase-treated cells, cholesterol efflux in presence of nonlipoprotein acceptors was not enhanced even when intracellular esterification was inhibited. (ii) Modulation of the sphingomyelinase induced cholesterol flow can be obtained by 100 microM verapamil which reduces it. In human skin fibroblast, interference with the delivery of free cholesterol to its site of esterification was found in the presence of brefeldin A. (iii) Aortic smooth muscle cells in culture are sensitive to low concentrations of sphingomyelinase and the increase in esterified cholesterol is evident also after exposure to the enzyme for 24 h. The present results suggest that in the plasma membrane, free cholesterol bound to sphingomyelin may be in a compartment which renders it more available for transport to the cell interior than for efflux. In view of the sensitivity of aortic smooth muscle cells to sphingomyelinase, this mechanism for enhanced esterification of cholesterol could be relevant to the transformation of arterial smooth muscle cells into foam cells in the process of atherogenesis.

Brefeldin A↗

PubMed1978

Relationship between high density lipoproteins and the rate of in vitro serum cholesterol esterification.

The rate of in vitro esterification of serum cholesterol and the concentrations of serum high density lipoprotein cholesterol (HDL-C) were measured in 18 women and 9 men, 74--95 years of age. Subjects in this age group can have HDL-C levels below accepted limits of normal. The subjects were divided into two groups, one with HDL-C less than 40 mg/dl and the other with HDL-C 40 mg/dl or higher. The rate of in vitro serum cholesterol esterification in the former group was 2.00 n. moles/ml/min, significantly higher (p less than 0.02) than 1.62 n. moles/ml/min present in the latter group. There was no correlation between the cholesterol esterification and a protein (s), which can produce an immune gamma globulin that completely inhibits in vitro serum cholesterol esterification. These findings are discussed with reference to the putative relationships between HDL-C and atherosclerosis.

Aged↗

PubMed1979

Esterification of cholesterol in fish plasma: studies on the cholesterol esterifying enzyme in plasma of char (Salmo alpinus L.).

1. Plasma of sea char (Salmo alpinus L.) has the ability to esterify cholesterol in vitro. Heat inactivation of the plasma totally inhibited the esterification. 2. Arrhenius plot of the esterification of [3H]cholesterol was linear in the temperature range 5-35 degrees C. 3. Cholesterol esterification in sea char plasma could not be reversibly inhibited by sulphydryl-blocking agents. Total equilibration of the added [3H]cholesterol and the endogenous cholesterol could therefore not be obtained. 4. Comparison of esterification of endogenous and labelled cholesterol revealed that the isotopic method was valid only in qualitative measurements.

Animals↗

PubMed1978

Serum cholesterol esterification in hyperthyroidism and hypothyroidism.

The rate of serum cholesterol esterification was measured in twenty healthy subjects and compared to similar data obtained with seventeen hyperthyroid and ten hypothyroid subjects. No significant differences were noted in the rate of cholesterol esterification while differences in the fractional rates were highly significant (p less than 0.001); the hyperthyroid group being higher and the hypothyroid group lower than normal. There were no clear trends observed in the changes of the rate of cholesterol esterification upon therapy. However, the fractional rates always increased when hypothyroid patients became euthyroid and always decreased in hyperthyroid patients as the result of therapy.

Cholesterol↗

PubMed1979

Enzymatic methyl esterification of pituitary polypeptides.

Methyl esterification of pituitary polypeptides by protein methylase II (S-adenosylmethionine:protein-carboxyl O-methyltransferase, EC. 2.1.1.24) has been investigated. Ovine lutropin and adrenocorticotropin (alpha1-39-ACTH) were found to be good methyl acceptor substrates, followed by beta-lipotropin. While the alpha-subunit of lutropin had nearly equal the methyl accepting activity of lutropin, the beta-subunit was devoid of accepting activity. The maximum amount of esterification occurred between 15 and 30 min at 37 degrees C) depending on the methyl acceptor molecule. The rate of the methyl esterification of adrenocorticotropin fragments was also studied. While alpha7-38-ACTH had less than half of alpha1-37-ACTH methyl accepting capacity, alpha1-17-ACTH did not serve as methyl acceptor. However, when a mixture of the two fragments was preincubated, the resulting mixture had full alpha1-39-ACTH activity.

Adrenocorticotropic Hormone↗

PubMed1992

Scavenger receptor-independent stimulation of cholesterol esterification in macrophages by low density lipoprotein extracted from human aortic intima.

There is a growing body of evidence that suggests that modification of low density lipoprotein (LDL) in the artery wall may contribute to atherogenesis. A number of physiologically plausible modifications have been studied in vitro, including oxidation, aggregation, formation of complexes with glycosaminoglycans, and generation of LDL-immune complexes. Several studies of the properties of LDL extracted from the aortic intima have been published, but these indicate disagreement about both the nature and the extent of modification of LDL in the artery wall. The objectives of the present study were to determine the nature and extent of modification of LDL extracted from both normal and diseased human aortic intimas and to correlate this with the rate of LDL uptake in cultured cells. Analyses were performed on LDLs isolated from aortic intimas obtained at autopsy or at the time of organ harvest from 33 subjects. LDL from normal intima showed no clear evidence of oxidation but had slightly increased electrophoretic mobility compared with native plasma LDL, whereas LDL from plaques or fatty streaks exhibited variable but usually modest signs of oxidative change. Aortic LDL was more rapidly degraded by cultured macrophages than was plasma LDL and resulted in a greater stimulation of cholesterol esterification. The degree of stimulation of cholesterol esterification was correlated with the extent of modification of LDL as reflected by the degree of apolipoprotein B fragmentation. However, in all aortic LDLs the extent of oxidative change, as assessed by electrophoretic mobility or other physical parameters, was less than that required for scavenger receptor-mediated uptake. In all cases where sufficient amounts of LDL were recovered to permit degradation experiments, the uptake of aortic LDL was nonsaturable and could not be inhibited by polyinosinic acid or acetylated LDL. Chromatography on Sepharose CL-4B showed that most LDLs isolated from plaque contained a fraction that eluted in the void volume, and the size of this void peak correlated well with the stimulation of cholesterol esterification. Electron microscopy showed that the high-molecular-weight fraction contained several different types of aggregates. Some appeared to be clusters of LDL-size particles, but large vesicular structures with numerous adherent LDL particles as well as lipid droplets were also identified. These results indicate that the accelerated uptake by macrophages of LDL isolated from the arterial intima can largely be attributed to phagocytosis of LDL-containing aggregates.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗