| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Prospective randomised trial in 1062 infants of diet low in saturated fat and cholesterol Lapinleimu, H., J. Viikari, et al. (1995), Lancet 345(8948): 471-6. Abstract: Interventions to avoid atherosclerosis might be more successful if launched early in life when eating and life-style patterns are formed, but dietary interventions have been limited by fears of diet-induced growth failure. We investigated the effects of a diet low in saturated fat and cholesterol on serum lipid concentrations and growth in 1062 healthy 7-month-old infants in a randomised study. Every 1-3 months, families in the intervention group received dietary advice aimed at adequate energy supply, with low fat intake (30-35% energy, polyunsaturated/monounsaturated/saturated fatty acid ratio 1/1/1, and cholesterol intake < 200 mg daily). Infants in control families consumed an unrestricted diet. 3-day food records were collected at ages 8 and 13 months. Growth was carefully monitored. Between 7 and 13 months serum cholesterol and non-high-density-lipoprotein cholesterol concentrations did not change significantly in the intervention group (mean change -0.03 SD 0.72 mmol/L and 0.01 0.67 mmol/L) but increased substantially in the control group (0.24 0.64 mmol/L and 0.23 0.60 mmol/L; p for difference in mean changes between groups < 0.001). Daily intakes of energy and saturated fat were lower in the intervention than in the control group at 13 months (4065 796 vs 4370 748 kJ, p = 0.033, and 9.3 3.5 vs 14.5 4.8 g, p < 0.001, respectively), and intake of polyunsaturated fat was higher (5.8 2.2 vs 4.4 1.4 g, p < 0.001). Growth did not differ between the groups and was as expected for children at this age. Serum cholesterol concentrations fell significantly in parents of intervention-group infants. The increases in serum cholesterol and non-high-density-lipoprotein cholesterol concentration that occur in infants between the ages of 7 and 13 months can be avoided by individualised diets, with no effect on the children's growth. |
| Prospective randomized trial of low-saturated-fat, low-cholesterol diet during the first 3 years of life. The STRIP baby project Niinikoski, H., J. Viikari, et al. (1996), Circulation 94(6): 1386-93. Abstract: BACKGROUND: The long-term consequences of modified fat intake in early childhood are poorly known. The randomized prospective STRIP baby project evaluates the effects of repeated dietary counseling on nutrient intakes and serum lipid values in children 7 months to 3 years old. METHODS AND RESULTS: One thousand sixty-two infants were randomized to intervention and control groups at 7 months of age. The families of the 540 intervention children were counseled to reduce the child's intake of saturated fat and cholesterol but to ensure adequate energy intake. Five hundred twenty-two control children consumed an unrestricted diet. Food records were kept, and serum lipids were measured at 5- to 12-month intervals. Intakes of saturated fat, fat as proportion of energy (E%), and cholesterol were lower in the intervention children than in control children at 13, 24, and 36 months of age. Fat intake by the intervention children decreased from 29 +/- 5 E% at 8 months of age to 26 +/- 6 E% at 13 months and then increased to 30 +/- 5 E% at 24 months and to 31 +/- 5 E% at 36 months. The control children consumed 29 +/- 4 E%, 28 +/- 5 E%, 33 +/- 5 E%, and 33 +/- 5 E% of fat at 8, 13, 24, and 36 months, respectively. The ratio of dietary poly-unsaturated to saturated fats of the intervention children was consistently higher than that of the control children (P <.0001). Baseline adjusted mean serum cholesterol concentration was lower in the intervention children than control children between 13 and 36 months (P <.0001; 95% confidence interval of the difference between the group means, -0.27 to -0.12 mmol/L). The effect was significant only in boys (95% confidence interval, -0.39 to -0.20 mmol/L in boys; -0.21 to 0.01 mmol/L in girls). CONCLUSIONS: Repeated individualized dietary counseling markedly reduces the increase in serum cholesterol concentration that occurs in control children during the first years of life. |
| Prospective study of serum cholesterol and site-specific cancers Chyou, P. H., A. M. Nomura, et al. (1992), J Clin Epidemiol 45(3): 287-92. Abstract: From 1965 to 1968, 7716 Japanese-American men were examined and tested for serum cholesterol. After 22 years, 1380 incident cancer cases were identified. Of the site-specific cancers, only colon cancer cases had a significantly lower mean serum cholesterol value than that of noncases (213.0 mg/dl vs 219.0 mg/dl). When the study subjects were separated into either a low, middle or high group, based on their serum cholesterol values, there was a significant inverse trend for cases of oral/pharyngeal/esophageal cancer combined. The association was present for cases diagnosed within 10 years of examination (p = 0.012), but not for cases diagnosed after 10 years. This suggests that the inverse association is due to the metabolic effects of undiagnosed oral/pharyngeal/esophageal cancer upon serum cholesterol levels. These results are discussed in relation to other studies on serum cholesterol. |
| Prospective study of serum cholesterol levels and large-bowel cancer Nomura, A. M., G. N. Stemmermann, et al. (1991), J Natl Cancer Inst 83(19): 1403-7. Abstract: Based on previous reports, it is uncertain whether serum cholesterol levels are inversely related to colon cancer risk. In this study, serum cholesterol levels were measured in 7926 Japanese-American men who were followed for over 20 years. Two hundred thirty-one incident cases of colon cancer and 97 cases of rectal cancer were identified. An increase in serum cholesterol levels was associated with a decrease in risk for colon cancer (P value for trend =.01) but not for rectal cancer. This association appeared stronger as the site of cancer moved from the sigmoid colon to the cecum. The data were further analyzed by interval from examination to diagnosis. The inverse association was present for colon cancer cases diagnosed within 10 years of examination (P value for trend less than.01), especially for cecum-ascending colon cancer cases (P less than.01). A similar inverse pattern was found for cecum-ascending colon cancer cases diagnosed after 10 years, but the association was not statistically significant. The results suggest that the preclinical effects of undiagnosed colon cancer contributed to the inverse association, but these effects do not entirely explain why the relationship with hypocholesterolemia was stronger in men who were subsequently diagnosed with right-sided colon cancer. |
| Prospective, randomized, infancy-onset trial of the effects of a low-saturated-fat, low-cholesterol diet on serum lipids and lipoproteins before school age: The Special Turku Coronary Risk Factor Intervention Project (STRIP) Rask-Nissila, L., E. Jokinen, et al. (2000), Circulation 102(13): 1477-83. Abstract: BACKGROUND: We showed previously that repeated dietary counseling during the first 3 years of life reduces the concentration of serum nonfasting cholesterol. We have now extended the study to children 5 years of age and analyzed fasting blood samples, enabling LDL cholesterol calculations for the first time. METHODS AND RESULTS: Families of 7-month-old infants (n=1062) were randomized to a control group (n=522) or an intervention group (n=540) that received individualized dietary counseling with the aims of a fat intake of 30% to 35% of daily energy, a saturated/monounsaturated/polyunsaturated fatty acid ratio of 1:1:1, and a cholesterol intake of <200 mg/d. Nutrient intakes were studied biannually, nonfasting serum lipid values were studied annually, and fasting values were studied at 5 years of age. The intervention children always had lower intakes of saturated fat and cholesterol than the control children. The intervention boys had 0.39 mmol/L (P:<0.0001) lower mean serum cholesterol values than the control boys between 13 and 60 months of age, but among girls, the difference was of marginal significance (0.15 mmol/L, P:=0.052). Five-year-old intervention boys had 9% lower mean serum LDL cholesterol concentrations than the control boys (P:=0.0002; 95% CI, -0.39 to -0.12 mmol/L), whereas no difference was observed in girls. In both sexes, serum triglyceride concentrations were similar in the 2 groups. CONCLUSIONS: The restriction of saturated fat and cholesterol intake by repeated, individualized dietary counseling since infancy resulted in lower serum total and LDL cholesterol concentrations at 5 years of age. However, the effect was significant only in boys. |
| Protease inhibitors' metabolic side effects: cholesterol, triglycerides, blood sugar, and "Crix belly." Interview with Lisa Capaldini, M.D. Interview by John S. James Capaldini, L. (1997), AIDS Treat News(No 277): 1-4. |
| Protection against atherosclerosis by estrogen is independent of plasma cholesterol levels in LDL receptor-deficient mice Marsh, M. M., V. R. Walker, et al. (1999), J Lipid Res 40(5): 893-900. Abstract: Low density lipoprotein (LDL) receptor-deficient (LDLR-/-) mice consuming a high fat diet were used to assess the effect of endogenous and exogenous estradiol (E2) on atherosclerosis. Sexually mature female mice were ovariectomized (OVX) and implanted with subcutaneous, slow-release pellets designed to release 6 microg/day of exogenous 17beta-estradiol (17beta-E2), 17alpha-estradiol (17alpha-E2), or placebo (E2- deficient). Sham-operated control female (endogenous E2) and male mice were studied as controls. Aortic atherosclerotic lesion area was reduced by physiologic amounts of both endogenous and exogenous E2 compared to E2-deficient female mice. Although plasma cholesterol levels were reduced by exogenous E2 despite the absence of the LDL receptor, endogenous E2 was not associated with any cholesterol changes. In contrast, only 17alpha-E2 was associated with decreased fasting triglyceride. In subgroup analyses matched for time-averaged plasma total cholesterol, aortic lesion area was reduced by the presence of estradiol (E2). E2 protected LDLR-/- female mice from atherosclerosis and this protection was independent of changes in plasma cholesterol levels. |
| Protection against carbon tetrachloride-induced hepatotoxicity by pretreating rats with the hemisuccinate esters of tocopherol and cholesterol Fariss, M. W., K. F. Bryson, et al. (1993), Environ Health Perspect 101(6): 528-36. Abstract: Previous studies have demonstrated that alpha-tocopheryl hemisuccinate (TS) protects hepatocyte suspensions from chemical-induced toxicity. It has been suggested that TS cytoprotection is related to unique properties of the TS molecule or is dependent on the cellular release and activity of unesterified alpha-tocopherol (T). To test the unique cytoprotective nature of TS in vivo, the protective ability of T and tocopherol esters against carbon tetrachloride (CCl4)-induced hepatotoxicity in rats was examined. Hepatoprotection determined by serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels and histopathology was not observed after T (or tocopheryl acetate and tocopheryl nicotinate) administration, even though this treatment resulted in a fivefold elevation in hepatic T content. Only pretreatment with TS (100 mg/kg, intraperitoneally) resulted in partial hepatoprotection against CCl4 (2.9 g/kg, orally) toxicity. These findings suggest that hepatoprotection results not from the cellular accumulation of T but rather from the intact TS molecule. To test this hypothesis, the hepatoprotective capacity of cholesteryl hemisuccinate (CS), unesterified cholesterol, and cholesteryl acetate (CA) was examined against CCl4 toxicity. As observed with the tocopherol derivatives, pretreatment with unesterified cholesterol or CA demonstrated no protective ability. However, when rats were pretreated with CS (100 mg/kg), the hepatotoxic effects of CCl4 (elevated serum AST and ALT levels and centrilobular necrosis) were completely prevented. The prevention of CCl4-induced hepatotoxicity by CS and TS do not appear to result from an alteration in hepatic drug metabolism. These data clearly demonstrate that CS and TS are unique and powerful cytoprotective agents against CCl4 hepatotoxicity in vivo.(ABSTRACT TRUNCATED AT 250 WORDS) |
| Protection by cholesterol-extracting cyclodextrins: a role for N-methyl-D-aspartate receptor redistribution Abulrob, A., J. S. Tauskela, et al. (2005), J Neurochem 92(6): 1477-86. Abstract: Cyclodextrins (CDs) are cyclic oligosaccharides composed of a lipophilic central cavity and a hydrophilic outer surface. Some CDs are capable of extracting cholesterol from cell membranes and can affect function of receptors and proteins localized in cholesterol-rich membrane domains. In this report, we demonstrate the neuroprotective activity of some CD derivatives against oxygen-glucose deprivation (OGD), N-methyl-D-aspartic acid (NMDA) and glutamate in cortical neuronal cultures. Although all CDs complexed with NMDA or glutamate, only beta-, methylated beta- and sulfated beta-CDs displayed neuroprotective activity and lowered cellular cholesterol. Only CDs that lowered cholesterol levels redistributed the NMDA receptor NR2B subunit, PSD-95 (postsynaptic density protein 95 kDa) and neuronal nitric oxide synthase (nNOS) from Triton X-100 insoluble membrane domains to soluble fractions. Cholesterol repletion counteracted the ability of methylated beta-CD to protect against NMDA toxicity, and reversed NR2B, PSD-95 and nNOS localization to Triton X-100 insoluble membrane fraction. Surprisingly, neuroprotective CDs had minimal effect on NMDA receptor-mediated increases in intracellular Ca(2+) concentration (Ca(2+)(i)), but did suppress OGD-induced increases in Ca(2+)(i). beta-CD, but not Mbeta-CD, also caused a slight block of NMDA-induced currents, suggesting a minor contribution to neuroprotection by direct action on NMDA receptors. Taken together, data suggest that cholesterol extraction from detergent-resistant microdomains affects NMDA receptor subunit distribution and signal propagation, resulting in neuroprotection of cortical neuronal cultures against ischemic and excitotoxic insults. Since cholesterol-rich membrane domains exist in neuronal postsynaptic densities, these results imply that synaptic NMDA receptor subpopulations underlie excitotoxicity, which can be targeted by CDs without affecting overall neuronal Ca(2+) levels. |
| Protection of superoxide-induced cholesterol oxidation by antioxidants in protic conditions Csallany, A. S., J. Hee-Lee, et al. (2002), Int J Food Sci Nutr 53(5): 403-9. Abstract: It was found in previous experiments that superoxide in the presence of added hydrogen peroxide in protic conditions produces oxysterols. The oxysterols formed under these conditions were 7beta-ketocholesterol, 7alpha-hydroxycholesterol and 7beta-hydroxycholesterol. In the present experiments, the inhibitory effects of three antioxidants, alpha-tocopherol (alpha-T), butylated hydroxyanisole (BHA) and butylated hydroxytoluene (BHT), on the oxidation of cholesterol in the presence of superoxide anion, water and hydrogen peroxide were investigated. It was found that BHA had the highest antioxidant activity on cholesterol oxidation, followed by alpha-T and BHT. The presence of antioxidants markedly retarded the formation of 7-ketocholesterol. The formation of 7beta-hydroxycholesterol or 7alpha-hydroxycholesterol was also reduced, but to a lesser degree. |
| Protective action of cholesterol against changes in membrane fluidity induced by malathion Blasiak, J. and Z. Walter (1992), Acta Biochim Pol 39(1): 49-52. |
| Protective action of cholesterol against changes in membrane fluidity induced by methylparathion Blasiak, J. (1993), Acta Biochim Pol 40(1): 35-8. |
| Protective action of phospholipid hydroperoxide glutathione peroxidase against membrane-damaging lipid peroxidation. In situ reduction of phospholipid and cholesterol hydroperoxides Thomas, J. P., M. Maiorino, et al. (1990), J Biol Chem 265(1): 454-61. Abstract: The general reactivity of membrane lipid hydroperoxides (LOOHs) with the selenoenzyme phospholipid hydroperoxide glutathione peroxidase (PHGPX) has been investigated. When human erythrocyte ghosts (lipid content: 60 wt % phospholipid; 25 wt % cholesterol) were treated with GSH/PHGPX subsequent to rose bengal-sensitized photoperoxidation, iodometrically measured LOOHs were totally reduced to alcohols. Similar treatment with the classic glutathione peroxidase (GPX) produced no effect unless the peroxidized membranes were preincubated with phospholipase A2 (PLA2). However, under these conditions, no more than approximately 60% of the LOOH was reduced; introduction of PHGPX brought the reaction to completion. Thin layer chromatographic analyses revealed that the GPX-resistant (but PHGPX-reactive) LOOH was cholesterol hydroperoxide (ChOOH) consisting mainly of the 5 alpha (singlet oxygen-derived) product. Membrane ChOOHs were reduced by GSH/PHGPX to species that comigrated with borohydride reduction products (diols). Sensitive quantitation of PHGPX-catalyzed ChOOH reduction was accomplished by using 14Ccholesterol-labeled ghosts. Kinetic analyses indicated that the rate of ChOOH decay was approximately 1/6 that of phospholipid hydroperoxide decay. Photooxidized ghosts underwent a large burst of free radical-mediated lipid peroxidation when incubation with ascorbate/iron or xanthine/xanthine oxidase/iron. These reactions were only partially inhibited by PLA2/GSH/GPX treatment, but totally inhibited by GSH/PHGPX treatment, consistent with complete elimination of LOOHs in the latter case. These findings provide important clues as to how ChOOHs are detoxified in cells and add new insights into PHGPX's protective role. |
| Protective effect of dietary monounsaturated fat on arteriosclerosis: beyond cholesterol Perez-Jimenez, F., J. Lopez-Miranda, et al. (2002), Atherosclerosis 163(2): 385-98. Abstract: The consumption of diets enriched in monounsaturated fat has been related to a lower rate of coronary heart disease. It is well known that this dietary model decreases LDL-cholesterol plasma levels when replacing a saturated fat enriched diet. For this reason, a high monounsaturated fat diet is now being advocated to prevent cardiovascular disease, especially in Mediterranean countries. However, some expert panels-the Joint Task Force of European and other Societies on Coronary Prevention and the International Task Force for Prevention of Coronary Heart Disease-recommend replacing dietary saturated fat by complex carbohydrates, limiting the intake of total fat to <30% of the energy and monounsaturated fat to no more than 10-15% of total calories, reaching a similar effect on LDL-cholesterol plasma levels to a high monounsaturated fat diet. The most appropriate nutritional model to prevent arteriosclerosis should be supported by research into other biological effects of both diets. Therefore, it is interesting to review the non-lipid effect of monounsaturated fat, starting with its influence on other cardiovascular risk factors, such as carbohydrate metabolism and blood pressure. Moreover, substantial evidence of the effect of dietary monounsaturated fat on a wide range of healthy benefits beyond cholesterol, which have been investigated in recent years, such as lipoprotein oxidation, coagulation, fibrinolysis and endothelium, will be discussed. Furthermore, many observational epidemiological studies suggest that a high intake of monounsaturated fat is associated with reduced coronary risk and this will be analyzed in accordance with the clinical evidence to discuss the best dietary model to prevent coronary artery disease. |
| Protective effects of CVPM on vascular endothelium in rats fed cholesterol diet Tu, Z., X. Han, et al. (2003), Clin Chim Acta 333(1): 85-90. Abstract: BACKGROUND: The cardiovascular protective mixture (CVPM) is a concoction of nine Chinese traditional medicines: Dan-shen root, Szechwan lovge rhizome, Chinese angelica, Hawthorn fruit, Safflower, Peach seed, Red peony root, earthworm, and membranous milkvetch root. These medicines are used to cure cardiovascular disease in China. METHODS: Animal models were established by feeding the Sprague-Dawley (SD) rats with lipid-rich forage. Serum total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) were measured. Malondialdehyde (MDA) content was determined to monitor lipid peroxidation. The 6-keto-prostaglandin F(1alpha)(6-keto-PGF(1alpha)) concentration was measured by radioimmunoassay to investigate the content of prostacyclin (PGI(2)). Electron microscope (JEM-1200EX) was used to observe the microstructure of the vascular endothelium. Rat aortic endothelial cell was cultured to investigate the effect of CVPM on vascular endothelial cell in vitro. RESULTS: CVPM inhibited the accumulation of TC, LDL-C, and MDA in vivo, when the rats were fed with cholesterol diet. CVPM promoted synthesizing and excreting of PGI(2), since it is capable of activating the proliferation of vascular endothelium in vitro. Electron micrographs showed that CVPM had notable protective effect on the vascular endothelium and prevented the shedding of these cells from subendothelial layer. CONCLUSIONS: CVPM could ameliorate the internal environment in which vascular endothelial cells lived, and activate the proliferation of these cells. Through these mechanisms, CVPM protect vascular endothelial cell from being harmed by excess cholesterol in vivo. |
| Protective effects of vitamin E and selenium on the renal morphology in rats fed high-cholesterol diets Gonca, S., S. Ceylan, et al. (2000), Pathobiology 68(6): 258-63. Abstract: The histopathological effects of cholesterol and the protective effects of vitamin E and selenium (Se) on renal histology were examined in Sprague-Dawley rats. Light-microscopic evaluation of the renal cortex revealed: glomerular fibrosis, cellular and mesangial proliferation, capillary obliteration and cholesterol crystals in the tubular lumina of the cholesterol-fed group. These results suggest that oxidated LDL (O-LDL) is a cytotoxic factor which stimulates mesangial cell and matrix proliferation. Ultrastructurally, small and large lipid vacuolization in intracapillary lumina, adhesion of epithelial foot processes, mesangial foam cells and polymorphonuclear leukocytes were seen in the cholesterol-fed group. In the groups fed cholesterol + vitamin E, cholesterol + Se and cholesterol + vitamin E + Se, morphological improvements were observed. It appeared that an excess in O-LDL, reactive oxygen species and growth factors might play an important role in the pathogenesis of glomerulosclerosis. In addition, it was concluded that antioxidant therapy may prevent LDL oxidation and generation of free radicals. |
| Protective role of biliary cholesterol and phospholipid lamellae against bile acid-induced cell damage Puglielli, L., L. Amigo, et al. (1994), Gastroenterology 107(1): 244-54. Abstract: BACKGROUND/AIMS: Bile salts (BS) are cytotoxic agents, but cell damage is not observed in the hepatobiliary system. We hypothesized that biliary lipid vesicles (unilamellae and multilamellae) could have a protective role against BS-induced cytotoxicity. METHODS: Biliary lipid lamellar secretion was induced by feeding rats with 0.5% diosgenin. Cytoprotection was assessed in bile duct-obstructed rats and by incubating human erythrocytes with sodium taurocholate. RESULTS: Biliary cholesterol concentration increased > 300% in diosgenin-fed rats; electron microscopic examination showed a great abundance of lipid lamellar vesicles in bile and within the canaliculi. After bile duct obstruction, serum hepatic enzyme activities were significantly lower in diosgenin-fed rats. Histologically severe and confluent hepatocellular necrosis was only observed in control rats. Biliary lamellar lipid material significantly reduced the BS-induced hemolytic effect in vitro in a concentration-dependent manner. This protective effect correlated to a progressive decrease in the intermicellar BS concentration. Phosphatidylcholine or cholesterol, alone or as lamellar structures, also showed cytoprotective effect in vitro but always less than native biliary lamellae. CONCLUSIONS: These results support the concept that native biliary cholesterol phospholipid lamellae represent an important cytoprotective factor for hepatocytes and biliary epithelial cells against BS-induced damage. |
| Protective role of intraperitoneally administrated vitamin E and selenium on the levels of total lipid, total cholesterol, and fatty acid composition of muscle and liver tissues in rats Yilmaz, O., S. Celik, et al. (1997), J Cell Biochem 64(2): 233-41. Abstract: The aim of this work was to determine the protective effects of intraperitoneally administrated vitamin E and Se on total lipid, total cholesterol, and fatty acid composition of rat liver and muscle tissues. Total lipid content of muscle tissue in Se and combination groups decreased as compared to the control group. However, the level of total lipid in the liver tissues was seen to decrease only in the combination group (P < 0.05). While the amount of total cholesterol in liver tissue was lower (P < 0.05) in the vitamin E and combination groups, the amount of total cholesterol in muscle tissue decreased (P < 0.05) in the combination group. The amount of linoleic acid in muscle tissue slightly decreased (P < 0.05), whereas the eicosenoic and eicosatrienoic acid amounts significantly increased (P < 0.01, P < 0.001) in the vitamin E group as compared to the control group. The amounts of most fatty acid decreased (P < 0.05) in the combination group. The proportions of eicosenoic, eicosatrienoic, and total polyunsaturated fatty acid (PUFA) within the total fatty acid were higher (P < 0.05) in vitamin E group, whereas these fatty acids proportions were lower (P < 0.05) in the Se group. Although the proportions of palmitic, linolenic, and total saturated fatty acids were low (P < 0.05), oleic and total unsaturated fatty acid proportions were higher (P < 0.05) in the combination group than in the control group. The amount of palmitic acid and total saturated fatty acid in liver tissue decreased (P < 0.01 and P < 0.05, respectively) in the vitamin E and combination groups. However, the amount of linoleic acid only decreased (P < 0.05) in the combination group. The amount of PUFA was slightly higher (P < 0.05) in vitamin E. The proportions of stearic acid and linoleic acid decreased (P < 0.05) both in the Se and combination groups. However, the proportions of eicosatrienoic, omega 6, and PUFA were slightly higher (P < 0.05) in the vitamin E group, but total saturated fatty acid proportion significantly decreased (P < 0.01) in both the vitamin E and combination groups. In conclusion, the level of total lipid and cholesterol in muscle and liver tissues were reduced by administrating vitamin E and Se together. Additionally, the fatty acid synthesis in the muscle and liver tissues was decreased by this process. However, it was observed that the protective effect of intraperitoneally administrated vitamin E was higher than Se on fatty acid composition in muscle and liver tissues. |
| Protein A carrying PMMA microbeads: adsorption of cholesterol and HlgG from human plasma Rad, A. Y., H. Ayhan, et al. (1997), Int J Artif Organs 20(10): 576-9. Abstract: Cholesterol and HIgG adsorbed from human plasma obtained from a hypercholesterolemic patient, onto protein A-immobilized polymethyl-methacrylate uniform microbeads carrying different amounts of protein A (0.264-1.682 mg protein A/g PMMA, or 0.66-4.2 mg protein A/m2 PMMA) were investigated in batchwise experiments. There was no interaction between protein A molecules and cholesterol when cholesterol aqueous solutions were used. However, there was significant cholesterol and HIgG adsorption from the plasma obtained from a patient with hypercholesterolemia. The maximum amounts of cholesterol and HIgG adsorbed were 3.96 micromol cholesterol/g PMMA (5.4 mg cholesterol/g PMMA) and 0.242 micromol IgG/g PMMA (35.4 mg IgG/g PMMA). |
| Protein and lipid sources affect cholesterol concentrations of juvenile Pacific white shrimp, Litopenaeus vannamei (Boone) Cheng, Z. J. and R. W. Hardy (2004), J Anim Sci 82(4): 1136-45. Abstract: Two experiments were conducted to evaluate the effects of protein and lipid sources on cholesterol, AA, and fatty acid content, and on biological performance of juvenile Pacific white shrimp, Litopenaeus vannamei (Boone). In Exp. 1, seven isonitrogenous and isocaloric diets were prepared using fish meal; soybean meal; casein; fish meal + soybean meal; fish meal + casein; soybean meal + casein; and fish meal + soybean meal + casein. In Exp. 2, seven isonitrogenous and isocaloric diets were prepared using fish oil; soy oil; poultry fat; fish oil + soy oil; fish oil + poultry fat; soy oil + poultry fat; and fish oil + soy oil + poultry fat. Nine shrimp (average BW 570 mg) were stocked per 60-L tank, with three tanks per diet in each experiment. Shrimp were fed to apparent satiation twice daily for 28 d. Protein sources affected shrimp cholesterol, feed consumption, feed efficiency, protein consumption, protein efficiency ratio, and crude body fat (P < or = 0.05), but not weight gain, survival, hepatosomatic index, body protein, ash, and AA composition. Body (without hepatopancreas) cholesterol concentrations were the highest in shrimp fed the diet containing fish meal (0.81%), lowest for those fed the casein diet (0.64%), and intermediate in the other dietary treatment groups (range 0.71 to 0.74%). Lipid source also affected shrimp body cholesterol, body fatty acid profiles, and fatty acid profiles in the hepatopancreas (P < or = 0.05), but not growth performance, body protein, fat, ash, and cholesterol concentrations in the hepatopancreas. Shrimp fed the fish oil diet had the highest body cholesterol (0.75%), whereas those fed the soy oil or poultry fat diets were lowest (0.66 and 0.65%, respectively). Results indicate that by replacing fish meal and fish oil with soybean meal and soy oil, shrimp growth performance is not affected, but body cholesterol concentration is reduced. |