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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Cholesterol intake (about 0-25 mmol/day) and the faecal excretion of cholesterol, coprostanol and coprostanone were determined in normolipidaemic control subjects and hyperlipidaemic patients, whose bile acid kinetics had been previously studied. 2. The combined excretion of the neutral steroids (excluding plant sterol and plant sterol metabolites) averaged 1-07 +/- 0-13 (+/-SEM)mmol/day in the control subjects (n=14). The corresponding values in patients with hyperlipoproteinaemia type IIa (n=19), IIb (n=12) and IV (n=23) were 0-86 +/- 0-10, 0-93 +/- 0-11 and 1-48 +/- 0-17 mmol/day respectively. 3. The mean values for the net steroid "balance", defined as the combined amount of bile acid synthesized (determined by an isotope-dilution technique) and the faecal excretion of neutral steroids minus cholesterol intake, were 1-83 +/- 0-22 mmol/day in the control subjects and 1-60 +/- 0-15, 1-81 +/- 0-19 and 3-53 +/- 0-23 mmol/day in patients with type IIa, IIb and IV lipoprotein patterns respectively. 4. No significant correlations between net steroid "balance" and sex, age, serum lipid concentrations, body weight or body surface area were found in any of the groups of subjects. 5. It is concluded that patients with type II hyperlipoproteinaemia eliminate cholesterol as bile acids and neutral faecal steroids normally. The type IV lipoprotein pattern is associated with increased bile acid synthesis and/or elevated faecal excretion of neutral steroids, so that the net steroid "balance" is usually above the normal limit.
Clin Sci Mol Med 1976 Oct
PMID:Elimination of cholesterol in hyperlipoproteinaemia. 97 79

1. Cholesterol esterification has been studied in the plasma of subjects on diets rich in saturated or polyunsaturated fat. 2. The diet rich in polyunsaturated fat was associated with lower rates of plasma cholesterol esterification in vitro. The data suggest that there was a reduction of plasma lecithin-cholesterol acyltransferase activity as well as decreased ability of the lipoprotein substrates of the enzyme to support esterification. 3. On this diet, there was no change in the proportion of the plasma cholesterol esterified but the plasma cholesterol and triglyceride concentrations were reduced.
Clin Sci Mol Med 1975 Dec
PMID:The relationship between dietary fat composition and plasma cholesterol esterification in man. 120 93

High concentrations of phospholipids determine destabilization of F1 histone-DNA complex at the weight ratios, histone:DNA, 0.8:1 and 1:1, but low concentrations cause only negligible destabilization. Cholesterol at high weight ratios has little effect on nucleohistone stability. Only linolenic acid of the fatty acids used reproduces similar changes in the thermal stability of F1 histone-DNA complex as phospholipids. The type of interaction of phospholipids with the F1 histone-DNA complex is analyzed, and the involvement of phospholipids in DNA replication in vivo is discussed.
Mol Cell Biochem 1976 Feb 25
PMID:Lipid-F1 nucleohistone interactions. 126 76

Cholesterol ester hydrolase (CEH) activity was characterized in the porcine adrenal gland and experiments conducted to determine the nature of its hormonal regulation. CEH activity was studied in the 14,000 gmax pellet (F4) and in the 192,000 gmax supernatant (F6). Characteristics associated with pH optima, product formation with time, linearity with increasing protein concentration, and equilibration of exogenous cholesterol esters added in acetone with endogenous cholesterol esters were determined. Scatchard analyses of saturation data demonstrated two-site models, which indicated the presence of lower velocity lower Km enzymes (catalytic sites) (L-VKm) and higher velocity higher Km enzymes (catalytic sites) (H-VKm) in both subcellular fractions. Neither ACTH (0.4 micrograms/kg body weight) nor 30-min restraint affected CEH activities at 0.5, 2, and 5 h after injection or initiation of restraint. However, 1 h after a longer restraint period (45 min), F4 H-VKm CEH activity increased concomitantly with decreased F6 L-VKm (P = 0.003). More modest increases in F4 H-VKm (P = 0.03) were still apparent 1 h after the last of nine daily 45-min restraints. Bromocriptine (CB154, a dopamine agonist) administration for 6 days (9.6 mg/daily) reduced plasma prolactin (PRL) by 53% (P < 0.05), but had no effect on CEH activities. ACTH treatment to CB154-induced hypoprolactinemic barrows dramatically reduced F4 (63%) and F6 (49%) L-VKm CEH activity (P = 0.03). These data are the first concerned with regulation of adrenal CEH activity in swine, and are the first to evaluate in vivo treatments on in vitro CEH activity in any species evolutionarily higher than rodents. In vivo regulation of porcine adrenal CEH activity appears complex. Stressor-associated hormonal perturbations apparently must surpass a certain threshold of duration and/or magnitude before they alter CEH activity. Differing Km and Vmax of CEH within and between the two subcellular fractions studied and the differential responses to restraint stressor suggest that as many as four different enzymes with CEH activity are involved. Additionally, the combined effect of ACTH and CB154-induced hypoprolactinemia argues for an interrelated modulatory function of ACTH and PRL (or dopamine) on specific porcine adrenal CEH activities.
J Steroid Biochem Mol Biol 1992 Dec
PMID:Hormonal and stressor-associated changes in porcine adrenocortical cholesterol ester hydrolase activity. 133 79

The present study correlated the reversibility of bile flow (BF) impairment with biochemical and morphological changes in the liver after injection of a cholestatic dose (12 mumole/100 g body weight) of lithocholic acid (LCA). BF declined maximally at 60 min but recovered totally at 210 min after LCA treatment. During the cholestatic period, there was an increase in tight junction permeability as measured by the bile to plasma (B/P) ratio of inulin and using lanthanum as a tracer. Cholesterol content and the cholesterol/phospholipid ratio in liver plasma membranes (LPM) were augmented while the fluidity of bile canalicular membranes (BCM) was decreased at 30 and 60 min after LCA injection. These changes in cholesterol content and membrane fluidity seemed to be correlated with LCA incorporation in LPM; their reversal at 120 min preceded the recovery of BF (210 min). Some biochemical disorders were evident after LCA injection, but they did not correlate with the variation in BF. These data suggest that increased tight junction permeability and decreased BCM fluidity are important pathogenic steps in LCA-induced cholestasis.
Exp Mol Pathol 1992 Aug
PMID:Tight junction permeability and liver plasma membrane fluidity in lithocholate-induced cholestasis. 139 92

In the mole crab Emerita asiatica, the main yolk proteins consist of two slow moving lipovitellins (Lv I and Lv II) of glycolipoprotein nature. Lv I cleaves into subunits (MW: 109,000 and 105,000) and Lv II gives rise to six subunits (MW: 65,000, 54,000, 50,000, 47,000, 44,000, and 42,000) in SDS-PAGE (with beta-mercaptoethanol). In order to observe the stability of Lv II as well as to achieve better resolution of the proteins, two different buffer systems (Phosphate buffered saline and tris-buffered saline), 40% sucrose, and glass distilled water were used as homogenizing media. Among them, better resolution was achieved with tris-buffered saline and 40% sucrose, and tris-buffered saline seems to be the ideal medium for elution of Lv II. The analysis of biochemical constituents of the major Lv II reveals a percentage composition of 69.325, 27.927, and 2.753 respectively for protein, lipid, and bound sugars. In the I stage embryo, protein comprises about 67.276%, lipid 29.65%, and bound sugars 3.015%. Vitellogenin (Vg) electrophoretically corresponding to the Lv I and Lv II was present in the female haemolymph during the entire period of embryogenesis. The number of subunits (8) of Vg in all stages remained unaltered and their approximate molecular weights were Vg1, 91,000; Vg2, 87,000; Vg3, 83,000; Vg4, 61,000; Vg5, 58,000; Vg6, 45,000; Vg7, 42,000; and Vg8, 38,000. Different proteins present in the embryos (I and IV stage) and the serum obtained from the animal carrying the I stage embryo were separated by gel-filtration in high performance liquid chromatography (HPLC). Sephadex (G-200) gel filtration chromatography was used to purify the Lv II in large quantity. Total lipid extracted from Lv II as well as the embryos belonging to different stages of development were separated into their constituent neutral, glycolipids, and phospholipids, using silicic acid column chromatography. Thin layer chromatography (TLC) was used to isolate the different phospholipids purified from various stages of embryos and Lv II. As many as seven different phospholipids were separated from Lv II and I and IX stage embryos; and whereas thin layer chromatogram of V and VI stage embryos showed six different phospholipids, embryos of VII and VIII stage contained four phospholipid species. Cholesterol, glycolipids, and individual phospholipids isolated from the Lv II and I stage embryo were quantified spectrophotometrically and the results were discussed.
Mol Reprod Dev 1992 Sep
PMID:Purification and characterization of vitellogenin and lipovitellins of the sand crab Emerita asiatica: molecular aspects of crab yolk proteins. 151 Aug 41

Cholesterol and cholesteryl ester concentrations and cholesteryl ester fatty acid substituents have been measured during the first 10 weeks of life in tissues of normal and dystrophic mice. In normal Swiss and 129ReJ(+/?) mice the concentrations of both cholesterol and cholesteryl esters remain essentially constant in liver, increase in brain and fall sharply in both thigh (mixed fiber type muscles) and chest muscles (predominantly slow oxidative muscles) over this period. In all cases the concentration of free cholesterol exceeds that of esterified cholesterol. In dystrophic mice, similar patterns are found in brain and liver. In both thigh and chest muscles, however, the developmental pattern is significantly different. After an initial decrease the concentrations of cholesterol and cholesteryl esters increase rapidly with the largest increase occurring in the concentration of cholesteryl esters which by 10 weeks of age exceeds the concentration of cholesterol in chest muscle. During the same period the pattern of esterified fatty acids changes gradually in dystrophic tissues towards an increasing ratio of unsaturated/saturated fatty acids. By 10 weeks of age this ratio is significantly higher in dystrophic tissues than normal in all tissues tested.
Mol Cell Biochem 1992 Mar 04
PMID:Cholesterol alterations in young dystrophic mice. 157 32

On repeated thawing at room temperature of frozen preparations of heavy microsomes from rat livers, HMGCoA reductase activity was solubilized due to limited proteolysis. This soluble enzyme was partially purified by fractionation with ammonium sulfate and filtration on Sephacryl S-200 column. The active enzyme was coeluted with a major 92 kDa-protein and was identified as a 58 kDa-protein after separation by SDS-PAGE and immunoblotting. Ethoxysilatrane, a hypocholesterolemic compound, which decreased the liver-microsomal activity of HMGCoA reductase on intra-peritonial treatment of animals, showed little effect on the enzyme activity with isolated microsomes or the 50 kDa-soluble enzyme when added in the assay. But it was able to inhibit the activity of the soluble 58 kDa-enzyme in a concentration-dependent, reversible manner. Cholesterol and an oxycholesterol were without effect whereas chlorophenoxyisobutyrate and ubiquinone showed small inhibition under these conditions. The extra region that links the active site domain (50 kDa protein) to the membrane, present in the 58 kDa-protein appears to be involved in mediating the inhibition by silatrane.
Mol Cell Biochem 1992 Mar 25
PMID:Preparation of a soluble 58 kDa-3-hydroxy-3-methylglutaryl CoA reductase from liver microsomes and its inhibition by ethoxysilatrane, a hypocholesterolemic compound. 158 3

Newborn rat glial cells in primary culture contain an active cholesterol side chain cleavage cytochrome P450. Cholesterol can be supplied either by biosynthesis or derive from low density lipoproteins (LDL), which bind apolipoprotein Band E (apoB,E) (LDL)-receptors and undergo receptor-mediated endocytosis. Using antibodies to purified human plasma LDL and antibodies to bovine adreno-cortical LDL-receptor, the presence of LDL-receptors was demonstrated on rat glial cells after 3-4 weeks of primary culture, by ligand blotting, immunoblotting, and indirect immunofluorescence staining. The latter approach indicated that oligodendrocytes express higher levels of LDL-receptors than astrocytes present in the same culture. The immunofluorescence staining was observed not only at the cell surface, but also within the cytoplasm, suggesting that the LDL-receptor complexes had been internalized. Western blotting of LDL-receptors extracted from glial cells indicated a band of approximately 130 kDa, the size expected for intact receptors. Their functionality was shown by the conversion of [3H]cholesterol linoleate, incorporated into reconstituted LDL and added to the cell cultures, to [3H]pregnenolone and/or its 20 alpha-hydroxy-metabolite. This is the first characterization of functional LDL-receptors on isolated, well characterized, normal brain cells.
J Steroid Biochem Mol Biol 1992 Jul
PMID:Low density lipoprotein-receptors in primary cultures of rat glial cells. 163 23

Cholesterol oxidase (3 beta-hydroxy-steroid oxidase) catalyzes the oxidation of cholesterol to 4-cholesten-3 one and other oxidized cholesterol derivatives. The purpose of the present study was to investigate its effects on cultured vascular smooth muscle cells. Cultured rabbit aortic smooth muscle cells were morphologically altered after exposure to cholesterol oxidase in the presence of culture medium containing 10% fetal calf serum. If fetal calf serum was absent, cells were unaffected by the treatment. The extent of morphological change of the smooth muscle cells was dependent upon the time of exposure to the enzyme and the concentration of cholesterol oxidase employed. After moderate treatment with cholesterol oxidase, cells excluded trypan blue. Further, a specific mitochondrial marker DASPMI (dimethyl aminostyryl-methyl-pyridiniumiodine) which was used as a fluorescent index of cell viability, revealed that cell viability was unchanged after moderate cholesterol oxidase treatment. Nile red, a hydrophobic probe which selectively stains intracellular lipid droplets, was applied to detect the cellular lipid content after treatment with cholesterol oxidase. Cellular nile red fluorescence intensity increased linearly with the time and concentration of cholesterol oxidase treatment. These results demonstrate that cholesterol oxidase alters lipid deposition in the cell and changes cell morphology. The primary site of action of cholesterol oxidase appears to be independent of the cell membrane itself and instead is dependent upon the lipid content in the surrounding culture media. These changes occur prior to the cytotoxic effects of extensive oxidation. Because oxidized cholesterol may play an important role in the pathogenesis of atherosclerosis, our results have implications for intracellular accumulation of lipids in smooth muscle cells during the atherosclerotic lesion.
Mol Cell Biochem 1991 Nov 13
PMID:Effects of cholesterol oxidase on cultured vascular smooth muscle cells. 177 Sep 44


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