| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Different trends in serum cholesterol levels among rural and urban populations aged 40-59 in Japan from 1960 to 1990 Okayama, A., H. Ueshima, et al. (1995), J Clin Epidemiol 48(3): 329-37. Abstract: In Japan, coronary heart disease mortality is low and has been declining since 1970, despite recent increases in serum cholesterol levels which have been reported in nationwide surveys. Longitudinal and cross-sectional surveys of serum cholesterol levels in rural and urban populations from 1960 to 1990 were reviewed. In the surveys in the 1960s, serum cholesterol levels in urban populations were higher than those in rural populations. An increase in serum cholesterol levels for men and women was observed in all longitudinal studies among rural populations; mean increases in serum cholesterol levels per year were 0.034 mmol/l (p < 0.001) and 0.033 mmol/l (p < 0.001), respectively. These trends were still observed after combining the data from the longitudinal and cross-sectional studies in both men and women (0.027 and 0.028 mmol/l per year, respectively), while there was no significant increase among urban populations. The results of National Nutrition Surveys are consistent with these findings and show that meat consumption per day per capita increased from 23.9 to 66.2 g in rural populations and 51.2 to 77.6 g in urban populations in the 1966 and 1990 surveys. It is suggested that different trends in coronary heart disease mortality should also be apparent in rural and urban populations over this period. |
| Different types of blood lipoproteins in psoriasis patients. 1. The relationship of dyslipoproteinemias due to disordered cholesterol transport and the course of psoriasis Keshileva, Z. B., A. B. Kosukhin, et al. (1990), Vestn Dermatol Venerol(2): 7-11. Abstract: Comparison of the course of psoriasis in patients with hypo- and hyperalphacholesterolemia, hypo- and hyperbetacholesterolemia (Type IIA hyperlipoproteinemia) with that in the patients without identified lipid metabolism disturbances has been carried out. Blood lipoproteins were typed in the progressive stage of psoriasis. In hypoalphacholesterolemia patients the period of the psoriatic process stabilization was prolonged. Furthermore the frequency of coming remissions in women correlated (q = 0.90) with the concentration of high density lipoprotein cholesterol. In men similar correlation (q = 0.97) was observed only in the range between the lowest (under 0.5 mmol/l) and the upper thresholds of the mean level (1.4-1.7 mmol/l) of high density lipoprotein cholesterol and then it was undetectable. Type IIA hyperlipoproteinemia had no unfavorable effect on the course of psoriasis. Possible mechanisms responsible for these results are discussed. |
| Differential accumulation of cholesterol in Golgi compartments of normal and Niemann-Pick type C fibroblasts incubated with LDL: a cytochemical freeze-fracture study Coxey, R. A., P. G. Pentchev, et al. (1993), J Lipid Res 34(7): 1165-76. Abstract: Cholesterol accumulation in the Golgi of normal and Niemann-Pick Type C (NP-C) fibroblasts was shown by freeze-fracture electron microscopy using filipin as a probe for unesterified cholesterol. The specific distribution of cholesterol within individual Golgi compartments could be examined because membrane cholesterol forms complexes with filipin that are visible as membrane deformations (pits and protuberances) in freeze-fracture replicas. The density of filipin-cholesterol deformations, quantitated for cis, medial, and trans Golgi cisternae and trans Golgi vacuoles, was shown to increase in a cis to trans direction. After addition of low density lipoproteins (LDL) to cultured fibroblasts for 24 h, the cholesterol content increased within specific compartments of the Golgi. Normal cells showed an increase in filipin-cholesterol deformations in membranes of cis/medial cisternae and trans Golgi vacuoles, whereas NP-C cells showed only an increase in membranes of trans Golgi cisternae. LDL uptake by cells appears to induce a disparate cholesterol enrichment of Golgi compartments of normal and mutant cells. The ability of cells to process endocytosed cholesterol may in part depend on modulation of cholesterol-enriched membrane transport through the Golgi, a function which appears to be defective in NP-C cells. |
| Differential alteration of vascular reactivity in rabbit aorta with modest elevation of serum cholesterol Merkel, L. A., L. M. Rivera, et al. (1990), Circ Res 67(3): 550-5. Abstract: The effect of diet-induced, moderate elevation of serum cholesterol on vascular reactivity in isolated rabbit abdominal aortic rings was examined by using a series of vasoconstrictor and vasodilator agonists. Serum cholesterol of rabbits that were fed a cholesterol-free, casein-rich diet for 10 weeks was elevated approximately 4.5-fold compared with values found in control rabbits that were fed standard lab chow (223 +/- 41 versus 51 +/- 5 mg/dl, respectively). Relaxation responses to carbamylcholine chloride and (+/-)-isoproterenol hydrochloride in vessels from hypercholesterolemic rabbits were markedly inhibited in the presence of norepinephrine, prostaglandin F2 alpha, 5-hydroxytryptamine, and angiotensin II but not in the presence of phorbol 12,13-dibutyrate. The depressed vasodilation in hypercholesterolemic vessels appeared to depend on the agonist initiating the contraction. Sodium nitroprusside-induced relaxations were unchanged in rings from hypercholesterolemic rabbits compared with rings from control rabbits for all contractile agonists except KCl. Isolated aortic rings from hypercholesterolemic rabbits exhibited a slight but significantly increased vasoconstrictor sensitivity to 5-hydroxytryptamine and KCl but not to norepinephrine, prostaglandin F2 alpha, angiotensin II, or phorbol 12,13-dibutyrate compared with aortic rings from control rabbits. These results demonstrate that modest elevation of serum cholesterol is sufficient to depress vasodilator and enhance vasoconstrictor responses to certain agonists. Vasodilator effects are impaired to a greater extent by a small increase in serum cholesterol than are responses to vasoconstrictor agonists. It is postulated that the induction of differential alterations in vascular reactivity with moderate increase in serum cholesterol may represent important early events predisposing arteries to vasospasm. |
| Differential and interactive effects of calcium channel blockers and cholesterol content of the diet on jejunal uptake of lipids in rabbits Hyson, D. A., A. B. Thomson, et al. (1994), Lipids 29(4): 281-7. Abstract: The present study was undertaken to determine the effects of two classes of calcium channel blockers (CCB), nisoldipine (N) and verapamil (V), on the jejunal uptake of lipids in rabbits. The uptake of cholesterol and long-chain fatty acids into rabbit jejunum was examined after 6 and 36 min of exposure to N or V in vitro ("acute" studies), and after 3-wk feeding of N or V ("chronic" studies). Animals were fed either a low (0.08%) cholesterol diet (LCD) or a high (2.8%) cholesterol diet (HCD), with or without N or V added. Acute in vitro exposure of the jejunum to N or V did not affect the uptake of cholesterol or palmitic acid in rabbits fed LCD or HCD. The effect of N or V feeding depended upon the cholesterol content of the diet; adding N or V to LCD increased cholesterol uptake while adding N or V to HCD enhanced or lowered cholesterol uptake, respectively. Both N and V increased the uptake of stearic acid in LCD. N in HCD had no effect on fatty acid uptake, whereas V lowered the uptake of stearic and linoleic acids and increased the uptake of oleic acid. These changes in lipid uptake were not due to variation in the animals' food intake, body weight gain, or intestinal mucosal surface area. The chronic administration of N or V results in an intestinal adaptative process that alters the jejunal uptake of lipids, the direction of which is influenced by the class of CCB, and by the cholesterol content of the diet. (ABSTRACT TRUNCATED AT 250 WORDS) |
| Differential capacity for cholesterol transport and processing in large and small rat luteal cells McLean, M. P., S. E. Nelson, et al. (1992), Endocrinology 131(5): 2203-12. Abstract: The aim of this investigation was to determine whether a specific luteal subpopulation is responsible for the hypertrophic development of the corpus luteum at midpregnancy in the rat and to determine whether there was an underlying cellular basis for the differential production of steroids by the luteal cell subtypes. To examine this, we have dispersed and separated rat luteal steroidogenic cell populations into small (< 20 microns) and large (> 30 microns) cell types by elutriation. Luteal cells were examined at early (day 3) and midpregnancy (day 14) for differences in protein content and for differential expression of proteins required for steroid production. Specific proteins examined include the P450side chain cleavage enzyme (P450scc), adrenodoxin and adrenodoxin reductase, proteins required for cholesterol conversion to progestagens in the corpus luteum, and sterol carrier protein-2 (SCP2), a protein thought to be involved in intracellular cholesterol transport. The cytochrome P450(17)alpha hydroxylase (P450(17)alpha), a key enzyme responsible for androgen biosynthesis was also examined in the isolated luteal cells. The large luteal cell population displayed an increase in total cellular protein content while the small cell type did not change with luteal development. In addition, the large luteal cells expressed proteins unique to or elevated in that cell type. Analysis by two-dimensional polyacrylamide gel electrophoresis revealed that the large cell-specific proteins had molecular masses of 23 K and 32 K and that a 14 kilodalton (kDa) protein was elevated in the large cell type relative to the small cells. The small luteal cell on day 3 of pregnancy expressed a 36 kDa protein which was barely detectable in the large cell. Immunocytochemical and Western analysis indicated that the large luteal cells contain 5.3-fold more SCP2 (P < 0.05) and 5.6-fold more P450scc (P < 0.001) relative to the small cell type. Immunocytochemical staining of adrenodoxin and adrenodoxin reductase indicate these proteins were elevated in the large cell as well. Human CG administration stimulated P450(17)alpha expression mainly in the large luteal cell population. The results of this investigation indicate, for the first time, that the large luteal cell of the rat, in contrast to the small cell type, undergoes a dramatic increase in protein content with luteal development, and that with this increase in cell size there is a concomitant increase in the large cell capacity to produce steroids. This occurs as a direct result of the enhanced expression of SCP2, P450scc, adrenodoxin and adrenodoxin reductase, proteins specifically required to transport and process cholesterol for steroid production in the large luteal cell. |
| Differential contribution of testosterone and estradiol in the determination of cholesterol and lipoprotein profile in healthy middle-aged men Van Pottelbergh, I., L. Braeckman, et al. (2003), Atherosclerosis 166(1): 95-102. Abstract: The role of endogenous sex steroids in the association between male gender and cardiovascular risk remains unclear. We performed a cross-sectional analysis of the role of endogenous testosterone (T) and estradiol (E2), as well as their respective biologically active fractions, in the determination of lipids and lipoproteins in an occupation-based cohort of 715 healthy middle-aged men. Serum T, sex hormone binding globulin (SHBG) and E(2) were measured by immunoassays; free T (FT) and free E2 (FE2) were calculated using a validated equation. Serum total cholesterol (Chol), HDL-cholesterol (HDL-Chol), apolipoproteins A1 (ApoA1), B (ApoB), E (ApoE), ApoE phenotype, lipoprotein a (Lpa), fibrinogen, C-reactive protein (CRP), systolic (SBP) and diastolic blood pressure (DBP) were assessed. Serum levels of T and FT, correlated positively with HDL-Chol and ApoA1 with Spearman correlation coefficients, partialised for age and body mass index (BMI), ranging between 0.14 and 0.17 (P<0.001); FT was associated with total Chol and ApoB levels (r=0.12 for both T and FT; P<0.01). After adjustment for age and BMI, both serum E2 and FE2 levels correlated significantly with ApoE (r=0.25 and r=0.26 for E2 and FE2, respectively; P<0.001). Free and total E2 were associated with both SBP and DBP with correlation coefficients partialised for age and BMI ranging between 0.11 and 0.13 (P<0.01). No correlation was found between any of the studied sex steroids, fibrinogen, Lpa or CRP. In multiple linear regression analyses, T was the most important independent hormonal determinant of HDL-Chol levels, when E2, SHBG and exogenous factors were considered in the model (P<0.01), whereas E2 contributed mostly in the determination of ApoE levels (P<0.001) and SBP (P<0.01). When FT and FE2 were considered in multivariate analyses as independent hormonal variables, FT was the most significant predictor of HDL-Chol (P<0.01) and ApoB (P<0.01) concentrations. Moreover, in the same multivariate model, ApoE (P<0.001) concentration as well as SBP (P<0.001) was most affected by FE2 levels in comparison with FT. In conclusion, our findings do suggest a differential role of T and E2 in the determination of traditional cardiovascular risk factors in healthy middle-aged men. In the determination of both HDL-Chol and ApoB levels endogenous (F)T may be involved, whereas (F)E2 may contribute to the determination of ApoE levels in this study group of 715 healthy middle-aged men. Regarding the observational design of the study, the physiological relationship of the observed associations between sex steroids and cardiovascular risk factors remains to be unravelled. |
| Differential control of cholesterol and fatty acid biosynthesis in sensitive and multidrug-resistant LoVo tumor cells Santini, M. T., M. Napolitano, et al. (2003), Anticancer Res 23(6C): 4737-46. Abstract: Multidrug resistance (MDR) describes the decrease in sensitivity of tumor cells to a wide variety of cytotoxic compounds. Although a central role has been ascribed to the P-glycoprotein (Pgp) pump in MDR, lipids also appear to be extremely important. However, their precise role in MDR is not yet fully understood. It was the aim of the present paper to gain a deeper understanding of intracellular lipid equilibrium in both sensitive and MDR tumor cells. In particular, intracellular cholesterol biosynthesis and cholesterol esterification were examined in LoVo-sensitive and Pgp-overexpressing resistant cells. The data presented seem to suggest that the higher synthesis of cholesteryl ester and triglyceride observed in resistant with respect to wild-type cells is due to a greater production of fatty acids in these cells. The results are discussed in view of the possible roles of sterol regulatory element-binding proteins and Pgp in these phenomena. |
| Differential deficiency of mevalonate kinase and phosphomevalonate kinase in patients with distinct defects in peroxisome biogenesis: evidence for a major role of peroxisomes in cholesterol biosynthesis Wanders, R. J. and G. J. Romeijn (1998), Biochem Biophys Res Commun 247(3): 663-7. Abstract: Peroxisomes catalyze a number of essential metabolic functions especially related to lipid metabolism. There is increasing evidence suggesting that peroxisomes are also involved in the synthesis of isoprenoids via the mevalonate pathway at least in rat liver. In order to obtain independent evidence for a role of peroxisomes in isoprenoid synthesis in man, we have measured the activity of two key enzymes of the mevalonate pathway in patients suffering from certain defined defects in peroxisome biogenesis. We now report that mevalonate kinase is not only deficient in livers from Zellweger patients in which peroxisome biogenesis is defective, but also in livers from rhizomelic chondrodysplasia punctata (RCDP) Type 1 patients. In the latter group of patients there is a selective defect in peroxisome biogenesis due to a genetic defect in the PTS2-receptor, a mobile receptor-protein guiding peroxisomal proteins with a certain peroxisomal targeting signal (PTS2) to the peroxisome. Phosphomevalonate kinase was found to be strongly deficient in Zellweger patients thus suggesting that this enzyme is also peroxisomal. Taken together, our data indicate that in human liver mevalonate kinase and phosphomevalonate kinase are truly peroxisomal enzymes which strongly suggests that peroxisomes play a major role in cholesterol biosynthesis. |
| Differential effect of aging on cholesterol modulation of carbachol-stimulated low-K(m) GTPase in striatal synaptosomes Denisova, N. A., S. A. Erat, et al. (1998), Exp Gerontol 33(3): 249-65. Abstract: Previous research has suggested that age-related decline in physiological functions may be the result of substantial alterations in membrane molecular structure. The purpose of the present experiments was to elucidate the role of cholesterol domains in the age-related decline in receptor-G-protein interactions in striatal synaptosomes. We observed a significant age-related deficit in muscarinic cholinergic stimulated Low-Km GTPase activity and its age-related susceptibility to cholesterol treatment in range of 10(-10)-10(-5) M. Treatment of synaptosomes from old rats with cholesterol in range of 10(-8)-10(-6) M restored the Low-Km GTPase activity up to the level seen in young animals and reached a maximum at 10(-7) M. In synaptosomes from young rats, however, cholesterol treatment did not have any effect on striatal Low-Km GTPase activity. We observed significant alterations in the membrane lipid composition of striatal synaptosomes as a function of age. Our results suggested a significant interaction of age and cholesterol treatment on physical properties of striatal synaptosomes. Thus, the present results of experiments in vitro support our previous results of experiments in vivo and suggested an interaction of cholesterol domains with muscarinic-cholinergic receptor G-protein alpha subunit coupling/uncoupling through regulation of physical properties of striatal synaptosomes. |
| Differential effect of dietary fat saturation and cholesterol on hepatic apolipoprotein gene expression in rats Osada, J., A. Fernandez-Sanchez, et al. (1994), Atherosclerosis 108(1): 83-90. Abstract: The effects of dietary cholesterol and fat saturation on hepatic apolipoprotein A-I, A-II, A-IV, B, C-I, C-III, E and LDL receptor mRNA levels were studied in male rats. Animals were maintained for 2 months on a high fat diet (40% w/w) containing 0.1% cholesterol. Two groups of control animals received either chow diet or chow plus 0.1% cholesterol, while experimental groups received as their fat supplement coconut, corn or olive oil. Olive oil fed animals had higher levels of hepatic apo A-I than the control cholesterol group (1.6 +/- 0.3 vs. 0.8 +/- 0.2). Apo E mRNA levels were 50% and 72% higher in animals consuming the saturated (coconut) and unsaturated (corn and olive) fat diet than the control cholesterol group. Apo B and apo C-I mRNA levels were not affected by the experimental conditions. Apo A-IV mRNA increased between 66% and 127% in groups in which cholesterol was present. LDL receptor mRNA increased 2 times in the corn fed group compared with the control groups. These results indicate that the expression of genes coding for products involved in lipoprotein metabolism have a differential susceptibility to dietary fat saturation and cholesterol. |
| Differential effect of genistein on the stimulation of cholesterol production by basic protein II in normal and hyperapoB fibroblasts Kwiterovich, P. O., Jr. and M. Motevalli (1998), Arterioscler Thromb Vasc Biol 18(1): 57-64. Abstract: We studied further the basis for the abnormal effect of human serum basic protein II (BP II) on cholesterol production in hyperapobetalipoproteinemia (hyperapoB) fibroblasts and whether this effect involves protein tyrosine kinase phosphorylation (TKP). Genistein, a specific inhibitor of TKP was used as a probe. Compared with normal cells, BP II stimulated significantly the cellular mass of total cholesterol (6.4-fold), unesterified cholesterol (3.6-fold), and esterified cholesterol (6.7-fold) in hyperapoB fibroblasts. The addition of genistein to BP II in hyperapoB cells markedly inhibited these abnormal stimulatory effects of BP II on cell sterol mass. In normal cells, the addition of genistein to BP II produced an opposite effect: a marked stimulation in the mass of total (5.5-fold) and esterified (18.3-fold) cholesterol and a decrease in unesterified cholesterol (3.4-fold). These effects of genistein on the formation of cellular cholesterol by BP II were both time and concentration dependent. The inhibition of the stimulatory effect of BP II on cholesterol production by genistein in hyperapoB cells may be mediated through 3-hydroxy 3-methylglutaryl coenzyme A reductase, the rate-limiting enzyme of cholesterol biosynthesis, since the rate of incorporation of 14Cacetate, but not 3Hmevalonate, into unesterified cholesterol was decreased by genistein in the hyperapoB cells. When the mass of cell total cholesterol in the cells treated with BP II was subtracted from those treated with BP II plus genistein, a negative number was produced in each of the six hyperapoB cell lines, while each of the normal cell lines retained a positive number. The mean difference for the mass of total cholesterol between the hyperapoB and normal fibroblasts under these conditions was 128.2 nmol/mg cell protein, a difference that was separated by >3 SD. This study supports further the tenet that there is a defect in the response of hyperapoB cells to BP II and that this defect results in an abnormality in cholesterol metabolism that appears mediated through a protein TKP-mediated process. |
| Differential effect of National Cholesterol Education Program (NCEP) Step II diet on HDL cholesterol, its subfractions, and apoprotein A-I levels in hypercholesterolemic women and men after 1 year: the beFIT Study Walden, C. E., B. M. Retzlaff, et al. (2000), Arterioscler Thromb Vasc Biol 20(6): 1580-7. Abstract: We previously reported that high density lipoprotein cholesterol (HDL-C) decreases more in hypercholesterolemic (HC) women than in HC men ingesting an National Cholesterol Education Program (NCEP) Step II diet for 6 months. We examined these subjects to determine whether the differential HDL-C reduction persists after 12 months and whether it is associated with decreased HDL(2)-C and apoprotein A-I. Subjects were screened from an industrial workforce and were defined as HC if 2 low density lipoprotein cholesterol measurements were >/=75th percentile or defined as combined hyperlipidemic (CHL) if triglycerides were also >/=75th percentile. The subjects were then taught the NCEP Step II diet in 8 weekly classes and counseled quarterly. Seventy-three HC and 92 CHL women (mean ages 43 and 44 years, respectively) and 112 HC and 106 CHL men (ages 45 and 41 years, respectively) were studied. All groups reported similar total fat (24% to 26% kcal) and saturated fat (7.1% to 7.9% kcal) intakes at 1 year. HDL-C decreased 7.6% in HC women (P<0.01), exceeding the nonsignificant 1.3% decrease in HC men (P=0.000). HDL(2)-C decreased 16.7% in HC women (P<0.01) compared with the nonsignificant 0.5% increase in HC men (P=0.000). In CHL women and men, HDL-C decreased 3.5% and 3.9% (both P<0.01); HDL(2)-C decreased more in women (7.1%, P<0.01) than in men (4.3%, a nonsignificant difference). Apoprotein A-I decreased significantly (5.3%, P<0.01) in HC women only. Plasma triglycerides were unchanged. Low density lipoprotein cholesterol and weight changes were not different among the 4 groups. HDL-C, HDL(2)-C, and apoprotein A-I levels decreased more in HC women than in HC men after following the NCEP Step II diet for 1 year, continuing a trend observed with HDL-C at 6 months. The total HDL-C and HDL(2)-C reductions narrow the baseline differences between men and women by 50%. Whether this reduction impacts women's protection from cardiovascular disease deserves future study. Nonetheless, the results point to sex-based differences in intrahepatic glucose and fatty acid metabolism linked to alterations in HDL formation and removal. |
| Differential effect of subspecies of lipoprotein containing apolipoprotein A-I on cholesterol efflux from cholesterol-loaded macrophages: functional correlation with lecithin: cholesterol acyltransferase Ohta, T., R. Nakamura, et al. (1992), Biochim Biophys Acta 1165(1): 119-28. Abstract: Two species of lipoprotein containing apoA-I, one containing only apoA-I (LpA-I), and the other containing apoA-I and apoA-II (LpA-I/A-II), were tested for their effects on macrophage foam cells. Rat macrophages were converted to foam cells by incubation with radiolabeled acetylated LDL. Incubation with LpA-I or LpA-I/A-II decreased the cellular cholesteryl esters (CE) mass. However, the free cholesterol (FC) mass was only reduced by LpA-I. All the radioactivity excreted into the medium was associated with LpA-I or LpA-I/A-II; 39% of the excreted radioactivity was esterified in LpA-I and 10% in LpA-I/A-II. Upon complete inactivation of lecithin: cholesterol acyltransferase (LCAT) activity with dithiobisnitrobenzoic acid, the cholesterol reducing capacity of LpA-I was weakened significantly. However, the CE mass reducing capacity of LpA-I/A-II was not affected. When LpA-I and LpA-I/A-II were combined, the cholesterol reducing capacity of the mixture was similar to that of LpA-I alone. However, LpA-I re-isolated from the medium showed a lower esterification rate than did the re-isolated LpA-I/A-II, thereby indicating that the cholesterol esterified in LpA-I was transferred to LpA-I/A-II. These results suggest that (i) the function of LpA-I is closely linked to the LCAT activity while that of LpA-I/A-II is not, and (ii) LpA-I in concert with LpA-I/A-II induces a series of extracellular events; LCAT-mediated esterification of excreted FC by LpA-I and a subsequent CE transfer to LpA-I/A-II. These mechanisms might be important for net cholesterol efflux from macrophage foam cells in physiological states. |
| Differential effect of triiodothyronine and thyroxine on liposomes containing cholesterol: physiological speculations Chehin, R. N., M. R. Rintoul, et al. (1995), J Membr Biol 147(2): 217-21. Abstract: The effect of thyroid hormones on the steady-state fluorescence polarization and on the release of the liposomal content was analyzed in liposomes composed of egg phosphatidylcholine and egg phosphatidyl choline:cholesterol in different molar ratios. Depending on liposome cholesterol composition, a dual effect of triiodothyronine was found. The fluorescence polarization of 1,6 diphenyl 1,3,5 hexatriene or 1-(4-trimethylaminophenyl) 6 phenyl-1, 3, 5 hexatriene decreased by the addition of the hormone when cholesterol content was in the range from 0 to 30 moles %, while it increased with cholesterol from 30 to 50 moles %. In the release experiments, the effect of triiodothyronine was also biphasic; the leakage was the highest at 0% and 50% and the lowest at 30 moles % of cholesterol. On the contrary, thyroxine was without effect on liposomes containing cholesterol from 30 to 50 mol %. This fact correlated with a lower incorporation of thyroxine, compared with that of triiodothyronine in liposomes containing up to 30 moles % of cholesterol. The fact that the above differential incorporation of thyroid hormones was also observed at physiological concentration and that most of the mammalian membrane cells have more than 25 moles % of cholesterol have for physiological implications to the observations reported here. |
| Differential effect of walnut oil and safflower oil on the serum cholesterol level and lesion area in the aortic root of apolipoprotein E-deficient mice Iwamoto, M., M. Kono, et al. (2002), Biosci Biotechnol Biochem 66(1): 141-6. Abstract: Walnut oil (WO) is a good source of alpha-linolenic acid. We compared the effects of WO and high-linoleic safflower oil (HLSO) on the serum lipid level and atherosclerosis development in male and female apolipoprotein (apo) E-deficient mice. The WO diet resulted in a higher level of serum cholesterol than with HLSO. Female mice fed on the WO diet had a greater lesion area in the aortic root than did those on the HLSO diet. There was no diet-dependent difference in the level of cholesterol and its oxidation products in the abdominal and thoracic aorta. These results suggest that the unpleasant effects of the WO diet on apo E-deficient mice may be attributable to alpha-linolenic acid. |
| Differential effects of an acyl-coenzyme A:cholesterol acyltransferase inhibitor on HDL-induced cholesterol efflux from rat macrophage foam cells Hakamata, H., A. Miyazaki, et al. (1995), FEBS Lett 363(1-2): 29-32. Abstract: When rat macrophages were converted to foam cells with acetylated low density lipoprotein (acetyl-LDL) and then reacted with high density lipoprotein (HDL) and an inhibitor of acyl-coenzyme A:cholesterol acyltransferase (58-035) (sequential incubation system), 58-035 did not enhance HDL-induced cholesterol efflux. In contrast, when macrophages were exposed to acetyl-LDL in the presence of both HDL and 58-035 (simultaneous incubation system), HDL-induced cholesterol efflux was enhanced 1.6-fold by 58-035. Cholesterol efflux with HDL alone was 2-fold greater in simultaneous incubation than in sequential incubation. These results suggest the presence of an efficient cholesterol efflux pathway in simultaneous incubation which is not available in sequential incubation. This pathway, which we refer to as the neutral cholesterol ester hydrolase-independent pathway, is characterized by the efflux of lysosome-derived cholesterol without re-esterification. |
| Differential effects of cholesterol and oxidised-cholesterol in egg lecithin bilayers Karolis, C., H. G. Coster, et al. (1998), Biochim Biophys Acta 1368(2): 247-55. Abstract: Low frequency impedance measurements of pure egg lecithin (phosphatidylcholine) bilayers have revealed the presence of four layers which can be attributed to the acyl chain, carbonyl, glycerol bridge and phosphatidylcholine regions of the lecithin molecule. Measurements on bilayers formed in the presence of unoxidised-cholesterol revealed that cholesterol molecules were located in the hydrocarbon region of the bilayer with its hydroxyl groups aligned with the carbonyl region of the lecithin molecules. Measurements of oxidised-cholesterol lecithin bilayers revealed that these molecules protruded less into the hydrocarbon region and their polar hydroxyl group aligned with the glycerol bridge region of the lecithin molecule. |
| Differential effects of cholesterol on acyl chain order in erythrocyte membranes as a function of depth from the surface. An electron paramagnetic resonance (EPR) spin label study Cassera, M. B., A. M. Silber, et al. (2002), Biophys Chem 99(2): 117-27. Abstract: The purpose of this work is to analyze the effects of cholesterol modulation on acyl chain ordering in the membrane of human erythrocytes as a function of depth from the surface. Partial cholesterol depletion was achieved by incubation of erythrocytes with liposomes containing saturated phospholipids, or with methyl-beta-cyclodextrin (MbetaCD). Cholesterol enrichment was achieved by incubation with liposomes formed by phospholipids/cholesterol, or with the complex MbetaCD/cholesterol. Acyl chain order was studied with electron paramagnetic resonance spectroscopy (EPR) using spin labels that sense the lipid bilayer at different depths. It is shown that the increase in cholesterol stiffens acyl chains but decreases the interaction among lipid headgroups, while cholesterol depletion causes the opposite behavior. It is likely that the observed cholesterol effects are related to those stabilizing the cholesterol-rich detergent-insoluble membrane domains (rafts), recently shown to exist in erythrocytes. |
| Differential effects of dietary cholesterol on aminopeptidase A, B and M in the frontal cortex of male and female mice Ramirez-Exposito, M. J., M. J. Garcia, et al. (2001), Nutr Neurosci 4(6): 461-8. Abstract: Although hypercholesterolemia and hypertension have been extensively associated, the regulatory mechanism underlying this relationship is poorly understood. Systemic and local renin-angiotensin systems are involved in the control of blood-pressure. Angiotensin II has been considered as the main effector peptide of renin-angiotensin system. However, other peptides derived from the metabolism of angiotensin II, as angiotensins III and IV have been shown to play significant roles. The aim of this study is to analyse the effect of dietary cholesterol on the activity of the enzymes involved in the metabolism of angiotensins II and III. Soluble and membrane-bound aminopeptidase A (aspartyl- and glutamyl-aminopeptidases), B (arginyl-aminopeptidase) and M (alanyl-aminopeptidase) activities were measured in the frontal cortex of male and female mice fed a cholesterol enriched-diet (1% cholesterol; 0.5 cholic acid). Soluble and membrane-bound aminopeptidases B and M did not change in male or female cholesterol groups. Significant increases were observed in membrane-bound aspartyl- and glutamyl-aminopeptidase activities in both cholesterol groups. Soluble aspartyl- and glutamylaminopeptidases did not change in male cholesterol group, but significant decreases were detected in female cholesterol group. Our results may indicate that the metabolism of angiotensin II to angiotensin III by aminopeptidase A is increased, but angiotensin III metabolism by aminopeptidases B and M is not modified after cholesterol intake; so cholesterol may enhance the effects of angiotensin III, at least, at the cortical level. |