Cholesterol Journal Articles

Record 4401 to 4420

Differential subcellular localization of cholesterol, gangliosides, and glycosaminoglycans in murine models of mucopolysaccharide storage disorders
McGlynn, R., K. Dobrenis, et al. (2004), J Comp Neurol 480(4): 415-26.
Abstract: The mucopolysaccharidoses (MPSs) are a complex family of lysosomal storage disorders characterized by failure to degrade heparan sulfate (HS) and/or other types of glycosaminoglycans (GAGs) secondary to the absence of specific lysosomal enzymes. An accompanying storage of glycosphingolipids (GSLs), most notably GM2 and GM3 gangliosides, has also been documented to occur in many types of MPS disease and is believed to be caused by secondary inhibition of GSL-degradative enzymes by intracellular GAG accumulation. We have documented the presence of secondary ganglioside accumulation in mouse models of several MPS disorders (types I, IIIA, IIIB, and VII) and report that this storage is accompanied by sequestration of free cholesterol in a manner similar to that observed in primary gangliosidoses. Using confocal microscopy, we evaluated the cellular distribution of cholesterol, GM2 and GM3 gangliosides, and HS in brains of mice with MPS IIIA disease. Unexpectedly, we found that although both gangliosides often accumulated in the same neurons, they were consistently located in separate populations of cytoplasmic vesicles. Additionally, GM3 ganglioside only partially co-localized with the primary storage material (HS), and cholesterol likewise only partially co-localized with the GM2 and GM3 gangliosides. These findings raise significant questions about the mechanism(s) responsible for secondary accumulation of storage materials in MPS disease. Furthermore, given that GSLs and cholesterol are constituents of membrane rafts believed critical in signal transduction events in neurons, their co-sequestration in individual neurons suggests the presence of defects in the composition, trafficking, and/or recycling of raft components and thus possible new mechanisms to explain neuronal dysfunction in MPS disorders.

Differentially expressed aortic genes in cholesterol-fed rabbits
Gyun Kim, T., M. Kyoo Jang, et al. (1998), Mol Cells 8(3): 324-9.
Abstract: In order to identify key genes involved in the development of atherosclerotic lesions, differentially expressed genes in atherosclerotic plaques obtained from diet-induced hypercholesterolemic rabbit aorta were screened using the differential display (DD) RT-PCR technique. Aortic RNAs were isolated from rabbits fed cholesterol-supplemented (2% cholesterol in lab-chow, w/w) chow diet for 12 weeks, followed by the synthesis of cDNAs by reverse-transcription using 2-base anchored oligo (dT) (5'-T11VN) as 3'-primers. Synthesized cDNAs were amplified by PCR using arbitrary 10-mers as 5'-primers and the same 3'-primers used in the reverse-transcription. Amplified cDNAs sized between 0.2 to 0.5kb obtained from control and cholesterol-fed rabbit aortas were displayed on the 6% DNA-sequencing gel for comparisons. The cDNA bands showing distinctive differences in patterns of display or in density of the band were extracted from the gel. A total of 66 differentially displayed cDNAs was isolated and subjected to the reverse-Northern and Northern blot analyses in order to confirm the differences. Through the extensive confirming processes, three cDNAs were finally selected (designated CRGRA-1 through -3) and their nucleotide sequences were determined. Two of those (CRGRA-1 and -2) were determined to be up regulated and the other (CRGRA-3) was down-regulated by the cholesterol-feeding. Upon homology search on databases for the identification of the genes, the first cDNA (CRGRA-1) turned out to be a part of a novel gene, the second one (CRGRA-2) was homologous (82%) to the corresponding segment of mitochondrial NADH dehydrogenase subunits 4 gene, and the last one (CRGRA-2) was identified to be homologous (94%) to a segment of human small GTP-binding protein (Rab7) gene.

Differentially expressed genes in cultured aortic smooth muscle cells by cholesterol-loading
Byun, S. J., M. K. Jang, et al. (1998), Mol Cells 8(6): 657-62.
Abstract: Differentially expressed genes generated by cholesterol-loading in the culture medium of aortic smooth muscle cells (SMC) were screened using the DDRT-PCR technique in order to identify the genes that are possibly involved in the pathogenesis of atherosclerosis in the artery. Twenty-eight genes were initially isolated and three differentially expressed cDNAs were finally selected by Northern blot analysis. All three cDNAs were up-regulated (designated CRGSM-1 through -3) by the cholesterol-loading. Upon nucleotide sequencing and homology search in the databases, the first cDNA (CRGSM-1) had a high homology (97%) with the corresponding segment of the acyl-CoA synthetase II gene from rat brain, which participates in fatty acid synthesis. The second one (CRGSM-2) had a high homology (91%) with a part of Mus musculus (mouse) LIM protein 1, and with human skeletal muscle LIM-protein 1 genes (80%) and the third gene (CRGSM-3) had no significant homology match in the database. A full size cDNA isolated from the cDNA library of rat aortic smooth muscle cell using the CRGSM-2 as a probe was identified to have a high homology with muscle LIM protein (MLP). The isolated cDNA contained a segment of DNA that encodes for a zinc-finger motif and two LIM domains. Proteins bearing the LIM domain, defined as a unique double zinc-finger structure associated with a subclass of proteins involved in the determination of cell identity, cell differentiation and control of cell growth, have previously been suggested to play an important role in the pathogenesis of atherosclerosis by others.

Differentiating the effects of raising low levels of high-density lipoprotein cholesterol versus lowering normal triglycerides: further insights from the Veterans Affairs High-Density Lipoprotein Intervention Trial
Miller, M. (2000), Am J Cardiol 86(12A): 23L-27L.
Abstract: In the Veterans Affairs High-Density Lipoprotein Intervention Trial (VA-HIT), a 6% increase in high-density lipoprotein cholesterol (HDL-C) was associated with a 22% reduction in the incidence of fatal and nonfatal myocardial infarction and death from coronary artery disease. A curvilinear correlation was demonstrated between incremental changes in HDL-C and outcome. However, triglyceride levels, which decreased by 31%, were not predictive of clinical events. Some design limitations may be implicated in this lack of statistical correlation between triglycerides and outcome. Evidence from other studies, notably the Framingham Heart Study, the Prospective Cardiovascular Munster Heart Study (PROCAM), and the Baltimore Coronary Observational Long-Term Study (COLTS) suggest that the triglyceride cutpoint of 200 mg/dL is too high. The Bezafibrate Infarction Prevention (BIP) trial found a significant correlation between reduction in death from coronary artery disease and nonfatal MI and reduced triglycerides in a subset of patients with baseline triglycerides >200 mg/dL.

Differentiation between calcium- and cholesterol-dominated types of arteriosclerotic lesions: antiarteriosclerotic aspects of calcium antagonists
Fleckenstein-Grun, G., M. Frey, et al. (1991), J Cardiovasc Pharmacol 18 Suppl 6: S1-9.
Abstract: In a series of animal studies we have clearly demonstrated since 1970 that calcium overload of the arterial wall is crucially involved in the pathogenesis of arteriosclerotic lesions. Following excessive calcium uptake, vascular stretch compliance and distensibility were lost together with structural integrity. Conversely, calcium antagonists that counteract abundant calcium uptake were found to prevent pathogenic mural calcium accumulation and damage. These effects were realized with light and electron microscopy as well as with measurements of calcium accumulation using atomic absorption spectrometry and radiocalcium. The experiments were carried out on rats exposed to various well-known risk factors such as nicotine, alloxan diabetes, high doses of vitamin D3, or dihydrotachysterol. Another particularly vasotoxic factor appeared to be hypertension, which develops in spontaneously hypertensive Okamoto rats (SHRs), in hypertensive NaCl-loaded salt-sensitive Dahl-S rats, and in rats with nephrogenic Goldblatt hypertension. Interestingly, aging arteries in animals and humans also exhibit, as a characteristic phenomenon, a steady increase in arterial calcium content. This natural age-dependent calcium accumulation is further enhanced in severe diabetics, heavy smokers, and hypertensive patients. However, the most excessive degree of toxic calcium overload, correlated with dramatic structural damage, occurred in human coronary artery plaques. Here, in "fatty streaks" (type I plaques according to World Health Organization classification), the mural calcium content exhibited a rise by 13 times above normal; in type II lesions (fibrous plaques), the increase in calcium was 24-fold; and in type III plaques, i.e., in "complicated lesions of stenosing character," calcium overload amounted to a value greater than 80 times above that found in healthy coronary segments.(ABSTRACT TRUNCATED AT 250 WORDS)

Differentiation of malignant and non-malignant origin of ascites by determination of levels of cholesterol and lactate dehydrogenase in ascitic fluid is not absolute
Gasko, R. and N. Klimova (2000), Vnitr Lek 46(1): 5-11.
Abstract: The authors Castaldo et al. (Clin. Chem., 1994, 30: 478-83) state, that the ascitic lactate dehydrogenase and ascitic cholesterol association correctly identified 100% of malignant ascites from ascites associated with cirrhosis and/or hepatocellular carcinoma, with help of stepwise multiple linear discriminant analysis. The free software Capsules--Ascites is via internet available (http: inverted question markwww.leeds.ac.uk/acb), which use the mathematical formula from this article. As we argue, Castaldo's state is not correct. Three independent multidimensional statistical methods--bivariate reference regions (program EVAL-KIT), cluster analysis (program BioAnalyst), geometrical distance classification (program GEODICLA) applicated on Castaldo's original data showed that lactate dehydrogenase and cholesterol have not satisfactory absolute discriminative power between malignant from nonmalignant ascites in general, but the probability to determinate the right diagnosis is about 91-93%. Research conducted in correctly selected probands should provide information which is valid not only for the selected sample but for the entire population, to achieve more generally valid conclusions, useful for practical decisions. In addition, in the compiled table show we sensitivity and specificity of different laboratory parameters publicated in 11 original articles in the nineties, all with diagnostic efficiency less 100%.

Differing effects of cholesterol and taurocholate on steady state hepatic HMG-CoA reductase and cholesterol 7 alpha-hydroxylase activities and mRNA levels in the rat
Shefer, S., L. B. Nguyen, et al. (1992), J Lipid Res 33(8): 1193-200.
Abstract: We investigated the effects of cholesterol, cholestyramine, and taurocholate feeding on steady state specific activities and mRNA levels of hepatic 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase and cholesterol 7 alpha-hydroxylase in the rat. Interruption of the enterohepatic circulation of bile acids (cholestyramine feeding) increased total HMG-CoA reductase activity 5-fold. Cholesterol and taurocholate administration suppressed total microsomal HMG-CoA reductase activities 87% and 65%, respectively. HMG-CoA reductase mRNA levels increased 3-fold with cholestyramine, did not decrease significantly with cholesterol feeding, but were markedly decreased after taurocholate treatment. Cholesterol 7 alpha-hydroxylase activity increased 4-fold with cholestyramine and 29% during cholesterol feeding, but decreased 64% with taurocholate. Cholesterol 7 alpha-hydroxylase mRNA levels rose 150% and 50% with cholestyramine and cholesterol feeding, respectively, but decreased 73% with taurocholate. The administration of cholesterol together with taurocholate prevented the decline in cholesterol 7 alpha-hydroxylase mRNA levels, but inhibition of enzyme activity persisted (-76%). Hepatic microsomal cholesterol concentrations increased 2-fold with cholesterol feeding but did not change with taurocholate or cholestyramine treatment. These results demonstrate that mRNA levels of HMG-CoA reductase are controlled by the hepatic taurocholate flux, whereas mRNA levels of cholesterol 7 alpha-hydroxylase are controlled by the cholesterol substrate supply. These end products, cholesterol and bile acids, exert post-transcriptional regulation on HMG-CoA reductase and cholesterol 7 alpha-hydroxylase, respectively.

Diffuse cholesterol embolism after fibrinolysis for myocardial infarction
Pochmalicki, G., P. Meunier, et al. (1993), Arch Mal Coeur Vaiss 86(2): 263-6.
Abstract: The authors report the case of a 57 year old man admitted to hospital 3 hours after the onset of an infero-latero-basal infarct who underwent thrombolytic therapy with intravenous streptokinase, in whom the immediate outcome was complicated by multiple cholesterol embolisation which cause renal failure, mesenteric ischemia, medullary ischemia and livedo reticulosis of the lower half of the body complicated by gangrene of the toes, despite the fact that cardiac catheterisation had not been performed. This case (fifth reported case) of multiple cholesterol embolisation from the abdominal aorta caused by thrombolysis is the earliest presentation of this complication in the literature.

Diffuse progressive pulmonary interstitial and intra-alveolar cholesterol granulomas in childhood
Sato, K., H. Takahashi, et al. (1996), Eur Respir J 9(11): 2419-22.
Abstract: We describe an 18 year old male with pulmonary interstitial and intra-alveolar cholesterol granulomas (PICG), which developed to severe respiratory failure over 15 yrs. The histological diagnosis was made on the basis of open lung biopsy findings at the age of 3 yrs and autopsy at 18 yrs of age. Although the pathological features of the lung were similar to that of paediatric patients with lipoid pneumonia coexisting with pulmonary alveolar proteinosis (PAP), gastro-oesophageal reflux (GOR) and a diverse group of severe primary diseases, the patient lacked evidence for any of these. We believe the present case provides a new example of a diffuse-type of lipoid pneumonia coexisting with pulmonary alveolar proteinosis, which we call cholesterol granulomas.

Diffusion of substances into human cholesterol gallstones
Sanabria, J. R., G. A. Upadhya, et al. (1994), Gastroenterology 106(3): 749-54.
Abstract: BACKGROUND/AIMS: The possibility that substances penetrate gallstones and accumulate after stones have formed has not been examined. The specific aims of this study were to determine whether cholesterol gallstones are permeable and, if so, the effect of molecular weight on permeability. METHODS: Cholesterol gallstones from patients with multiple stones were collected during surgery and incubated in fluorescein solution or in solutions of fluoresceinated albumin or immunoglobulin (Ig) G. To determine egress from the stones, some stones were removed from the fluoresceinated solution after incubation and placed in bicarbonate buffer. The total area of the stone and the area of dye that had diffused into the calculi were calculated. To determine mass of penetrating IgG, stones were powdered after incubation, and IgG was measured by an enzyme-linked immunosorbent assay. RESULTS: All substances penetrated stones. Although all compounds tested diffused back out of the stones when they were replaced in buffer, proteins did so more slowly than fluorescein. CONCLUSIONS: Substances of different molecular weights can diffuse into and out of cholesterol gallstones. These findings must be taken into account when considering the role of substances contained in stones on stone formation and growth.

Dihydropyridine calcium antagonist modulates cholesterol metabolism and eicosanoid biosynthesis in vascular cells
Nicholson, A. C., O. R. Etingin, et al. (1992), J Cell Biochem 48(4): 393-400.
Abstract: Recent clinical studies have shown that calcium channel blockers can retard and possibly reduce the angiographic progression of coronary artery disease. Calcium channel blockers also inhibit dietary-induced atherosclerosis in animal models of this disease. In this study, we delineate potential cellular and molecular mechanisms by which nicardipine, a dihydropyridine calcium antagonist, may alter lipoprotein and cholesterol trafficking, affect the regulatory signal transduction pathways involved in accelerating cholesteryl ester (CE) catabolism in vascular smooth muscle cells, and modulate cell-cell interactions of vascular and inflammatory cells. We demonstrate in arterial smooth muscle cells that nicardipine increases 1) LDL binding, uptake, and degradation, 2) RNA transcript levels for the LDL receptor, 3) CE catabolic activity, 4) PGI2 release, and 5) RNA transcript levels for cyclooxygenase. Furthermore, nicardipine blocked cytokine-induced monocyte adhesion to endothelial cells and smooth muscle cells. Taken together, these findings support the hypothesis that nicardipine may function as an anti-atherosclerotic agent by promoting CE catabolism and cholesterol clearance and by reducing monocyte adhesion to the activated endothelium.

Diminished rate of mouse peritoneal macrophage cholesterol efflux is not related to the degree of HDL glycation in diabetes mellitus
Passarelli, M., A. F. Shimabukuro, et al. (2000), Clin Chim Acta 301(1-2): 119-34.
Abstract: The efflux of (14)C-cholesterol from mouse peritoneal macrophages mediated by in vivo and in vitro glycation of intact HDL(3) and by HDL(3) apolipoproteins was investigated. Cholesterol-laden cells were incubated a long time with HDL(3) from control subjects (C), poorly controlled diabetes mellitus patients (D) and with HDL C submitted to in vitro glycation (G), as well as with all their respectively isolated apolipoproteins. A diminished cholesterol efflux rate occurred in incubations with intact HDL(3) D but not with intact HDL(3)G or with apoHDL(3)C, G or D. The specific binding of (125)I-HDL(3)G to the cell receptor, obtained upon incubation in the absence and in the presence of excess unlabelled HDL(3), was lower than the control. The role of apoE secretion by cholesterol-laden macrophages on cholesterol efflux was analyzed by incubating apoE knockout and control mice macrophages with HDL C or HDL G: a lower cholesterol efflux was observed from apoE knockout macrophages but glycation of HDL(3) did not influence this process either. The diminished capacity to remove cholesterol by the HDL drawn from diabetic subjects must be attributed to other modifications of the lipoproteins, except for non enzymatic glycation. Thus, events that impair the cell cholesterol removal in diabetes mellitus are multifaceted.

Diosgenin-induced biliary cholesterol secretion in mice requires Abcg8
Kosters, A., R. J. Frijters, et al. (2005), Hepatology 41(1): 141-50.
Abstract: The plant sterol diosgenin has been shown to stimulate biliary cholesterol secretion in mice without affecting the expression of the adenosine triphosphate-binding cassette transporter heterodimer Abcg5/g8. The aim of this study was to investigate the mechanism of diosgenin-induced cholesterol hypersecretion and to identify the genes involved. Surprisingly, despite its lack of effect on Abcg5/g8 expression in wild-type mice, diosgenin did not stimulate biliary cholesterol secretion in mice deficient for Abcg8. Analysis of the kinetics of cholesterol secretion suggested that diosgenin probably activates a step before Abcg5/g8. To identify potential diosgenin targets, gene expression profiling was performed in mice fed a diosgenin-supplemented diet. Diosgenin feeding increased hepatic expression of genes involved in cholesterol synthesis as well as genes encoding for several cytochrome P450s. No significant change in expression of known cholesterol transporters was found. Comparison with published expression-profiling data for Srebp2-overexpressing mice, another mouse model in which biliary cholesterol secretion is elevated, revealed a number of genes with unknown function that were upregulated in both diosgenin-fed mice and mice overexpressing Srebp2. In conclusion, we found that although Abcg8 is essential for most diosgenin-induced biliary cholesterol hypersecretion, diosgenin probably does not interact directly with Abcg5/Abcg8, but rather increases cholesterol delivery to the heterodimer. Supplementary material for this article can be found on the HEPATOLOGY website (http://interscience.wiley.com/jpages/0270-9139/suppmat/index.html).

Dipalmitoylphosphatidylcholine (DPPC) and DPPC/cholesterol liposomes as predictors of the cytotoxicity of bis-GMA related compounds
Fujisawa, S., Y. Kadoma, et al. (2004), J Liposome Res 14(1-2): 39-49.
Abstract: In light of recent development, dental materials such as 2, 2-bis 4-2(-hydroxy-3-methacryloyloxypropoxy)phenyl propane, (bis-GMA); 2, 2-bis 4-(1-hydroxymethyl-2-methacryloxy)phenyl propane, (iso-bis-GMA); and triethyleneglycol dimethacrylate, (TEGDMA) were investigated to determine whether their phase transition properties (phase transition temperature, temperature width, cooperativity) could be induced in samples of DPPC or DPPC/cholesterol (CHOL) liposomes using differential scanning calorimetry (DSC). The changes in phase transition properties of DPPC liposomes caused by addition of TEGDMA were greater than those caused by addition of bis-GMA or iso-bis-GMA, but the extent of changes in the properties of DPPC/CHOL (10:1 or 4:1) liposomes declined in the order of bis-GMA > iso-bis-GMA > TEGDMA. The degree of alteration was related to the cytotoxicity of these compounds. DPPC/CHOL liposomes were found to be better predictors of cytotoxicity than DPPC liposomes. Whether the computational approach to studying the molecular mechanism of alteration is applicable using descriptors such as reactivity of energy of the highest occupied molecular orbital (HOMO) and/or lowest unoccupied molecular orbital (LUMO) was investigated, and the data suggested that these descriptors are useful for studying the interactive roles of dental materials.

Dipalmitoylphosphatidylcholine and cholesterol in monolayers spread from adsorbed films of pulmonary surfactant
Yu, S. H. and F. Possmayer (2001), J Lipid Res 42(9): 1421-9.
Abstract: Pulmonary surfactant forms a surface film that consists of a monolayer and a monolayer-associated reservoir. The extent to which surfactant components including the main component, dipalmitoylphosphatidylcholine (DPPC), are adsorbed into the monolayer, and how surfactant protein SP-A affects their adsorptions, is not clear. Transport of cholesterol to the surface region from dispersions of bovine lipid extract surfactant BLES(chol) with or without SP-A at 37 degrees C was studied by measuring surface radioactivities of 4-(14)Ccholesterol-labeled BLES(chol), and the Wilhelmy plate technique was used to monitor adsorption of monolayers. Results showed that transport of cholesterol was lipid concentration dependent. SP-A accelerated lipid adsorption but suppressed the final level of cholesterol in the surface. Surfactant adsorbed from a dispersion with or without SP-A was transferred via a wet filter paper to a clean surface, where the surface radioactivity and surface tension were recorded simultaneously. It was observed that 1) surface radioactivity was constant over a range of dispersion concentrations; 2) cholesterol and DPPC were transferred simultaneously; and 3) SP-A limited transfer of cholesterol.These results indicate that non-DPPC components of pulmonary surfactant can be adsorbed into the monolayer. Studies in the transfer of 1-(14)CDPPC-labeled BLES(chol) to an equal or larger clean surface area revealed that SP-A did not increase selective adsorption of DPPC into the monolayer. Evaluation of transferred surfactant with a surface balance indicated that it equilibrated as a monolayer. Furthermore, examination of transferred surfactants from dispersions with and without prespread BLES(chol) monolayers revealed a functional contiguous association between adsorbed monolayers and reservoirs.

Dipalmitoylphosphatidylcholine liposomes with soybean-derived sterols and cholesterol as a carrier for the oral administration of insulin in rats
Muramatsu, K., Y. Maitani, et al. (1996), Biol Pharm Bull 19(8): 1055-8.
Abstract: Dipalmitoylphosphatidylcholine (DPPC) liposomes with a soybean-derived sterol mixture (SS) or cholesterol (Ch) were examined as a carrier for the oral administration of insulin in rats. Four kinds of liposomes were prepared: liposomes containing SS or Ch (molar ratio of DPPC/X = 7:2 or 7:4, X = SS or Ch), respectively. The pharmacological availability was greater and the lag time for the glucose reduction was later in the order of DPPC/SS (7:4) > DPPC/SS (7:2) > DPPC/Ch (7:4) > > DPPC/Ch (7:2)-liposomes. This order appears to correspond well with that of the rigidity of the liposomal membrane. In particular, DPPC/SS (7:4)-liposomes reduced blood glucose levels for up to 21 h in rats after oral administration. The highest absolute pharmacological availability was 31.6% at a dose of 20.0 IU/kg of DPPC/SS (7:4)-liposomes among the liposomes in comparison to intravenous administration.

Direct and correlated responses to divergent selection for serum cholesterol concentration on day 56 in swine
Young, L. D., W. G. Pond, et al. (1993), J Anim Sci 71(7): 1742-53.
Abstract: Divergent selection for serum cholesterol concentration on d 56 was practiced in a four-breed, composite population for three generations. High and Low lines, representing high and low levels of serum cholesterol, respectively, were each maintained with approximately 10 males and 25 females per generation. Pigs from a contemporary Control line were evaluated only in the last generation. In the last generation, mean serum cholesterol concentration was significantly different among lines (107.1, 85.6, and 65.5 mg/dL for High, Control, and Low lines, respectively). Realized heritability was.31.33, and.31 for high, low, and divergent selection (SE =.03), respectively. Terminal evaluation indicated that average birth and weaning (28 d of age) weight was lower (P <.05) for Low pigs (1.25 and 6.25 kg, respectively) than for High pigs (1.43 and 7.10 kg, respectively) and was intermediate for Control pigs (1.34 and 6.53 kg, respectively). At 56 d of age, High (15.1 kg) and Control (13.5 kg) pigs were heavier (P <.05) than Low pigs (11.9 kg). However, pigs sampled after 56 d did not differ (P >.05) in average daily gain, 164-d weight, feed consumption, or feed efficiency. Serum cholesterol concentration at 165 d of age was significantly different among lines (110.1, 98.5, and 85.6 mg/dL for High, Control, and Low pigs, respectively), although differences were smaller than at 56 d of age. When slaughtered at approximately 106 kg (188 to 195 d of age), Low pigs had significantly shorter carcasses than High and Control pigs (77.5 vs 78.7 and 78.9 cm, respectively). Low pigs had significantly more fat at the first rib (5.70 vs 5.28 cm) than High pigs. Lines did not differ significantly for fat thickness at the last rib, last lumbar vertebrae or 10th rib, or for longissimus muscle area. At 60 d of gestation, ovulation rate, measured as number of corpora lutea, was lower (P <.05) for High (9.84 eggs) than for Low (11.79 eggs) or Control (11.17 eggs) gilts. Differences in ovulation rate were reflected in smaller but nonsignificant differences in number of fetuses (7.97, 9.00, and 8.55 fetuses for High, Low, and Control, respectively).

Direct assay method for LDL-cholesterol
Yoshino, G., T. Hirano, et al. (2001), Nippon Rinsho 59 Suppl 2: 778-87.

Direct association between high-density lipoprotein cholesterol and endothelial function in hyperlipemia
Lupattelli, G., S. Marchesi, et al. (2002), Am J Cardiol 90(6): 648-50.

Direct binding of cholesterol to the purified membrane region of SCAP: mechanism for a sterol-sensing domain
Radhakrishnan, A., L. P. Sun, et al. (2004), Mol Cell 15(2): 259-68.
Abstract: Mammalian cells control their membrane composition by regulating the vesicular transport of membrane-bound sterol regulatory element binding proteins (SREBPs) from endoplasmic reticulum (ER) to Golgi. Transport is blocked by cholesterol, which triggers SCAP, the SREBP escort protein, to bind to Insigs, which are ER retention proteins. The cholesterol trigger mechanism is unknown. Using recombinant SCAP purified in detergent, we show that cholesterol acts by binding with high affinity and specificity to the 767 amino acid octahelical membrane region of SCAP. This octahelical region contains a conserved pentahelical sterol-sensing domain found in six other polytopic membrane proteins. We show that the membrane domain of SCAP is a tetramer and that cholesterol binding is inhibited by cationic amphiphiles, raising the possibility of allosteric regulation by positively charged phospholipids. The current studies show that cells control their cholesterol content through receptor-ligand interactions and not through changes in the physical properties of the membrane.

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Cholesterol Journal Articles