Статті в журналах: "Cholesterol control"

1

Kiberstis, P. A. "Idolizing Cholesterol Control." Science Signaling 2, no. 78 (July 7, 2009): ec232-ec232. http://dx.doi.org/10.1126/scisignal.278ec232.

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2

Fletcher, Gerald F. "Fat and Cholesterol Control." Journal of Cardiopulmonary Rehabilitation 12, no. 3 (May 1992): 162–63. http://dx.doi.org/10.1097/00008483-199205000-00002.

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3

Marecic, Maryfrances, and Robin Bagby. "Take Control of Cholesterol." Nutrition Today 23, no. 5 (September 1988): 47. http://dx.doi.org/10.1097/00017285-198809000-00011.

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4

Belavic, Jennifer. "Drugs to control cholesterol." Nursing 42, no. 3 (March 2012): 68. http://dx.doi.org/10.1097/01.nurse.0000398753.52565.6a.

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5

Haug, Anna, Arne T. Høstmark, Øystein Spydevold, and Einar Eilertsen. "Hypercholesterolaemia, hypotriacylglycerolaemia and increased lipoprotein lipase activity following orchidectomy in rats." Acta Endocrinologica 113, no. 1 (September 1986): 133–39. http://dx.doi.org/10.1530/acta.0.1130133.

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Abstract. Plasma lipoproteins, faecal cholesterol excretion, and activities of lecithin: cholesterol acyltransferase (LCAT) hepatic lipase (HL), and lipoprotein lipase (LPL) were determined in castrated rats, in rats treated with testosterone propionate after castration, and in sham-operated controls. Compared to control rats, whole-plasma total cholesterol (TC) rose, and triacylglycerols (TG) fell in castrated rats, but were normalized by androgen substitution. VLDL components tended to be reduced, whereas HDL2 components rose following castration. In general, testosterone substitution normalized the alterations induced by castration. Adipose tissue LPL was higher in castrated rats than in control rats, whereas activities of HL and LCAT were not significantly affected by the treatments. Hepatic cholesterol concentration, and faecal excretion of cholesterol and bile acids were not significantly altered by the treatments. Considering all 3 groups together, there was a significant positive correlation between the concentration of plasma cholesterol and cholesterol in liver, between plasma HDL2-cholesteryl esters and hepatic cholesterol, and also between HL and faecal cholesterol excretion. The results suggest that short term castration of rats causes increased levels of lipoprotein lipase and thereby brings about a lowering of VLDL and an increased concentration of LDL and HDL2. These effects are reflected in hypotriacylglycerolaemia and hypercholesterolaemia.

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6

Khan, B., H. G. Wilcox, and M. Heimberg. "Cholesterol is required for secretion of very-low-density lipoprotein by rat liver." Biochemical Journal 258, no. 3 (March 15, 1989): 807–16. http://dx.doi.org/10.1042/bj2580807.

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To study potential effects of hepatic cholesterol concentration on secretion of very-low-density lipoprotein (VLDL) by the liver, male rats were fed on unsupplemented chow, chow with lovastatin (0.1%), or chow with lovastatin (0.1%) and cholesterol (0.1%) for 1 week. Livers were isolated from these animals and perfused in vitro, with a medium containing [2-14C]acetate, bovine serum albumin and glucose in Krebs-Henseleit buffer, and with an oleate-albumin complex. With lovastatin feeding, the hepatic concentrations of cholesteryl esters and triacylglycerols before perfusion were decreased, although free cholesterol was unchanged. However, hepatic secretion of all the VLDL lipids was decreased dramatically by treatment with lovastatin. Although total secretion of VLDL triacylglycerol, phospholipid, cholesterol and cholesteryl esters was decreased, the decrease in triacylglycerol was greater than that in free cholesterol or cholesteryl esters, resulting in secretion of a VLDL particle enriched in sterols relative to triacylglycerol. In separate studies, the uptake of VLDL by livers from control animals or animals treated with lovastatin was measured. Uptake of VLDL was estimated by disappearance of VLDL labelled with [1-14C]oleate in the triacylglycerol moiety, and was observed to be similar in both groups. During perfusion, triacylglycerol accumulated to a greater extent in livers from lovastatin-fed rats than in control animals. The depressed output of VLDL triacylglycerols and the increase in triacylglycerol in the livers from lovastatin-treated animals was indicative of a limitation in the rate of VLDL secretion. Addition of cholesterol (either free cholesterol or human low-density lipoprotein) to the medium perfusing livers from lovastatin-fed rats, or addition of cholesterol to the diet of lovastatin-fed rats, increased the hepatic concentration of cholesteryl esters and the output of VLDL lipids. The concentration of cholesteryl esters in the liver was correlated with the secretion of VLDL by the liver. These data suggest that cholesterol is an obligate component of the VLDL required for its secretion. It is additionally suggested that cholesteryl esters are in rapid equilibrium with a small pool of free cholesterol which comprises a putative metabolic pool available and necessary for the formation and secretion of the VLDL. Furthermore, the specific radioactivity (d.p.m./mumol) of the secreted VLDL free cholesterol was much greater than that of hepatic free cholesterol, suggesting that the putative hepatic metabolic pool is only a minor fraction of total hepatic free cholesterol.

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7

Anonymous. "Steps Overlooked in Cholesterol Control." Journal of Gerontological Nursing 20, no. 12 (December 1994): 47. http://dx.doi.org/10.3928/0098-9134-19941201-13.

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8

Florez, Hermes, Kelly J. Hunt, and Willy Marcos Valencia. "Reducing Disparities in Cholesterol Control." JAMA 328, no. 8 (August 23, 2022): 714. http://dx.doi.org/10.1001/jama.2022.13284.

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9

Björkhem, Ingemar. "Do oxysterols control cholesterol homeostasis?" Journal of Clinical Investigation 110, no. 6 (September 15, 2002): 725–30. http://dx.doi.org/10.1172/jci0216388.

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10

Kiberstis, P. A. "MiR-33 in Cholesterol Control." Science Signaling 3, no. 127 (June 22, 2010): ec189-ec189. http://dx.doi.org/10.1126/scisignal.3127ec189.

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11

Collins, Sonya. "Statin therapy for cholesterol control." Pharmacy Today 19, no. 10 (October 2013): 36–37. http://dx.doi.org/10.1016/s1042-0991(15)31126-9.

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12

Gilutz, Harel, Julian Zelingher, Yaakov Henkin, Dan Y. Bonneh, Zvi Liss, Roni Peleg, Max Mayslus, Reuben Ilia, and Avi Porath. "Computerized community cholesterol control (4C)." Journal of the American College of Cardiology 39 (March 2002): 263. http://dx.doi.org/10.1016/s0735-1097(02)81178-0.

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13

Nugraheni, Kartika, and Siti Harnina Bintari. "Aktivitas antidislipidemia Tepung tempe dan susu kedelai pada profil lipid tikus diabetes yang diinduksi streptozotocin." Jurnal Gizi dan Dietetik Indonesia (Indonesian Journal of Nutrition and Dietetics) 4, no. 3 (May 22, 2017): 147. http://dx.doi.org/10.21927/ijnd.2016.4(3).147-153.

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ABSTRACTBackground : dyslipidemia increases risk of cardiovascular disease on diabetes patients. Soybean contain many bioactive compounds which can help control lipid profile.Objectives : analyze the difference between fermented soybean (tempe flour) and unfermented soybean (soymilk) on lipid profile in diabetic rats.Methods : thirty male sprague dawley rats divided into 3 groups (1) diabetic control (2) tempe flour 1,8 gr (3) soymilk 1,35 gr. Tempe flour and soymilk were given for 28 days. Profile lipid measured including total cholesterol, triglycerides, LDL cholesterol and HDL cholesterol. The data then were analyzed using Anova with confidence level of 95%.Results : the decrease values of total cholesteril, triglycerides and LDL cholesterol were better in tempe flour group (p<0,05). In addition, tempe flour group also showed better increase in the value of HDL cholesterl (p<0,05)Conclusion :fermented soybean (tempe flour) showed better antidyslipidemic activity than unfermented ones

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14

Slotte, J. P., and E. L. Bierman. "Depletion of plasma-membrane sphingomyelin rapidly alters the distribution of cholesterol between plasma membranes and intracellular cholesterol pools in cultured fibroblasts." Biochemical Journal 250, no. 3 (March 15, 1988): 653–58. http://dx.doi.org/10.1042/bj2500653.

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This study examines the relationship between cellular sphingomyelin content and the distribution of unesterified cholesterol between the plasma-membrane pool and the putative intracellular regulatory pool. The sphingomyelin content of cultured human skin fibroblasts was reduced by treatment of intact cells with extracellularly added neutral sphingomyelinase, and subsequent changes in the activities of cholesterol-metabolizing enzymes were determined. Exposure of fibroblasts to 0.1 unit of sphingomyelinase/ml for 60 min led to the depletion of more than 90% of the cellular sphingomyelin, as determined from total lipid extracts. In a time-course study, it was found that within 10 min of the addition of sphingomyelinase to cells, a dramatic increase in acyl-CoA:cholesterol acyltransferase activity could be observed, whether measured from the appearance of plasma membrane-derived [3H]cholesterol or exogenously added [14C]oleic acid, in cellular cholesteryl esters. In addition, the cholesteryl ester mass was significantly higher in sphingomyelin-depleted fibroblasts at 3 h after exposure to sphingomyelinase compared with that in untreated fibroblasts [7.1 +/- 0.4 nmol of cholesterol/mg equivalents of esterified cholesterol compared with 4.2 +/- 0.1 nmol of cholesterol/mg equivalents of cholesteryl ester in control cells (P less than 0.05)]. The sphingomyelin-depleted cells also showed a reduction in the rate of endogenous synthesis of cholesterol, as measured by incorporation of sodium [14C]acetate into [14C]cholesterol. These results are consistent with a rapid movement of cholesterol from sphingomyelin-depleted plasma membranes to the putative intracellular regulatory pool of cholesterol. This mass movement of cholesterol away from the plasma membranes presumably resulted from a decreased capacity of the plasma membranes to solubilize cholesterol, since sphingomyelin-depleted cells also had a decreased capacity to incorporate nanomolar amounts of [3H]cholesterol from the extracellular medium, as compared with control cells. These findings confirm previous assumptions that the membrane sphingomyelin content is an important determinant of the overall distribution of cholesterol within intact cells.

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15

Hallikainen, Maarit, Henri Tuomilehto, Tarja Martikainen, Esko Vanninen, Juha Seppä, Jouko Kokkarinen, Jukka Randell, and Helena Gylling. "Cholesterol Metabolism and Weight Reduction in Subjects with Mild Obstructive Sleep Apnoea: A Randomised, Controlled Study." Cholesterol 2013 (May 16, 2013): 1–9. http://dx.doi.org/10.1155/2013/769457.

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To evaluate whether parameters of obstructive sleep apnoea (OSA) associate with cholesterol metabolism before and after weight reduction, 42 middle-aged overweight subjects with mild OSA were randomised to intensive lifestyle intervention (N=23) or to control group (N=18) with routine lifestyle counselling only. Cholesterol metabolism was evaluated with serum noncholesterol sterol ratios to cholesterol, surrogate markers of cholesterol absorption (cholestanol and plant sterols) and synthesis (cholestenol, desmosterol, and lathosterol) at baseline and after 1-year intervention. At baseline, arterial oxygen saturation (SaO2) was associated with serum campesterol (P<0.05) and inversely with desmosterol ratios (P<0.001) independently of gender, BMI, and homeostasis model assessment index of insulin resistance (HOMA-IR). Apnoea-hypopnoea index (AHI) was not associated with cholesterol metabolism. Weight reduction significantly increased SaO2and serum cholestanol and decreased AHI and serum cholestenol ratios. In the groups combined, the changes in AHI were inversely associated with changes of cholestanol and positively with cholestenol ratios independent of gender and the changes of BMI and HOMA-IR (P<0.05). In conclusion, mild OSA seemed to be associated with cholesterol metabolism independent of BMI and HOMA-IR. Weight reduction increased the markers of cholesterol absorption and decreased those of cholesterol synthesis in the overweight subjects with mild OSA.

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16

Shahnaz, Begum, Satoshi Tada, Tatsushi Kajikawa, Toshihiko Ishida, and Koichi Kawanishi. "Automated Fluorimetric Determination of Cellular Cholesterol." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 35, no. 5 (September 1998): 665–70. http://dx.doi.org/10.1177/000456329803500511.

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We developed a completely automated fluorimetric method for the determination of cellular cholesterol, consisting of enzymatic hydrolysis of cholesteryl ester to free cholesterol and enzymatic oxidation of free cholesterol in the presence of an indicator substrate to produce a fluorescent product. For control preparations of monocytes, the mean detection limit was 2.57 μmol/5 × 105 cells and the mean within-batch coefficients of variation were 9.30, 600 and 3.73% at mean cholesterol concentrations of 1.94, 9.05 and 12.49 μmol/5 × 105 cells, respectively. The results correlated well with those obtained by gas-liquid chromatography.

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17

Bakkeren, H. F., F. Kuipers, R. J. Vonk, and T. J. C. Van Berkel. "Evidence for reverse cholesterol transport in vivo from liver endothelial cells to parenchymal cells and bile by high-density lipoprotein." Biochemical Journal 268, no. 3 (June 15, 1990): 685–91. http://dx.doi.org/10.1042/bj2680685.

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Acetylated low-density lipoprotein (acetyl-LDL), biologically labelled in the cholesterol moiety of cholesteryl oleate, was injected into control and oestrogen-treated rats. The serum clearance, the distribution among the various lipoproteins, the hepatic localization and the biliary secretion of the [3H]cholesterol moiety were determined at various times after injection. In order to monitor the intrahepatic metabolism of the cholesterol esters of acetyl-LDL in vivo, the liver was subdivided into parenchymal, endothelial and Kupffer cells by a low-temperature cell-isolation procedure. In both control and oestrogen-treated rats, acetyl-LDL is rapidly cleared from the circulation, mainly by the liver endothelial cells. Subsequently, the cholesterol esters are hydrolysed, and within 1 h after injection, about 60% of the cell- associated cholesterol is released. The [3H]cholesterol is mainly recovered in the high-density lipoprotein (HDL) range of the serum of control rats, while low levels of radioactivity are detected in serum of oestrogen-treated rats. In control rats cholesterol is transported from endothelial cells to parenchymal cells (reverse cholesterol transport), where it is converted into bile acids and secreted into bile. The data thus provide evidence that HDL can serve as acceptors for cholesterol from endothelial cells in vivo, whereby efficient delivery to the parenchymal cells and bile is assured. In oestrogen-treated rats the radioactivity from the endothelial cells is released with similar kinetics as in control rats. However, only a small percentage of radioactivity is found in the HDL fraction and an increased uptake of radioactivity in Kupffer cells is observed. The secretion of radioactivity into bile is greatly delayed in oestrogen-treated rats. It is concluded that, in the absence of extracellular lipoproteins, endothelial cells can still release cholesterol, although for efficient transport to liver parenchymal cells and bile, HDL is indispensable.

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18

Redgrave, T. G., C. L. Elsegood, J. C. L. Mamo, and M. J. Callow. "Effects of hypothyroidism on the metabolism of lipid emulsion models of triacylglycerol-rich lipoproteins in rats." Biochemical Journal 273, no. 2 (January 15, 1991): 375–81. http://dx.doi.org/10.1042/bj2730375.

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Methimazole-treated hypothyroid rats were injected intravenously with triacylglycerol/cholesteryl oleate/cholesterol/phospholipid emulsions designed to model the composition of chylomicrons. Compared with controls, hypothyroidism decreased the clearance rates of emulsion cholesteryl oleate. Clearance of emulsion triolein was affected much less and could be accounted for by residual triolein in remnants, suggesting that triacylglycerol lipolysis by lipoprotein lipase was unaffected by hypothyroidism but that clearance of remnants from plasma was decreased. Assays in vitro showed increased activities of lipoprotein lipase and hepatic lipase in hypothyroid rats. Emulsions were incubated with post-heparin plasma lipoprotein lipase to prepare remnants in vitro. The clearance from plasma of pre-formed remnants was slower after injection into hypothyroid rats than in control rats. Uptake of remnant cholesteryl oleate by the liver was significantly decreased in the hypothyroid rats. Treatment of hypothyroid rats for 7 days with 3,3′,5′-tri-iodo-L-thyronine (T3) reversed the inhibition of hepatic remnant uptake and normalized plasma cholesterol. A thyroid hormone analogue with decreased hypermetabolic side-effects, L-94901, attenuated plasma cholesterol and improved but did not normalize remnant clearance. Emulsions incubated with plasma from hypothyroid rats had a decreased ratio of apolipoprotein E/apolipoprotein C compared with control rats or hypothyroid rats treated with T3. The change in the apolipoprotein E/apolipoprotein C ratio probably accounts for the defect in remnant clearance in hypothyroidism.

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19

HIGGINS, MALCOLM J. P., and DESPINA K. PAPACHRISTODOULOU. "Control of hepatic acyl-CoA: cholesterol acyltransferase in cholesterol-fed rats." Biochemical Society Transactions 17, no. 1 (February 1, 1989): 156. http://dx.doi.org/10.1042/bst0170156.

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20

Hussain, Syed Saad, Megan T. Harris, Alex J. B. Kreutzberger, Candice M. Inouye, Catherine A. Doyle, Anna M. Castle, Peter Arvan, and J. David Castle. "Control of insulin granule formation and function by the ABC transporters ABCG1 and ABCA1 and by oxysterol binding protein OSBP." Molecular Biology of the Cell 29, no. 10 (May 15, 2018): 1238–57. http://dx.doi.org/10.1091/mbc.e17-08-0519.

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In pancreatic β-cells, insulin granule membranes are enriched in cholesterol and are both recycled and newly generated. Cholesterol’s role in supporting granule membrane formation and function is poorly understood. ATP binding cassette transporters ABCG1 and ABCA1 regulate intracellular cholesterol and are important for insulin secretion. RNAi interference–induced depletion in cultured pancreatic β-cells shows that ABCG1 is needed to stabilize newly made insulin granules against lysosomal degradation; ABCA1 is also involved but to a lesser extent. Both transporters are also required for optimum glucose-stimulated insulin secretion, likely via complementary roles. Exogenous cholesterol addition rescues knockdown-induced granule loss (ABCG1) and reduced secretion (both transporters). Another cholesterol transport protein, oxysterol binding protein (OSBP), appears to act proximally as a source of endogenous cholesterol for granule formation. Its knockdown caused similar defective stability of young granules and glucose-stimulated insulin secretion, neither of which were rescued with exogenous cholesterol. Dual knockdowns of OSBP and ABC transporters support their serial function in supplying and concentrating cholesterol for granule formation. OSBP knockdown also decreased proinsulin synthesis consistent with a proximal endoplasmic reticulum defect. Thus, membrane cholesterol distribution contributes to insulin homeostasis at production, packaging, and export levels through the actions of OSBP and ABCs G1 and A1.

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21

Bouillet, Benjamin, Thomas Gautier, Damien Denimal, Maxime Samson, David Masson, Jean Paul Pais de Barros, Guillaume Maquart, et al. "Glucocorticoids impair HDL-mediated cholesterol efflux besides increased HDL cholesterol concentration: a proof of concept." European Journal of Endocrinology 183, no. 3 (September 2020): 297–306. http://dx.doi.org/10.1530/eje-20-0477.

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Objective: Glucocorticoids (GC) are associated with increased cardiovascular morbidity despite increased HDL-C concentration. HDL-mediated cholesterol efflux, a major anti-atherogenic property of HDL particles, is negatively associated with CVD risk. We aimed to determine whether HDL-mediated cholesterol efflux was influenced by GC. Design: Prospective, observational study. Methods: Lipid parameters, HDL composition, HDL-mediated cholesterol efflux, cholesteryl ester transfer protein, phospholipid transfer protein and lecithin cholesterol acyl-transferase (LCAT) activities were determined in ten patients with giant cell arteritis before and 3 months after GC introduction and in seven control subjects. HDL concentration and composition, HDL-mediated cholesterol efflux and LCAT activity were determined in GC-treated mice. Results: In patients, HDL-C concentration was higher after than before treatment GC-treatment (P = 0.002), while HDL-mediated cholesterol efflux was decreased (P = 0.008) and negatively associated with the proportion of cholesteryl ester in HDL (P = 0.04), independently of CRP. As well, in mice, HDL-C level was increased after GC exposure (P = 0.04) and HDL-mediated cholesterol efflux decreased (P = 0.04). GC-treated patients had higher cholesteryl ester content in HDL, higher HDL2-to-HDL3 ratio and higher LCAT activity than before treatment (P = 0.008, P = 0.02 and P = 0.004, respectively). Conclusions: We report, for the first time, that in patients with giant cell arteritis and mice treated with GC, HDL-mediated cholesterol efflux was impaired by GC besides an increased HDL-C level. This impaired HDL functionality, possibly related to HDL enrichment in cholesteryl ester, could contribute to the increased CVD risk observed in GC-treated patients. Further studies are needed in larger populations, to further decipher the effect of GC on HDL.

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22

Poli, Andrea, Franca Marangoni, Alberto Corsini, Enzo Manzato, Walter Marrocco, Daniela Martini, Gerardo Medea, and Francesco Visioli. "Phytosterols, Cholesterol Control, and Cardiovascular Disease." Nutrients 13, no. 8 (August 16, 2021): 2810. http://dx.doi.org/10.3390/nu13082810.

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The use of phytosterols (or plant sterols) for the control of plasma cholesterol concentrations has recently gained traction because their efficacy is acknowledged by scientific authorities and leading guidelines. Phytosterols, marketed as supplements or functional foods, are formally classified as food in the European Union, are freely available for purchase, and are frequently used without any health professional advice; therefore, they are often self-prescribed, either inappropriately or in situations in which no significant advantage can be obtained. For this reason, a panel of experts with diverse medical and scientific backgrounds was convened by NFI—Nutrition Foundation of Italy—to critically evaluate and summarize the literature available on the topic, with the goal of providing medical doctors and all health professionals useful information to actively govern the use of phytosterols in the context of plasma cholesterol control. Some practical indications to help professionals identify subjects who will most likely benefit from the use of these products, optimizing the therapeutic outcomes, are also provided. The panel concluded that the use of phytosterols as supplements or functional foods to control Low Density Lipoprotein (LDL) cholesterol levels should be preceded by the assessment of some relevant individual characteristics: cardiovascular risk, lipid profile, correct understanding of how to use these products, and willingness to pay for the treatment.

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23

Brown, Andrew J., and Joanne Hsieh. "Foiling IDOL to Help Control Cholesterol." Circulation Research 118, no. 3 (February 5, 2016): 371–73. http://dx.doi.org/10.1161/circresaha.116.308191.

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24

Topping, David. "Hydroxypropylmethylcellulose, Viscosity, and Plasma Cholesterol Control." Nutrition Reviews 52, no. 5 (April 27, 2009): 176–78. http://dx.doi.org/10.1111/j.1753-4887.1994.tb01416.x.

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25

Russell, David W. "Nuclear Orphan Receptors Control Cholesterol Catabolism." Cell 97, no. 5 (May 1999): 539–42. http://dx.doi.org/10.1016/s0092-8674(00)80763-1.

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26

Strzyz, Paulina. "Cholesterol feeds into cell growth control." Nature Reviews Molecular Cell Biology 18, no. 5 (April 5, 2017): 277. http://dx.doi.org/10.1038/nrm.2017.41.

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27

Franceschini, Guido, JoséP werba, and Laura Calabresi. "Drug control of reverse cholesterol transport." Pharmacology & Therapeutics 61, no. 3 (January 1994): 289–324. http://dx.doi.org/10.1016/0163-7258(94)90014-0.

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28

Thompson, P. D. "Putting Cholesterol Control on a Diet." JAMA: The Journal of the American Medical Association 262, no. 21 (December 1, 1989): 2998. http://dx.doi.org/10.1001/jama.1989.03430210036018.

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29

Grove, David D. "Putting Cholesterol Control on a Diet." JAMA: The Journal of the American Medical Association 262, no. 21 (December 1, 1989): 2998. http://dx.doi.org/10.1001/jama.1989.03430210036020.

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30

Klipsic, Devon, Danilo Landrock, Gregory G. Martin, Avery L. McIntosh, Kerstin K. Landrock, John T. Mackie, Friedhelm Schroeder, and Ann B. Kier. "Impact of SCP-2/SCP-x gene ablation and dietary cholesterol on hepatic lipid accumulation." American Journal of Physiology-Gastrointestinal and Liver Physiology 309, no. 5 (September 1, 2015): G387—G399. http://dx.doi.org/10.1152/ajpgi.00460.2014.

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While a high-cholesterol diet induces hepatic steatosis, the role of intracellular sterol carrier protein-2/sterol carrier protein-x (SCP-2/SCP-x) proteins is unknown. We hypothesized that ablating SCP-2/SCP-x [double knockout (DKO)] would impact hepatic lipids (cholesterol and cholesteryl ester), especially in high-cholesterol-fed mice. DKO did not alter food consumption, and body weight (BW) gain decreased especially in females, concomitant with hepatic steatosis in females and less so in males. DKO-induced steatosis in control-fed wild-type (WT) mice was associated with 1) loss of SCP-2; 2) upregulation of liver fatty acid binding protein (L-FABP); 3) increased mRNA and/or protein levels of sterol regulatory element binding proteins (SREBP1 and SREBP2) as well as increased expression of target genes of cholesterol synthesis ( Hmgcs1 and Hmgcr) and fatty acid synthesis ( Acc1 and Fas); and 4) cholesteryl ester accumulation was also associated with increased acyl-CoA cholesterol acyltransferase-2 (ACAT2) in males. DKO exacerbated the high-cholesterol diet-induced hepatic cholesterol and glyceride accumulation, without further increasing SREBP1, SREBP2, or target genes. This exacerbation was associated both with loss of SCP-2 and concomitant downregulation of Ceh/Hsl, apolipoprotein B (ApoB), MTP, and/or L-FABP protein expression. DKO diminished the ability to secrete excess cholesterol into bile and oxidize cholesterol to bile acid for biliary excretion, especially in females. This suggested that SCP-2/SCP-x affects cholesterol transport to particular intracellular compartments, with ablation resulting in less to the endoplasmic reticulum for SREBP regulation, making more available for cholesteryl ester synthesis, for cholesteryl-ester storage in lipid droplets, and for bile salt synthesis and/or secretion. These alterations are significant findings, since they affect key processes in regulation of sterol metabolism.

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31

Chang, Chen-Kang, and Jean T. Snook. "The cholesterolaemic effects of dietary fats in cholesteryl ester transfer protein transgenic mice." British Journal of Nutrition 85, no. 6 (June 2001): 643–48. http://dx.doi.org/10.1079/bjn2001320.

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In order to investigate the role of cholesteryl ester transfer protein (CETP) in the cholesterolaemic response to dietary fats, we analysed plasma lipid profiles of CETP-transgenic and control C57BL/6 mice fed standard chow (AIN-93G; AIN), a low-fat diet, and diets high in butter (saturated fatty acids; SFA), high-oleic acid safflower oil (monounsaturated fatty acids; MUFA), and safflower oil (polyunsaturated fatty acids; PUFA) for 5 weeks. Each group contained four or five mice. There were significant diet and diet×genotype effects on plasma total cholesterol (TC; P = 0·035 and P = 0·008 respectively), liver TC (P < 0·001 and P = 0·002 respectively), and esterified cholesterol (EC; P = 0·002 and P = 0·001 respectively); diet effects on plasma triacylglycerol (P = 0·007), liver free cholesterol (P < 0·001), and body weight (P = 0·027); a genotype effect on body-weight gain (P = 0·014); and a diet×genotype effect on energy intake (P = 0·006). In transgenic mice the SFA diet caused significantly higher plasma TC than the PUFA diet (P < 0·05). In control mice MUFA and PUFA diets, but not the SFA diet, caused significantly higher plasma TC than the low-fat and AIN diets (P < 0·05). Transgenic mice fed PUFA had lower plasma TC (P = 0·040), while transgenic mice fed MUFA had lower LDL+VLDL-cholesterol (P = 0·013) than controls in the same dietary groups. Transgenic mice fed MUFA and PUFA diets also had significantly higher liver TC (P = 0·020 and P = 0·002 respectively) and EC (P = 0·040 and P = 0·036 respectively) than controls fed the same diets. In the present study we showed that: (1) CETP transgenic mice had a cholesterolaemic response to dietary fats similar to that in human subjects; (2) CETP transgenic mice fed PUFA showed significantly lower plasma TC, while those fed MUFA had lower LDL+VLDL-cholesterol than controls; (3) hepatic accumulation of cholesterol, possibly resulting from the combination of the enhanced cholesteryl ester transfer to apolipoprotein B-containing lipoproteins and increased hepatic uptake of cholesterol, may contribute to the cholesterol-lowering effect of MUFA and PUFA in CETP-transgenic mice; (4) CETP may play a role in appetite and/or energy regulation.

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32

Neary, Richard H., Mark D. Kilby, Padma Kumpatula, Francis L. Game, Deepak Bhatnagar, Paul N. Durrington, and P. M. Shaughn O'Brien. "Fetal and Maternal Lipoprotein Metabolism in Human Pregnancy." Clinical Science 88, no. 3 (March 1, 1995): 311–18. http://dx.doi.org/10.1042/cs0880311.

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1. Lipid, apolipoprotein concentration and composition were determined in maternal venous and umbilical arterial and venous blood at delivery by elective Caesarean section in 13 full-term pregnancies and in 25 healthy non-pregnant females. The indications of Caesarean section were a previous Caesarean section or breech presentation. None of the women was in labour and there were no other complications of pregnancy or fetal distress. 2. The objectives of the study were to establish whether the placenta has a role in feto-maternal cholesterol metabolism through either synthesis or transplacental cholesterol flux. The potential for free cholesterol diffusion between mother and fetus and rates of cholesterol esterification and transfer between lipoproteins were determined and related to the differences in composition between fetal and maternal lipoproteins. 3. Pregnant women had raised levels of all lipid and lipoprotein fractions compared with control subjects. The greatest increases were in free cholesterol and triacylglycerol (P < 0.0001). Lipoprotein (a) levels were significantly greater in the pregnant women [112(12.2) mg/l] than in the control women [50 (10.0) mg/l]. 4. The only significant correlation between maternal and fetal lipoprotein concentrations was in lipoprotein (a) levels (r = 0.791, P = 0.002). In both umbilical venous and arterial blood, concentrations of very-low- and low-density lipoproteins, particularly apolipoprotein B, cholesteryl ester and triacylglycerol, were lower than in maternal blood (P < 0.0001), but high-density lipoprotein levels were similar. 5. There was no umbilical arteriovenous differences in lipoprotein concentration or composition. This suggests that cholesterol synthesis or free cholesterol diffusion does not occur in the placenta. The relative concentrations of free cholesterol to phospholipid in maternal and fetal lipoproteins do not indicate the existence of a concentration gradient favouring free cholesterol diffusion across the placenta. 6. The esterification of free cholesterol was significantly reduced in maternal [17.7 (2.4) μmol h−1 l−1, P < 0.001] and fetal [6.7 (3.5) μmol h−1 l−1, P < 0.0001] compared with control [40.9 (13.2) μmol h−1 l−1] blood. 7. In fetal compared with maternal high-density lipoproteins the ratios cholesteryl ester/apoliproprotein A-I [0.84 (0.35) versus 0.40 (0.05), P < 0.01] and phospholipid/apolipoprotein A-I [1.66 (0.14) versus 0.58 (0.10), P < 0.0001] indicated lipid enrichment of these particles in the fetus. 8. Lipid enrichment of high-density lipoprotein is due in part to a marked reduction in transfer of cholesteryl ester in the fetus [1.0 (0.6) μmol h−1 l−1] compared with maternal [6.15 (1.3) μmol h−1 l−1, P = 0.004] and control [17.3 (7.2) μmol h−1 l−1, P < 0.0001] blood. 9. In conclusion, there was no evidence for involvement of the placenta in cholesterol metabolism during pregnancy. In fetal life high-density lipoproteins are lipid rich, partly because of a reduction in transfer of esterified cholesterol to other particles. Maternal and fetal lipoprotein levels are not correlated, although the results suggested that lipoprotein (a) levels may be related.

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33

NAPOLITANO, Mariarosaria, Kelly V. BATT, Michael AVELLA, Elena BRAVO, and Kathleen M. BOTHAM. "Lipid synthesis in macrophages derived from the human cell line THP-1: modulation of the effects of native and oxidized chylomicron-remnant-like particles by oestrogen." Clinical Science 101, no. 4 (September 14, 2001): 403–13. http://dx.doi.org/10.1042/cs1010403.

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The effects of native and oxidized chylomicron remnants on the synthesis of cholesteryl ester and triacylglycerol in macrophages, and the way that this is influenced by exposure of the cells to oestrogen, was investigated using the human monocyte cell line THP-1 and chylomicron-remnant-like particles containing human apolipoprotein E (CRLPs). Synthesis of the lipids was measured by the incorporation of [3H]oleate into cholesteryl ester and triacylglycerol. CRLPs (5-40μg of cholesterol/ml) containing either trilinolein or triolein as the triacylglycerol component caused a dose-dependent decrease in cholesteryl ester formation, while triacylglycerol production was unchanged. After oxidation of the CRLPs, the level of thiobarbituric acid-reactive substances was increased by 6.3-fold and 2.2-fold in particles containing trilinolein and triolein respectively. Furthermore, CRLPs containing oxidized trilinolein lost their ability to down-regulate cholesterol esterification, while CRLPs containing oxidized triolein did not. Both types of oxidized CRLPs decreased triacylglycerol synthesis. Treatment of the macrophages with 17β-oestradiol caused increases of approx. 94% and 34% in the synthesis of cholesteryl ester and triacylglycerol respectively in the absence of CRLPs. The differences between control and oestrogen-treated cells were abolished, however, when CRLPs (40μg of cholesterol/ml) were added to the incubations. In addition, in contrast with their lack of effect in control cells, CRLPs containing oxidized trilinolein decreased cholesterol esterification in oestrogen-treated cells by approx. 48%. These findings with CRLPs suggest that chylomicron remnants have significant effects on cholesteryl ester and triacylglycerol synthesis in macrophages, which may be modulated both by the oxidation state of the particles and by oestrogen.

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34

Vecka, Marek, Magdalena Dušejovská, Barbora Staňková, Ivan Rychlík, and Aleš Žák. "A Matched Case-Control Study of Noncholesterol Sterols and Fatty Acids in Chronic Hemodialysis Patients." Metabolites 11, no. 11 (November 12, 2021): 774. http://dx.doi.org/10.3390/metabo11110774.

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Dyslipidemia is common among patients on hemodialysis, but its etiology is not fully understood. Although changes in cholesterol homeostasis and fatty acid metabolism play an important role during dialysis, the interaction of these metabolic pathways has yet to be studied in sufficient detail. In this study, we enrolled 26 patients on maintenance hemodialysis treatment (high-volume hemodiafiltration, HV HDF) without statin therapy (17 men/9 women) and an age/gender-matched group of 26 individuals without signs of nephropathy. The HV-HDF group exhibited more frequent signs of cardiovascular disease, disturbed saccharide metabolism, and altered lipoprotein profiles, manifesting in lower HDL-C, and raised concentrations of IDL-C and apoB-48 (all p < 0.01). HV-HDF patients had higher levels of campesterol (p < 0.01) and β-sitosterol (p = 0.06), both surrogate markers of cholesterol absorption and unchanged lathosterol concentrations. Fatty acid (FA) profiles were changed mostly in cholesteryl esters, with a higher content of saturated and n-3 polyunsaturated fatty acids (PUFA) in the HV-HDF group. However, n-6 PUFA in cholesteryl esters were less abundant (p < 0.001) in the HV-HDF group. Hemodialysis during end-stage kidney disease induces changes associated with higher absorption of cholesterol and disturbed lipoprotein metabolism. Changes in fatty acid metabolism reflect the combined effect of renal insufficiency and its comorbidities, mostly insulin resistance.

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35

Lucić, A., V. Bradamante, M. Peraica, B. Radić, A.-M. Domijan, and R. Fuchs. "Changes in plasma lipids after a non-lethal dose of cycloheximide in rats." Human & Experimental Toxicology 22, no. 5 (May 2003): 245–48. http://dx.doi.org/10.1191/0960327103ht355oa.

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This paper describes a study of the effect of a single intraperitoneal non-lethal dose of cycloheximide (CHM; 2.0 mg/kg body weight) on the concentration of plasma lipids and lipoproteins in male rats killed one, two, three, four and nine days after receiving the dose. The concentration of triglycerides, total cholesterol, high-density lipoproteins (HDL)-cholesterol and low-density lipoproteins (LDL)-cholesterol was measured in treated and control animals. The effect of CHM on the concentration of triglycerides, total cholesterol, HDL-cholesterol, and LDL-cholesterol was visible in rat plasma throughout the study. Total cholesterol and HDL-cholesterol concentrations showed the same pattern of changes, probably due to the reversible inhibition of apolipoprotein apo A-I synthesis by CHM. The concentration of triglycerides decreased after a lag period of three days when the reserves of apolipoprotein apo B, the main apolipoprotein of very low-density lipoproteins (VLDL)-cholesterols produced in the liver, were consumed.

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36

Feingold, K. R., and A. H. Moser. "Effect of lactation on cholesterol synthesis in rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 249, no. 2 (August 1, 1985): G203—G208. http://dx.doi.org/10.1152/ajpgi.1985.249.2.g203.

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Lactation induces a variety of morphological and functional changes in the gastrointestinal tract. In the present study we employed tritiated water as the substrate to demonstrate that in the intact rat lactation results in a twofold increase in cholesterol synthesis in the small intestine. Feeding a high-cholesterol diet did not markedly inhibit small intestinal cholesterol synthesis in either control or lactating animals, and the difference in cholesterol synthesis between the two groups persisted. In the large intestine, cholesterol synthesis is increased threefold in the lactating animals, and feeding a high-cholesterol diet did not affect synthesis in either the control or lactating animals. In the liver, lactation stimulated cholesterol synthesis, and quantitatively this increase in hepatic cholesterol synthesis is much greater than the increase observed in the intestines. Feeding the rats a high-cholesterol diet markedly inhibited hepatic cholesterol synthesis in both control and lactating animals, a finding that demonstrates that the feedback inhibition of cholesterol synthesis in the liver is not impaired by lactation. In the lactating animals, the quantity of labeled cholesterol in 1 ml of serum is 2.4 times greater than observed in controls. Feeding the rats a high-cholesterol diet markedly decreased the quantity of labeled cholesterol in the serum in both groups and obliterated the difference between control and lactating animals. This suggests that the increased hepatic cholesterol synthesis in the lactating animals is responsible for the differences in labeled cholesterol in the serum. Cholesterol feeding also reduced the quantity of labeled cholesterol localized to the mammary glands in lactating animals.(ABSTRACT TRUNCATED AT 250 WORDS)

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37

Singh, Pravin Kumar. "Hyperlipidemia: Etiology and Possible Control Through Homoeopathic Remedies." International Journal of Advanced Ayurveda, Yoga, Unani, Siddha and Homeopathy 11, no. 1 (May 26, 2022): 696–700. http://dx.doi.org/10.23953/cloud.ijaayush.518.

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Hyperlipidemia is a condition characterized by an elevation of any or all lipid profile and/or lipoproteins in the blood. Hyperlipidemia is the most important atherosclerotic risk factor. Review of population-based studies in India shows increasing mean total cholesterol levels. Recent studies have reported that high cholesterol is present in 25–30% of urban and 15–20% rural subjects. This prevalence is lower than high-income countries. The most common Hyperlipidemia in India are borderline high LDL cholesterol, low HDL cholesterol and high triglycerides. Studies have reported that over a 20-years period total cholesterol, LDL cholesterol and triglyceride levels have increased among urban populations. Homoeopathy can play vital role not only in prevention and promotion but also as treatment in pre-clinical condition of borderline high-risk lipid levels and clinical condition of Hyperlipidemia with the proper use of Repertory and Homoeopathic materia medica.

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38

Reboulleau, Anne, Véronique Robert, Benoît Vedie, Aline Doublet, Alain Grynberg, Jean-Louis Paul, and Natalie Fournier. "Involvement of cholesterol efflux pathway in the control of cardiomyocytes cholesterol homeostasis." Journal of Molecular and Cellular Cardiology 53, no. 2 (August 2012): 196–205. http://dx.doi.org/10.1016/j.yjmcc.2012.05.015.

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39

Terlingen, J. B., H. J. van Dreumel, A. van Heiningen, G. J. Boerma, and J. C. Koedam. "Improved preparation of cholesterol calibration and control sera." Clinical Chemistry 31, no. 7 (July 1, 1985): 1201–3. http://dx.doi.org/10.1093/clinchem/31.7.1201.

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Abstract We prepared several serum batches with various cholesterol concentrations, to be used as calibrators and controls in a proficiency testing program of an organization in The Netherlands that is in charge of the standardization of cholesterol determinations for epidemiological purposes. The sera were of human origin, to avoid abnormal matrix effects. To decrease the cholesterol content in some samples, we adsorbed them onto colloidal silicic acid. To increase it, we added lipoproteins that had been precipitated from human serum with heparin and calcium ions. The precipitation method we used allowed us to dilute the serum as little as possible and to keep the final concentrations of calcium and heparin as low as possible, while maintaining a high cholesterol content. By mixing these sera having high and low cholesterol concentrations, we could prepare batches with any desired concentration. The stabilities of these sera were excellent. We used the sera to calibrate enzymic determinations of cholesterol.

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40

Gudbrandsen, Oddrun A., Hege Wergedahl, Bjørn Liaset, Marit Espe, and Rolf K. Berge. "Dietary proteins with high isoflavone content or low methionine–glycine and lysine–arginine ratios are hypocholesterolaemic and lower the plasma homocysteine level in male Zucker fa/fa rats." British Journal of Nutrition 94, no. 3 (September 2005): 321–30. http://dx.doi.org/10.1079/bjn20051496.

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It has previously been demonstrated that soya protein, which contains isoflavones and low methionine–glycine and lysine–arginine ratios, has a hypocholesterolaemic effect. In the present study, the hypocholesterolaemic effects of an isoflavone-enriched casein diet (HDI) and a single-cell protein-based diet (SCP) devoid of isoflavones but with low methionine–glycine and lysine–arginine ratios were investigated in obese Zucker rats after 6 weeks of feeding. The control diet contained casein, which has high ratios of methionine–glycine and lysine–arginine. HDI and SCP feeding reduced the concentrations of total cholesterol and cholesteryl esters in plasma and liver, and changed the fatty acid composition of the hepatic cholesteryl esters. Faecal cholesterol and bile acid levels were markedly higher in SCP-fed rats than in controls, whereas HDI feeding had only minor effects. However, both HDI and SCP feeding increased the hepatic gene expression of cholesterol 7α hydroxylase. In contrast, the hepatic acyl-CoA synthetase and acyl-CoA:cholesterol acyltransferase activities and the gene expression of the LDL receptor were increased by HDI, but not by SCP feeding. The present results suggested that the cholesterol-lowering effect of SCP was related to the enterohepatic circulation, whereas HDI seemed to lower the plasma cholesterol via the circulation. Plasma homocysteine level was reduced in rats fed HDI and SCP compared to rats fed casein. In summary, diets enriched in isoflavones or containing proteins with low methionine–glycine and lysine–arginine ratios lowered the plasma cholesterol and homocysteine levels, changing the plasma profile from atherogenic to cardioprotective.

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41

Rymaszewski, Z., R. L. Yunker, M. Ashraf, M. Park, and M. T. Subbiah. "Regulation of cholesterol metabolism in fetal rabbit aorta: role of amniotic fluid factors." American Journal of Physiology-Heart and Circulatory Physiology 255, no. 1 (July 1, 1988): H160—H168. http://dx.doi.org/10.1152/ajpheart.1988.255.1.h160.

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This study shows that amniotic fluid enhances cholesterol esterification in arterial wall, as measured by in vitro assay of acyl-CoA:cholesterol acyltransferase (ACAT) activity and by incorporation of oleic acid to cholesteryl esters in cultured fetal aortas and smooth muscle cells. This property is mostly evident in the fraction of molecular weight greater than 100,000, and it is abolished by delipidation, indicating that stimulating factor is probably lipoprotein in nature. Despite an increased cholesterol esterification by the presence of amniotic fluid in medium of cultured fetal aortas, the content of cholesterol and cholesteryl esters was much lower. The cellular structures are better preserved in explants cultured with amniotic fluid than in control animals. This study indicates that amniotic fluid contains factors that may have a pronounced effect on arterial wall during development.

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42

Zhang, Hanrui, Jianting Shi, Melanie A. Hachet, Chenyi Xue, Robert C. Bauer, Hongfeng Jiang, Wenjun Li, et al. "CRISPR/Cas9-Mediated Gene Editing in Human iPSC-Derived Macrophage Reveals Lysosomal Acid Lipase Function in Human Macrophages—Brief Report." Arteriosclerosis, Thrombosis, and Vascular Biology 37, no. 11 (November 2017): 2156–60. http://dx.doi.org/10.1161/atvbaha.117.310023.

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Objective— To gain mechanistic insights into the role of LIPA (lipase A), the gene encoding LAL (lysosomal acid lipase) protein, in human macrophages. Approach and Results— We used CRISPR (clustered regularly interspaced short palindromic repeats)/Cas9 (CRISPR–associated protein 9) technology to knock out LIPA in human induced pluripotent stem cells and then differentiate to macrophage (human-induced pluripotent stem cells–derived macrophage [IPSDM]) to explore the human macrophage LIPA loss-of-function phenotypes. LIPA was abundantly expressed in monocyte-derived macrophages and was markedly induced on IPSDM differentiation to comparable levels as in human monocyte–derived macrophage. IPSDM with knockout of LIPA ( LIPA −/− ) had barely detectable LAL enzymatic activity. Control and LIPA −/− IPSDM were loaded with [ 3 H]-cholesteryl oleate–labeled AcLDL (acetylated low-density lipoprotein) followed by efflux to apolipoprotein A-I. Efflux of liberated [ 3 H]-cholesterol to apolipoprotein A-I was abolished in LIPA −/− IPSDM, indicating deficiency in LAL-mediated lysosomal cholesteryl ester hydrolysis. In cells loaded with [ 3 H]-cholesterol–labeled AcLDL, [ 3 H]-cholesterol efflux was, however, not different between control and LIPA −/− IPSDM. ABCA1 (ATP-binding cassette, subfamily A, member 1) expression was upregulated by AcLDL loading but to a similar extent between control and LIPA −/− IPSDM. In nonlipid loaded state, LIPA −/− IPSDM had high levels of cholesteryl ester mass compared with minute amounts in control IPSDM. Yet, with AcLDL loading, overall cholesteryl ester mass was increased to similar levels in both control and LIPA −/− IPSDM. LIPA −/− did not impact lysosomal apolipoprotein-B degradation or expression of IL1B , IL6 , and CCL5. Conclusions— LIPA −/− IPSDM reveals macrophage-specific hallmarks of LIPA deficiency. CRISPR/Cas9 and IPSDM provide important tools to study human macrophage biology and more broadly for future studies of disease-associated LIPA genetic variation in human macrophages.

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43

Talamillo, Ana, Leiore Ajuria, Marco Grillo, Orhi Barroso-Gomila, Ugo Mayor, and Rosa Barrio. "SUMOylation in the control of cholesterol homeostasis." Open Biology 10, no. 5 (May 2020): 200054. http://dx.doi.org/10.1098/rsob.200054.

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SUMOylation—protein modification by the small ubiquitin-related modifier (SUMO)—affects several cellular processes by modulating the activity, stability, interactions or subcellular localization of a variety of substrates. SUMO modification is involved in most cellular processes required for the maintenance of metabolic homeostasis. Cholesterol is one of the main lipids required to preserve the correct cellular function, contributing to the composition of the plasma membrane and participating in transmembrane receptor signalling. Besides these functions, cholesterol is required for the synthesis of steroid hormones, bile acids, oxysterols and vitamin D. Cholesterol levels need to be tightly regulated: in excess, it is toxic to the cell, and the disruption of its homeostasis is associated with various disorders like atherosclerosis and cardiovascular diseases. This review focuses on the role of SUMO in the regulation of proteins involved in the metabolism of cholesterol.

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44

Safavi, Seyyed Morteza, Rahele Ziaei, and Mohammad Reza Maracy. "Association of Serum Ceruloplasmin Level with Obesity: Some Components of Metabolic Syndrome and High-Sensitive C-Reactive Protein in Iran." Journal of Obesity 2012 (2012): 1–5. http://dx.doi.org/10.1155/2012/951093.

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Background. One of the mechanisms that has been suggested for obesity related metabolic disturbances is obesity-induced inflammation. Pro-inflammatory cytokines generated in adipose tissue can increase hepatic synthesis of inflammation-sensitive plasma proteins (ISPs) including ceruloplasmin (Cp). In this study we aimed to investigate the relation between serum Cp level and obesity.Methods. 61 persons with body mass index (BMI) ≥ 25 kg/m2(case group) and 61 persons with BMI < 25 kg/m2(control group) were included in this study with a case-control design. Serum Cp levels, triglyceride level, fating blood glucose, total cholesterol, LDL-cholesterol, HDL-cholesterol and hsCRP were measured in both groups.Results. We did not observe any significant association between serum Cp level and BMI in all subjects [OR: 1.02 (CI, 0.967 to 1.07)] and in case (β=0.012,P=0.86) and control groups (β=0.49,P=0.07) separately. However, in control group, this positive association was marginally significant. We found a positive correlation between serum Cp level and serum triglyceride level.Conclusion. Serum Cp level was not related to obesity in this group of subjects. None of the baseline variables could predict obesity in this group of subjects, including serum Cp level, FBS, total cholesterol, LDL and HDL- cholesterols and hsCRP.

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45

Garg, M. L., and J. R. Sabine. "Homoeostatic control of membrane cholesterol and fatty acid metabolism in the rat liver." Biochemical Journal 251, no. 1 (April 1, 1988): 11–16. http://dx.doi.org/10.1042/bj2510011.

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Experiments were designed to assess the effect of cholesterol feeding, with or without high levels of either saturated (coconut oil) or unsaturated (sunflower-seed oil) fat on the fatty acid composition of hepatic microsomal membrane lipids, as well as on the activities of several membrane-bound enzymes of cholesterol synthesis and metabolism. Administration of 2% (w/w) cholesterol in the rat diet inhibited hydroxymethylglutaryl-CoA reductase activity, and this inhibition was much more pronounced when cholesterol was fed in combination with unsaturated rather than with saturated fat. Cholesterol 7 alpha-hydroxylase activity was increased by all the high-cholesterol diets and inhibited by both the high-fat diets. Cholesterol esterification, as assessed by acyl-CoA:cholesterol acyltransferase (ACAT) activity, was enhanced after unsaturated-fat feeding. Cholesterol supplement, without any added fat, failed to elicit any significant increase in ACAT activity, whereas consumption of cholesterol in combination with unsaturated fat led to the greatest increase in ACAT activity. After cholesterol feeding, C18:1 and C18:2 fatty acids in the microsomal phospholipids were increased, with concomitant decreases in C18:0, C20:4 and C22:6 fatty acids, leading to an overall decrease in membrane unsaturation, irrespective of the particular fat supplement. It can be concluded that the inhibition of cholesterol biosynthesis and the enhancement of cholesterol utilization, either by increased bile formation or by increased cholesterol esterification, after cholesterol feeding, may not be enough to prevent cholesterol accumulation in the microsomal membranes. Then, to compensate for the altered fluidity resulting from cholesterol enrichment, the unsaturation of membrane phospholipids is decreased, which would in turn have an effect on membrane lipid fluidity opposite to that of increased cholesterol.

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46

Caudill, Samuel P., Gerald R. Cooper, S. Jay Smith, and Gary L. Myers. "Assessment of current National Cholesterol Education Program guidelines for total cholesterol, triglyceride, HDL-cholesterol, and LDL-cholesterol measurements." Clinical Chemistry 44, no. 8 (August 1, 1998): 1650–58. http://dx.doi.org/10.1093/clinchem/44.8.1650.

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Abstract We examine the effect of systematic bias and random error, quality control, and intraperson biological variation on the National Cholesterol Education Program (NCEP) clinical classifications for reported lipid measurements. We consider misclassification to occur if a true lipid homeostatic set point is within a desirable range but the reported lipid value is in a high-risk range, or if a true lipid homeostatic set point is in a high-risk range but the reported lipid value is in a desirable range. To evaluate the overall adequacy of the NCEP guidelines to ensure correct patient classification, we construct operating characteristic curves for total cholesterol, triglycerides, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol. We demonstrate that if laboratories are meeting the NCEP guidelines for inherent bias and analytic precision and are using standard quality-control (QC) procedures incorporating at least two QC samples per analytical run from each of two QC pools (for a total of 4 QC samples), the current NCEP guidelines are adequate to ensure (probability >0.90) correct patient classifications regardless of the size of the systematic bias of the laboratory or increased random analytic error. Thus we suggest that at least two concentrations of QC material be included in the QC scheme to ensure that the measurement system is operating within desired specifications across the entire range of desirable and high-risk lipid concentrations and to ensure with high probability that patients are correctly classified.

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47

Franzini, C., and P. Luraschi. "Commutability of control materials in cholesterol measurement." Scandinavian Journal of Clinical and Laboratory Investigation 53, no. 1 (February 1, 1993): 51–55. http://dx.doi.org/10.3109/00365519309092531.

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48

Franzini, C., and P. Luraschi. "Commutability of control materials in cholesterol measurement." Scandinavian Journal of Clinical and Laboratory Investigation 53, no. 1 (January 1993): 51–55. http://dx.doi.org/10.1080/00365519309092531.

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49

MINEGISHI, YOSHIHIKO. "Tissue-specificity of cholesterol biosynthesis control mechanism." Kagaku To Seibutsu 41, no. 6 (2003): 375–77. http://dx.doi.org/10.1271/kagakutoseibutsu1962.41.375.

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50

Passey, Sarah. "Cholesterol control might help treat Alzheimer's disease." Lancet Neurology 3, no. 12 (December 2004): 700. http://dx.doi.org/10.1016/s1474-4422(04)00923-8.

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