Cholesterol Articles and Abstracts

For medical practitioners and the general public - Cholesterol Journal Article Catalog.

Cholesterol Journal Articles



Record 1641 to 1660
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Ceramide and cholesterol composition of the skin of patients with atopic dermatitis
Di Nardo, A., P. Wertz, et al. (1998), Acta Derm Venereol 78(1): 27-30.
Abstract: Atopic dermatitis skin tends to be easily irritated and appears dry. These clinical peculiarities correspond to impaired barrier function and to increased transepidermal water loss (TEWL) values. A few studies suggest that a reduced amount of total ceramides (especially of ceramide 1) is responsible for functional abnormalities of the skin of atopic dermatitis patients. The aim of this study was to analyze the relationship between epidermal lipids and barrier impairment in the skin of patients with atopic dermatitis. The quantity of ceramides, cholesterol sulphate and free cholesterol of 47 patients with atopic dermatitis and 20 age- and sex-matched healthy subjects was assessed by cyanoacrylate stripping and thin layer chromatography. Capacitance and TEWL were recorded at the same site of the lipid sample. In patients with atopic dermatitis, the levels of ceramide 1 and 3 were significantly lower and values of cholesterol significantly higher with respect to healthy subjects. Moreover, the CER/CH ratio was significantly lower with respect to normal skin. Patients with active signs of eczema also had higher TEWL values and lower capacitance values. By contrast, patients with no active signs of atopic dermatitis had a normal barrier function and intermediate values of ceramides and cholesterols, when compared to patients with atopic dermatitis with active lesions and normal subjects. The quantity of ceramide 3 was significantly correlated with TEWL impairment. These findings suggest that a decrease in ceramides in the stratum corneum is involved in barrier impairment in atopic dermatitis skin. Our data confirm those of other authors and support the view that impaired metabolism of ceramides may be the cause of dry skin and impaired barrier function in atopic dermatitis.

Ceramide enhances cholesterol efflux to apolipoprotein A-I by increasing the cell surface presence of ATP-binding cassette transporter A1
Witting, S. R., J. N. Maiorano, et al. (2003), J Biol Chem 278(41): 40121-7.
Abstract: It is widely accepted that functional ATP-binding cassette transporter A1 (ABCA1) is critical for the formation of nascent high density lipoprotein particles. However, the cholesterol pool(s) and the cellular signaling processes utilized by the ABCA1-mediated pathway remain unclear. Sphingomyelin maintains a preferential interaction with cholesterol in membranes, and its catabolites, especially ceramide, are potent signaling molecules that could play a role in ABCA1 regulation or function. To study the potential role of ceramide in this process, we treated a variety of cell lines with 20 microM C2-ceramide and examined apolipoprotein-mediated cholesterol efflux to lipid-free apoA-I. We found that cell lines expressing ABCA1 displayed 2-3-fold increases in cholesterol efflux to apoA-I. Cell lines not expressing ABCA1 were unaffected by ceramide. We further characterized the cholesterol efflux effect in Chinese hamster ovary cells. Ceramide treatment did not cause significant cytotoxicity or apoptosis and did not affect cholesterol efflux to non-apolipoprotein acceptors. Raising endogenous ceramide levels increased cholesterol efflux to apoA-I. Using a cell surface biotinylation method, we found that the total cellular ABCA1 and that at the plasma membrane were increased with ceramide treatment. Also ceramide enhanced the binding of fluorescently labeled apoA-I to Chinese hamster ovary cells. These data suggest that ceramide may increase the plasma membrane content of ABCA1, leading to increased apoA-I binding and cholesterol efflux.

Ceramide selectively displaces cholesterol from ordered lipid domains (rafts): implications for lipid raft structure and function
Megha and E. London (2004), J Biol Chem 279(11): 9997-10004.
Abstract: Ceramide is a membrane lipid involved in a number of crucial biological processes. Recent evidence suggests that ceramide is likely to reside and function within lipid rafts; ordered sphingolipid and cholesterol-rich lipid domains believed to exist within many eukaryotic cell membranes. Using lipid vesicles containing co-existing raft domains and disordered fluid domains, we find that natural and saturated synthetic ceramides displace sterols from rafts. Other raft lipids remain raft-associated in the presence of ceramide, showing displacement is relatively specific for sterols. Like cholesterol-containing rafts, ceramide-rich "rafts" remain in a highly ordered state. Comparison of the sterol-displacing abilities of natural ceramides with those of saturated diglycerides and an unsaturated ceramide demonstrates that tight lipid packing is critical for sterol displacement by ceramide. Based on these results, and the fact that cholesterol and ceramides both have small polar headgroups, we propose that ceramides and cholesterol compete for association with rafts because of a limited capacity of raft lipids with large headgroups to accommodate small headgroup lipids in a manner that prevents unfavorable contact between the hydrocarbon groups of the small headgroup lipids and the surrounding aqueous environment. Minimizing the exposure of cholesterol and ceramide to water may be a strong driving force for the association of other molecules with rafts. Furthermore, displacement of sterol from rafts by ceramide is very likely to have marked effects upon raft structure and function, altering liquid ordered properties as well as molecular composition. In this regard, certain previously observed physiological processes may be a result of displacement. In particular, a direct connection to the previously observed sphingomyelinase-induced displacement of cholesterol from plasma membranes in cells is proposed.

Cerebral cholesterol granuloma in homozygous familial hypercholesterolemia
Francis, G. A., R. L. Johnson, et al. (2005), Cmaj 172(4): 495-7.
Abstract: Familial hypercholesterolemia (FH) is characterized by the accumulation of excess cholesterol in tissues including the artery wall and tendons. We describe a patient with homozygous FH who presented with asymptomatic cholesterol granuloma of the brain. The patient's plasma low-density lipoprotein cholesterol level was remarkably responsive to combination hypolipidemic therapy with statin plus ezetimibe. This case illustrates another potential complication of whole-body cholesterol excess and underscores the differences in phenotype and in response to therapy among patients with FH.

Cerebral CO2 reactivity, cholesterol, and high-density lipoprotein cholesterol in the elderly
Bakker, S. L., F. E. de Leeuw, et al. (2000), Neurology 54(4): 987-9.
Abstract: Cholesterol and its subfractions play a role in the development of atherosclerosis. Cerebral CO2 reactivity reflects the compensatory capacity of cerebral arterioles. The authors investigated the relationship between total cholesterol, high-density lipoprotein (HDL), their ratio, and cerebral CO2 reactivity in 826 participants from the Rotterdam Study. Cerebral CO2 reactivity increased significantly with increasing levels of HDL and decreased significantly with an increasing total cholesterol/HDL ratio. This suggests that blood lipids may also affect smaller cerebral blood vessels.

Cerivastatin induces carotid artery plaque stabilization independently of cholesterol lowering in patients with hypercholesterolaemia
Kurata, T., M. Kurata, et al. (2001), J Int Med Res 29(4): 329-34.
Abstract: To prevent cardiovascular events in hyperlipidaemic patients, plaque stabilization by inhibition of localized inflammatory reactions in the blood vessels is important in addition to cholesterol lowering. Cerivastatin, a 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor (statin), has more potent enzyme-inhibitory effects than other statins and has also been reported in vitro to inhibit, at low concentrations, various inflammatory reactions due to plaque instability. Cerivastatin was therefore administered over 12 months to five patients with hypercholesterolaemia and atherosclerotic plaque diagnosed by ultrasonography of the carotid artery, and changes in the plaque composition were determined. The mean cholesterol level decreased over the study period, although not significantly. However, the mean percentage of fibrous matrix of the plaque increased significantly from a mean of 11.2 +/- 7.7% at study entry to 18.3 +/- 5.9% at the end of the study. Additionally, the mean maximum plaque height was significantly reduced from 3.7 +/- 0.9 mm to 3.0 +/- 0.7 mm. These results indicate that cerivastatin induces plaque stability independently of cholesterol lowering.

Cerivastatin prevents angiotensin II-induced renal injury independent of blood pressure- and cholesterol-lowering effects
Park, J. K., D. N. Muller, et al. (2000), Kidney Int 58(4): 1420-30.
Abstract: BACKGROUND: Statins are effective in prevention of end-organ damage; however, the benefits cannot be fully explained on the basis of cholesterol reduction. We used an angiotensin II (Ang II)-dependent model to test the hypothesis that cerivastatin prevents leukocyte adhesion and infiltration, induction of inducible nitric oxide synthase (iNOS), and ameliorates end-organ damage. METHODS: We analyzed intracellular targets, such as mitogen-activated protein kinase and transcription factor (nuclear factor-kappaB and activator protein-1) activation. We used immunohistochemistry, immunocytochemistry, electrophoretic mobility shift assays, and enzyme-linked immunosorbent assay techniques. We treated rats transgenic for human renin and angiotensinogen (dTGR) chronically from week 4 to 7 with cerivastatin (0.5 mg/kg by gavage). RESULTS: Untreated dTGR developed hypertension, cardiac hypertrophy, and renal damage, with a 100-fold increased albuminuria and focal cortical necrosis. dTGR mortality at the age of seven weeks was 45%. Immunohistochemistry showed increased iNOS expression in the endothelium and media of small vessels, infiltrating cells, afferent arterioles, and glomeruli of dTGR, which was greater in cortex than medulla. Phosphorylated extracellular signal regulated kinase (p-ERK) was increased in dTGR; nuclear factor-kappaB and activator protein-1 were both activated. Cerivastatin decreased systolic blood pressure compared with untreated dTGR (147 +/- 14 vs. 201 +/- 6 mm Hg, P < 0.001). Albuminuria was reduced by 60% (P = 0.001), and creatinine was lowered (0.45 +/- 0.01 vs. 0.68 +/- 0.05 mg/dL, P = 0. 003); however, cholesterol was not reduced. Intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 expression was diminished, while neutrophil and monocyte infiltration in the kidney was markedly reduced. ERK phosphorylation and transcription factor activation were reduced. In addition, in vitro incubation of vascular smooth muscle cells with cerivastatin (0.5 micromol/L) almost completely prevented the Ang II-induced ERK phosphorylation. CONCLUSION: Cerivastatin reduced inflammation, cell proliferation, and iNOS induction, which led to a reduction in cellular damage. Our findings suggest that 3-hydroxy-3-methylglutaryl coenzyme (HMG-CoA) reductase inhibition ameliorates Ang II-induced end-organ damage. We suggest that these effects were independent of cholesterol.

Certification of cholesterol measurements by the National Reference Method Laboratory Network with routine clinical specimens: effects of network laboratory bias and imprecision
Bennett, S. T., J. H. Eckfeldt, et al. (1992), Clin Chem 38(5): 651-7.
Abstract: The National Reference Method Laboratory Network has initiated a program to certify clinical laboratory cholesterol measurement performance by using routine clinical specimens. Clinical laboratory and reference laboratory measurements of split samples are used to assess whether the clinical laboratory is meeting the Laboratory Standardization Panel's goals for accuracy and precision. We used a computer-based Monte Carlo simulation model of split-sample proficiency testing to evaluate the certification program and, in particular, to analyze the effects of reference laboratory bias and imprecision. Results of our simulations indicate that the accuracy of the certification program is strongly influenced by reference laboratory bias and less influenced by reference laboratory imprecision. The certification program is potentially highly accurate, but unless reference laboratory bias is tightly controlled, the number of classification errors may limit its utility. Moreover, the decision limit of the certification program needs to be higher than the Laboratory Standardization Panel's goal (3.5% instead of 3.0%) to ensure that an acceptably high proportion of well-performing clinical laboratories can become certified.

CETP activity in liver perfusates and plasma from rabbits hypo- or hyperresponsive to dietary cholesterol
Meijer, G. W., J. E. Groener, et al. (1996), Comp Biochem Physiol B Biochem Mol Biol 114(4): 403-7.
Abstract: We investigated the relationship between the development of hypercholesterolemia in rabbits and cholesteryl ester transfer protein (CETP) activity secretion by their perfused livers. Two inbred strains of rabbits were compared which differ markedly in their hypercholesterolemic response to dietary cholesterol. Feeding a high-cholesterol (0.3%) diet, increased plasma and liver cholesterol level in the two strains, the increments being 15 mM and 30 mumol/g greater in the hyperresponders, respectively. The high-cholesterol diet caused an about 2-fold increased hepatic secretion of CETP activity, but there was no difference between the two rabbit strains. Feeding a lower amount of dietary cholesterol (0.08%) also caused higher cholesterolemic (2 mM) and hepatocholesterolic (28 mumol/g) responses in hyper- than in hyporesponsive rabbits. The activity of hepatic CETP secretion was not increased by the low-cholesterol diet, and there was no difference between hypo- and hyperresponsive rabbits. Cholesterol feeding increased plasma CETP activity by 90% in both rabbit strains, but there was no difference between the strains. Our combined data suggest that with increasing plasma cholesterol levels hepatic CETP secretion may be increased in a parabolic manner, reaching its maximum rate for before plasma cholesterol concentrations are maximal. There were no differences in hepatic CETP activity secretion of plasma CETP activity levels between the genetically different strains of hypo- and hyperresponsive rabbits.

CETP is a determinant of serum LDL-cholesterol but not HDL-cholesterol in healthy Japanese
Kinoshita, M., T. Teramoto, et al. (1996), Atherosclerosis 120(1-2): 75-82.
Abstract: Cholesteryl ester transfer protein (CETP) is one of the factors that regulate plasma levels of HDL-cholesterol. To identify the factors that may regulate CETP activity, and to determine to what extent CETP is correlated with physiologic concentrations of lipoprotein, we performed an epidemiologic study in 586 healthy volunteers (317 males and 269 females mean age 52.2 +/- 10.9 years). CETP activity in these subjects was 192.96 +/- 48.73 (mean +/- S.D.) nmol/ml/h and distributed to a wide range (60-450 nmol/ml/h). Using multiple regression analysis, we found significant positive correlations between CETP activity and LDL-cholesterol (P < 0.03), apolipoprotein (apo) E (P < 0.005) and LCAT activity (P < 0.001). CETP activities showed significant negative correlation with apo A-I (P < 0.03). However, CETP activity showed no significant correlation either with HDL cholesterol or with apo B. One-way layout analysis of variance showed that alcohol drinking and cigarette smoking significantly reduced CETP activity, but there was no significant association between CETP activity and body mass index. Although CETP activities were significantly higher in females than in males (P < 0.001), multiple regression analysis showed no correlation between CETP activity and age in either the males or the females. Our results suggest that CETP activity regulates the concentration of apo A-I and LDL-cholesterol, and that such activity may be influenced by gender, alcohol consumption and cigarette smoking.

Challenges to implementing the current pediatric cholesterol screening guidelines into practice
Dennison, B. A., P. L. Jenkins, et al. (1994), Pediatrics 94(3): 296-302.
Abstract: OBJECTIVE. The Expert Panel on Blood Cholesterol Levels in Children and Adolescents of the National Cholesterol Education Program (NCEP) recommends selective screening of children for high blood cholesterol. We determined the number of children, who, according to the guidelines, should be targeted for cholesterol screening. DESIGN. Population survey. SETTING. Permanent household residents in Otsego County, NY. PARTICIPANTS. Total population-based sample of 17,444 households (86.6% response rate) including 44,565 participants, of whom 10,457 were children, aged 2 through 19 years. MAIN OUTCOME MEASURES. Percent of children qualifying for cholesterol screening under the NCEP Children's Panel guidelines. RESULTS. Children from two-parent families were more likely to have known family history of coronary heart disease (CHD) before 60 years of age (41.8% vs 25.8%, P <.001), and twice as likely as children from single-parent families to have known parental hypercholesterolemia (18.8% vs 9.5%, P <.001). Only 39% of parents reported having had their cholesterol level checked; they were better educated and more likely to have health insurance. Parents with a first-degree relative with CHD before 60 years of age were more likely to report having their cholesterol level checked and to report a high cholesterol level. We calculated that 27% of children (18% of children from single-parent households and 29% of children from two-parent households) would report a known family history of premature CHD (ie, CHD before 55 years of age) and qualify for lipoprotein analysis, and that 11% of children would qualify for total cholesterol screening because of known parental hypercholesterolemia without a family history of premature CHD. Thirty-five percent of children had incomplete or unavailable family health history and/or unknown parental cholesterol status. CONCLUSIONS. In this population, 38% of children would be targeted for cholesterol screening, exceeding the estimate of the NCEP Children and Adolescents Panel. The selection process, however, would tend to miss children from single-parent families, children with incomplete family health history, and children whose parents have not had their cholesterol levels measured. The currently recommended pediatric cholesterol screening policy needs to be evaluated further in additional communities and population settings. Alternative cholesterol screening strategies are needed when family health history is incomplete and/or parental cholesterol status is unknown.

Change in cholesterol awareness and action. Results from national physician and public surveys
Schucker, B., J. T. Wittes, et al. (1991), Arch Intern Med 151(4): 666-73.
Abstract: The National Heart, Lung, and Blood Institute, Bethesda, Md, sponsored national telephone surveys of practicing physicians and the adult public in 1983, 1986, and 1990 to assess attitudes and practices regarding high serum cholesterol levels. Each time, approximately 1600 physicians and 4000 adults were interviewed. Trends show continuing change in medical practice and public health behavior relating to serum cholesterol. In 1990, physicians reported treating serum cholesterol at considerably lower levels than in 1986 and 1983. The median range of serum cholesterol at which diet therapy was initiated was 5.17 to 5.66 mmol/L (200 to 219 mg/dL) in 1990, down from 6.21 to 6.70 mmol/L (240 to 259 mg/dL) in 1986 and 6.72 to 7.21 mmol/L (260 to 279 mg/dL) in 1983. The median ranges for initiating drug therapy were 6.21 to 6.70 mmol/L (240 to 259 mg/dL) in 1990, 7.76 to 8.25 mmol/L (300 to 319 mg/dL) in 1986, and 8.79 to 9.28 mmol/L (340 to 359 mg/dL) in 1983. The number of adults who reported having had their cholesterol level checked rose from 35% to 46% to 65% in 1983, 1986, and 1990, respectively. Between 1983 and 1990, the number of adults reporting a physician diagnosis of high serum cholesterol increased from 7% to 16%; the number reporting a prescribed cholesterol-lowering diet increased from 3% to 9%. Reports of self-initiated diet efforts reached a high of 19% in 1986 and decreased to 15% in 1990 compared with 1% in earlier years. In 1990, over 90% of physicians reported awareness and use of the recommendations from the Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults, and the public reported marked increases in awareness of dietary methods to lower serum cholesterol. These changes suggest educational gains; the data also suggest areas for continued cholesterol educational initiatives.

Change in cholesterol levels and in lipid fatty acid composition in safflower oil fed lambs
Muci, M. R., A. R. Cappello, et al. (1992), Int J Vitam Nutr Res 62(4): 330-3.
Abstract: The influence of safflower oil supplemented (5%) diet both on cholesterol level and on lipid fatty acid composition was investigated in serum, liver and muscle (Longissimus dorsi) of lambs. The fatty acid pattern varied similarly in all the three tissues. An increase in linoleic acid and in some other polyunsaturated fatty acids, and a simultaneous reduction of the saturated fatty acids (mostly palmitic and stearic acid) were observed. On the contrary, cholesterol content decreased notably (44%) in the liver, with a much less evident decrease in serum and muscle of treated animals.

Change in cholesterol metabolism in HepG2 cells caused by antisense RNA to the oxysterol-binding protein gene
Krylov, A. S., A. Shevelev, et al. (1999), Dokl Akad Nauk 368(6): 830-2.

Change in concentration of cholesterol and lipoprotein fractions of rabbit blood serum in the dynamics of hypercholesterolemia
Bozhko, H., V. M. Kulabukhov, et al. (1992), Ukr Biokhim Zh 64(2): 61-6.
Abstract: Three quantitatively different periods have been detected as a result of 21-week monitoring of blood serum total cholesterol at hypercholesterolemia in rabbits. The first of them (4th week) ends by a relative decrease of cholesterol concentration: the second one (4th-13th weeks) is characterized by its sharp increase; in the third period (13th-21st weeks) the sterol accumulation slows down. Concentration variations of all main lipoprotein fractions are observed in each of the above periods. Their specific features enable us to suppose that in the first period the cholesterol transport system is activated which, probably, reflects the development of adaptation mechanisms of hypocholesterolemia. The second period can be considered as a transition stage from norm to pathology and is most likely, connected with atherogenesis induction. In the third period, in spite of relative stabilization of total cholesterol level clear signs of hyperbeta and hypoalpha dyslipoproteinemias are observed.

Change of high density lipoprotein receptor of hepatocyte during cholesterol gallstone formation in rabbit model
Shu, Y., L. Xiao, et al. (1999), Hua Xi Yi Ke Da Xue Xue Bao 30(3): 296-8.
Abstract: In order to study the formation of cholesterol gallstone through rabbit model which was induced by high cholesterol diet (HCD), we investigated the high density lipoprotein receptor (HDLr) activities of hepatocytes, total bile acids and cholesterol of common duct bile at 1 week(1 w), 2 weeks(2 w), 3 weeks (3 w) and 4 weeks(4 w) in comparison with those of a control group respectively. The results were as follows: 1. The HDLr Bmax decreased and the kd value increased significantly (1 w group vs control group, P < 0.05); In 2 w group the two variables recovered to the level of control group; and after that, the HDLr Bmax increased and Kd value decreased markedly (3 w and 4 w groups vs control group, P < 0.05). 2. Total bile acids in bile increased slightly in 1 w group (vs control group, P > 0.05), then decreased in 2 w, 3 w and 4 w groups (4 w group vs control group, P < 0.05). 3. The concentration of cholesterol in bile increased gradually as the time of feeding HCD went on (3 w and 4 w groups vs control group, P < 0.05). The results demonstrated that owing to the intake of HCD with the passage of time, the activity of HDLr was up at the beginning and down gradually in the rest period. The change in concentrations of bile acids was similar to that of HDLr, and the concentration of cholesterol in bile was foreign to the change of HDLr. These results suggest that the decrease of HDLr activity may cause the absence of material for bile acids synthesis and it may play an important role in the formation of gallstone.

Change of motion and localization of cholesterol molecule during L(alpha)-H(II) transition
Hayakawa, E., M. Naganuma, et al. (1998), Biophys J 74(2 Pt 1): 892-8.
Abstract: Formation of the inverted hexagonal (H(II)) phase from the lamellar (L(alpha)) phase of bovine brain-extracted phosphatidylcholine (BBPC) and phosphatidylethanolamine (BBPE) was investigated using 31P-NMR with or without cholesterol. When the ratio of BBPC to BBPE was 1:1, the H(II) formation was observed in the presence of 33 mol% cholesterol (i.e., BBPC:BBPE:cholesterol = 1:1:1) at 47 degrees C. The fraction of the H(II) phase in the BBPC/BBPE/cholesterol system could be controlled by the addition of dioleoylglycerol. The change of molecular motion of cholesterol affected by the H(II) formation was measured at various ratios of the L(alpha) to H(II) phase with the time-resolved fluorescence depolarization method, using dehydroergosterol as a fluorescent probe. It is observed that the motion of cholesterol became vigorous in the mixture state of the L(alpha) and the H(II) phases compared to that in the L(alpha) or the H(II) phase only. These facts show that cholesterol has the strong ability to induce the H(II) phase, probably by special molecular motion, which includes change of its location from the headgroup area to the acyl-chain area.

Change of serum lipid, apolipoprotein during cholesterol gallstone formation in rabbit model
Zhao, J., L. Xiao, et al. (1997), Hua Xi Yi Ke Da Xue Xue Bao 28(4): 361-4.
Abstract: In order to study the formation of cholesterol gallstone through rabbit model which was induced by high cholesterol diet (HCD), we investigated the rabbits' serum lipoprotein cholesterols and apolipoprotein (apo) at 1 week (1w), 2 weeks (2w), 3 weeks (3w) and 4 weeks (4w) in comparison with those of a control group respectively. The results were as follows: (1) of 10 rabbits subjected to experiment, 4, 6, and 7 rabbits were found to have induced-cholesterol gallstones in the 2w, 3w and 4w groups respectively. (2) The serum concentrations of total cholesterol (TC), triglyceride (TG), phospholipid (PL), low density lipoprotein cholesterol (LDL-C) and very low density lipoprotein chloesterol (VLDL) increased significantly (1w, 2w, 3w and 4w groups vs control group, P < 0.05), especially in the 3w and 4w groups; the surum concentrations of high density lipoprotein cholesterol and its subfractions (HDL-C, HDL2-C, HDL3-C) decreased slightly (vs control group, P > 0.05). (3) The serum contents of apoB100, apoC II and apoC III increased significantly (vs control group, P < 0.05), especially in the 3w and 4w groups; the serum apoA I reduced gradually in 1w, 2w and 3w groups, and decreased greatly in 4w group (vs control group, P < 0.05). The results demonstrated that owing to the intake of high cholestrol diet with the passage of time, the increased concentrations of serum VLDL-C, apoB, apoC II and apoC III possibly caused an enhanced secretion of biliary cholesterol into bile; that the decreased serum apoA I level might reduce the secretion of anti-nucleating factor into bile. All of these factors and changes may play important roles during the formation of cholesterol gallstones.

Changes during hibernation in different phospholipid and free and esterified cholesterol serum levels in black bears
Chauhan, V., A. Sheikh, et al. (2002), Biochimie 84(10): 1031-4.
Abstract: During hibernation, fat is known to be the preferred source of energy. A detailed analysis of different phospholipids, as well as free and esterified cholesterol, was conducted to investigate lipid abnormalities during hibernation. The levels of total phospholipids and total cholesterol in the serum of black bears were found to increase significantly in hibernation as compared with the active state. Both free and esterified cholesterol were increased in the hibernating state in comparison with the active state (P < 0.05). The percentage increase during hibernation was more in free cholesterol (57%) than in esterified cholesterol (27%). Analysis of subclasses of serum phospholipids showed that choline containing phospholipids, i.e., sphingomyelin (SPG) (14%) and phosphatidylcholine (PC) (76%), are the major phospholipids in the serum of bear. The minor phospholipids included 8% of phosphatidylserine (PS) + phosphatidylinositol (PI), while phosphatidylethanolamine (PE) was only 2% of the total phospholipids. A comparison of phospholipid subclasses showed that PC, PS + PI and SPG were significantly increased, while PE was significantly decreased (P < 0.05) in the hibernating state as compared with the active state in black bears. These results suggest that the catabolism of phospholipids and cholesterol is decreased during hibernation in black bears, leading to their increased levels in the hibernating state as compared with the active state. In summary, our results indicate that serum cholesterol and phospholipid fractions (except PE) are increased during hibernation in bears. It is proposed that the increase of these lipids may be due to the altered metabolism of lipoproteins that are responsible for the clearance of the lipids.

Changes in 1H-NMR chemical shifts of Bis-GMA and its related methacrylates induced by their interaction with phosphatidylcholine/cholesterol liposomes
Fujisawa, S., Y. Kadoma, et al. (1991), Dent Mater J 10(2): 121-7.
Abstract: To clarify the hemolytic mechanism of Bis-GMA and its related methacrylates, the interaction of five methacrylates (Bis-GMA, MMA, NPGDMA, TEGDMA, and UDMA) with DPPC/Cholesterol (CS) liposomes, as a model for erythrocyte membranes, was studied by 1H-NMR spectroscopy. Exogenous Bis-GMA partitioning into the DPPC/CS liposomes caused disappearances of its proton signals. With NPGDMA, its signals broadened markedly in DPPC/CS liposomes. UDMA partitioning caused changes in chemical shifts to a higher field, whereas MMA and TEGDMA partitioning did not cause any changes in chemical shifts. It was concluded from these observations that Bis-GMA has a stronger interaction with the DPPC/CS liposomes than the other methacrylates used. The high hemolytic activity of Bis-GMA reported previously seemed to be due to its migration into the lipid bilayer of phospholipids containing CS in erythrocyte membranes.


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