| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Effect of dietary chitin on cholesterol absorption and metabolism in rats Zacour, A. C., M. E. Silva, et al. (1992), J Nutr Sci Vitaminol (Tokyo) 38(6): 609-13. Abstract: The effect of chitin at the level of 5% in the diet on cholesterol absorption and metabolism was studied in Wistar rats fed on diet containing beef tallow (7%) and cholesterol (1%). When compared with pair-fed controls, rats fed on diet containing chitin had: (1) similar weight gain and feed efficiency, (2) lower apparent protein digestibility, (3) equivalent liver steatosis, (4) reduced levels of liver triglycerides and cholesterol, (5) similar levels of serum and fecal cholesterol, (6) higher excretion of triglycerides in feces. |
| Effect of dietary chitosans with different viscosity on plasma lipids and lipid peroxidation in rats fed on a diet enriched with cholesterol Chiang, M. T., H. T. Yao, et al. (2000), Biosci Biotechnol Biochem 64(5): 965-71. Abstract: To investigate the effect of dietary chitosan on lipid metabolism, male SD (Sprague-Dawley) rats were fed a cholesterol-enriched diet containing 5% cellulose (CE), 5% chitosan (CCS; high viscosity), or 5% chitosan (FCS; low viscosity) for 4 weeks. The two types of chitosan with a comparable degree of deacetylation had a different molecular weight and intrinsic viscosity. Significantly (p < 0.05) lower plasma total cholesterol, LDL-cholesterol and VLDL-cholesterol concentrations were observed in the rats fed on the chitosan diets. In addition, chitosan significantly increased the fecal cholesterol and triglyceride contents. Although no significant difference in body weight was found among the dietary groups, the rats fed on the chitosan diets had lower relative liver weight when compared with those fed on the cellulose diet. Both of the chitosan groups had significantly lower liver total lipid and total cholesterol contents compared to the cellulose group, although the FCS group was less effective. The plasma and liver thiobarbituric acid reactive substances (TBAR) values were similar in the CE and FCS groups, while the CCS group had increased liver TBAR values. Although a significant increase in liver glucose-6-phosphate dehydrogenase activity was observed in the CCS group, no significant change was found in the FCS group. The observed influence of chitosans with different viscosity on the plasma lipid level, liver lipids and lipid peroxidation suggests that, while the hypocholesterolemic action of chitosans with different viscosity was similar, changes in the liver lipids and liver peroxidation status depended on their molecular weight when the deacetylation degree was comparable. |
| Effect of dietary cholesterol and alloxan-diabetes on tissue cholesterol and apolipoprotein E mRNA levels in the rabbit Lenich, C. M., A. V. Chobanian, et al. (1991), J Lipid Res 32(3): 431-8. Abstract: Alloxan-diabetic rabbits develop hypercholesterolemia and hypertriglyceridemia in response to cholesterol feeding. To determine whether alterations in apolipoprotein composition of plasma lipoproteins were due to changes in apolipoprotein gene expression, we measured the steady state apoE mRNA levels in several tissues from both control and diabetic rabbits. Control rabbits were fed either chow or chow plus 1.5% cholesterol (chow-fed or cholesterol-fed groups) and diabetic rabbits were fed either chow or chow plus 0.5% cholesterol for dietary periods of 5, 21, and 42 days. The tissues examined were liver, small intestine, brain, adrenals, and aorta. ApoE mRNA levels were measured by Northern and dot blot analysis with a human apoE cDNA probe. In control rabbits fed either chow or cholesterol diets for up to 42 days, the steady state apoE mRNA levels remained relatively constant in all of the tissues examined. In contrast, in alloxan-diabetic rabbits fed a 0.5% cholesterol diet, apoE mRNA was reduced in liver, brain, and adrenals (46 +/- 19%, 56 +/- 5%, and 39 +/- 18% of chow-fed control, respectively), but showed little change in the aorta (91 +/- 22% of chow-fed control). Despite a similar increase in plasma cholesterol, the cholesterol content of the liver and adrenals of cholesterol-fed diabetic rabbits were 20% and 50%, respectively, of that of the liver and adrenals in cholesterol-fed control rabbits. The result that apoE mRNA levels and tissue cholesterol content are altered in the diabetic cholesterol-fed rabbit suggests that insulin deficiency in the rabbit may influence apoE gene expression and tissue cholesterol homeostasis. |
| Effect of dietary cholesterol and carbohydrate on small intestinal structure and function in prematurely weaned rats Dunsford, B. R. and W. E. Haensly (1991), J Anim Sci 69(7): 2894-903. Abstract: A study using the prematurely weaned rat as a model for the pig was undertaken to determine the effect of dietary cholesterol and carbohydrate source on small intestinal structure and function. Duodenal and jejunal samples were obtained at 18, 24, and 30 d of age from rats weaned at 15 d of age and from unweaned rats at 15, 18, 24, and 30 d of age. Four 20% CP diets were formulated: two diets used lactose and glucose as the carbohydrate source and two used sucrose and starch as the carbohydrate source; 1% cholesterol was substituted for either glucose or starch in one of each diet type. The unweaned rats consistently gained weight at a faster rate (P less than.01), had greater concentrations of Alcian blue (AB+) and periodic acid-Schiff (PAS+) goblet cells (P less than.03), and had more favorable villus height than did the weaned rats. The animals fed cholesterol tended to gain more weight, had more AB+ and PAS+ goblet cells (P less than.03), and had longer villi than did those not fed cholesterol. Lactase activities tended to be greater in the unweaned rats. Sucrase activities were greater in the weaned rats at 18 d (P less than.02). The data indicate that the addition of cholesterol to weaning diets is beneficial in maintaining small intestinal integrity. |
| Effect of dietary cholesterol and fat levels on lipid peroxidation and the activities of antioxidant enzymes in rats Lu, Y. F. and C. F. Chiang (2001), Int J Vitam Nutr Res 71(6): 339-46. Abstract: The aim of this study was to investigate the effect of dietary fat levels, with or without cholesterol, on lipid peroxidation and the activities of antioxidant enzymes in rats. Thirty-two Wistar rats aged 4 weeks were divided into 4 groups and fed high (20%; HF) or low (5%; LF) fat, with or without 1% cholesterol, for 6 weeks. Cholesterol feeding resulted in significantly higher concentrations of serum cholesterol, but lowered serum triacylglycerol levels. Cholesterol feeding also led to markedly decreased levels of hepatic thiobarbituric acid reactive substances (TBARS) and lower activities of hepatic superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase, and glucose-6-phosphate dehydrogenase (G6PDH) when compared with cholesterol-free counterparts in both HF and LF diets. On the other hand, rats fed high-fat diets showed increased serum and liver TBARS, but decreased hepatic GSH-Px, SOD, and G6PDH activities. Hepatic catalase activity was lower in rats fed cholesterol-containing diets, but higher in rats fed high-fat diets, and interaction existed between cholesterol and fat feeding. These results suggested that dietary cholesterol might delay lipid peroxidation and decrease the activities of the hepatic antioxidant enzymes. The degree of lipid peroxidation was also influenced by dietary fat levels. |
| Effect of dietary cholesterol and fat on the expression of hepatic sterol 27-hydroxylase and other hepatic cholesterol-responsive genes in baboons (Papio species) Kushwaha, R. S., B. Guntupalli, et al. (1995), Arterioscler Thromb Vasc Biol 15(9): 1404-11. Abstract: Our studies of baboons with low and high responses to dietary cholesterol and fat suggest that low-responding baboons increase the activity of hepatic sterol 27-hydroxylase, an important enzyme of bile acid synthesis, considerably more than do high-responding baboons when challenged with a high-cholesterol, high-fat (HCHF) diet. The present studies were conducted to determine whether hepatic sterol 27-hydroxylase mRNA levels and plasma 27-hydroxycholesterol concentrations also differed with dietary responsiveness. Sixteen adult male baboons with a wide range of VLDL cholesterol plus LDL cholesterol (VLDL+LDL cholesterol) response to an HCHF diet were selected. They were examined first while on a chow diet and then after 1, 3, 6, 10, 18, 26, 36, 52, 72, and 104 weeks on the HCHF diet. Plasma and lipoprotein cholesterol concentrations increased rapidly during the first 3 weeks and stabilized thereafter. On the basis of the response in VLDL/LDL cholesterol, we selected five low-responding, four medium-responding, and five high-responding baboons for more intensive study in more detail. In low responders, the major increase in serum cholesterol concentration was in HDL cholesterol, whereas in medium and high responders it was in both VLDL+LDL and HDL cholesterol. In low and medium responders, serum or VLDL+LDL cholesterol did not change after 3 weeks of consumption of the HCHF diet, whereas in high responders VLDL+LDL cholesterol declined between 78 and 104 weeks.(ABSTRACT TRUNCATED AT 250 WORDS) |
| Effect of dietary cholesterol and taurocholate on cholesterol 7 alpha-hydroxylase and hepatic LDL receptors in inbred mice Dueland, S., J. Drisko, et al. (1993), J Lipid Res 34(6): 923-31. Abstract: Compared to BALB/c mice, inbred C57BL/6 mice are more susceptible to developing fatty streak atherosclerotic lesions when fed a cholesterol-rich diet containing taurocholate. We examined the metabolic basis for the taurocholate requirement. In contrast to widely accepted assumptions, taurocholate did not increase cholesterol absorption in either strain of mouse. However, in susceptible C57BL/6 mice, taurocholate was required to increase plasma concentrations of apoB. In both strains, the cholesterol-rich diet increased both the activity and mRNA for 7 alpha-hydroxylase, a compensatory response to maintain cholesterol homeostasis. In both strains, adding taurocholate to the diet suppressed both the activity and mRNA for 7 alpha-hydroxylase, thus blocking this important compensatory response. The cholesterol-rich diet (without taurocholate) significantly increased hepatic cholesterol content in both strains of mice, but repressed low density lipoprotein (LDL) receptor mRNA only in BALB/c mice (not in C57BL/6 mice). However, adding taurocholate to the cholesterol-rich diet did decrease LDL receptor mRNA in C57BL/6 mice. In C57BL/6, but not in BALB/c mice, there was a linear parallel relationship between 7 alpha-hydroxylase mRNA and LDL receptor mRNA. These data show the existence of strain-specific differences in the effects of dietary cholesterol and taurocholate on 7 alpha-hydroxylase and LDL receptor expression. The combined data suggest that genetic factors determine how the expression of hepatic LDL receptors responds to dietary cholesterol and taurocholate. |
| Effect of dietary cholesterol on activity and mRNA levels of hepatic lipase in rat Sultan, F., F. Benhizia, et al. (1995), Life Sci 56(1): 31-7. Abstract: Female lean Zucker rats were fed for four weeks with either a control diet or the same diet enriched with 2% (w/w) cholesterol and cholic acid (0.5%, w/w). This treatment resulted in a 6-fold increase in plasma total cholesterol. A 30% decrease was observed in plasma post-heparin HL activity, in contrast with lipoprotein lipase, which was unmodified in the cholesterol/cholate-fed rats. HL activity measured in liver homogenate from these rats was also decreased (-30%, p < 0.05), as was its protein mass, quantified by immunoblot analysis (-57%, (p < 0.01), whereas HL mRNA levels were 3-fold lower in the cholesterol/cholate-fed rats. We conclude that the cholesterol/cholate-enriched diet decreases the HL gene expression by acting at the transcriptional level and/or by affecting HL mRNA stability, or both. |
| Effect of dietary cholesterol on cholesterol synthesis in breast-fed and formula-fed infants Wong, W. W., D. L. Hachey, et al. (1993), J Lipid Res 34(8): 1403-11. Abstract: The fractional synthesis rate (FSR) of cholesterol was measured in 6 breast-fed and 12 formula-fed infants (ages 4 to 5 months) using the 2H2O method. The breast-fed infants had higher cholesterol intakes (18.2 +/- 4.0 vs. 3.4 +/- 1.8 mg/kg per day, P = 0.001), plasma total cholesterol (183 +/- 47 vs. 112 +/- 22 mg/dl, P = 0.013), and plasma low density lipoprotein (LDL)-cholesterol (83 +/- 26 vs. 48 +/- 16 mg/day, P = 0.023) than the formula-fed infants (6.9 +/- 2.6 vs. 2.1 +/- 0.6%/day, P < 0.001). Among all infants, there was a significant inverse relationship (P = 0.002, r = 0.66) between the FSR of cholesterol and dietary cholesterol intake. Our findings indicate that the greater cholesterol intake of the breast-fed infants was associated with elevated plasma LDL-cholesterol concentrations and that cholesterol synthesis in human infants may be efficiently regulated via HMG-CoA reductase when infants are challenged with high intakes of dietary cholesterol. |
| Effect of dietary cholesterol on low density lipoprotein-receptor, 3-hydroxy-3-methylglutaryl-CoA reductase, and low density lipoprotein receptor-related protein mRNA expression in healthy humans Boucher, P., M. de Lorgeril, et al. (1998), Lipids 33(12): 1177-86. Abstract: We investigated the possibility that dietary cholesterol downregulates the expression of low density lipoprotein (LDL) receptor and 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase genes of circulating mononuclear cells in vivo in healthy humans. We also studied the variations of the LDL receptor-related protein (LRP) gene in the same conditions. Dieters (n = 5) were submitted to a 4-d fat restriction (mean cholesterol intake: 6+/-4 mg/d), followed by a 7-d cholesterol (a mean of 791+/-150 mg/d) supplementation. Controls (n = 3) did not change their diet. During fat restriction, serum total and LDL cholesterol decreased significantly (P < 0.05), and LDL receptor and HMG-CoA reductase mRNA copy numbers in mononuclear cells increased by 57 and 147%, respectively (P < 0.05). After reintroducing cholesterol, serum cholesterol was stable whereas LDL receptor and HMG-CoA reductase mRNA decreased by 46 and 72% (P < 0.05) and LRP mRNA increased by 59% (P < 0.005). The changes in LDL receptor and HMG-CoA reductase mRNA abundance were correlated (r = +0.79, P = 0.02) during cholesterol reintroduction as were LDL receptor and LRP mRNA levels, but negatively (r = -0.70, P = 0.05). Also, 70% of the variability in LRP mRNA (P < 0.005) was explained by dietary cholesterol. Thus, the basic mechanisms regulating cellular cholesterol content, the coordinate feedback repression of genes governing the synthesis and uptake of cholesterol, are operating in vivo in humans. However, serum cholesterol did not increase in response to dietary cholesterol, suggesting that these mechanisms may not play as predominant a role as previously believed in the short-term control of serum cholesterol in vivo in humans. A new finding is that LRP gene is also sensitive to dietary cholesterol, suggesting that it may participate in the control of serum cholesterol. Further in vivo studies in humans are warranted to explore the molecular mechanisms of the physiological response to dietary cholesterol in humans. |
| Effect of dietary cholesterol on membrane properties and immune functions in rainbow trout Bowden, L. A., B. Weitzel, et al. (1994), Biochem Soc Trans 22(3): 339S. |
| Effect of dietary cholesterol on postprandial lipoproteins in three phenotypic groups Clifton, P. M. and P. J. Nestel (1996), Am J Clin Nutr 64(3): 361-7. Abstract: Dietary cholesterol appears to be associated with long-term cardiovascular risk even after its potential for cholesterol elevation has been accounted for, but the mechanism is unknown. Our aim in this study was to determine the postprandial lipoprotein changes after a high-cholesterol load (equal to about three eggs) eaten with a low-fat meal by three phenotypic groups normal, high low-density-lipoprotein (LDL)-cholesterol concentration, and high plasma triacylglycerol concentration and compare them with the changes seen after a low-fat meal without cholesterol. Twenty-one normolipidemic and hyperlipidemic men and women were studied on two occasions after a single meal, one containing 19 g fat and 700 mg cholesterol, the other containing a similar amount of fat but no cholesterol. Their plasma intermediate-density lipoproteins (IDLs), LDLs, and high-density lipoproteins (HDLs) were separated by isopycnic ultracentrifugation. The addition of 700 mg cholesterol to the meal increased the amount of cholesterol and triacylglycerol in the large triacylglycerol-rich lipoproteins (Sf > 1000), particularly in the hypertriacylglycerolemic group (P = 0.02, fat meal compared with fat and cholesterol meal). In the hypertriacylglycerolemic group the normal fall in HDL cholesterol after a fat meal was reduced by 87% (P = 0.02, fat meal compared with fat and cholesterol meal). Both of these changes may be atherogenic. There was no increase in any candidate atherogenic particle (e.g., small very-low-density lipoprotein, IDL, or LDL) with the acute dietary cholesterol load. Thus, dietary cholesterol does not acutely alter postprandial lipoproteins to produce a more atherogenic profile except possibly in hypertriacylglycerolemic subjects. |
| Effect of dietary cholesterol on rat glomerular cholesterol esterase Roh, D. D., P. Kwak, et al. (1993), Am J Nephrol 13(6): 478-82. Abstract: The accumulation of tissue cholesterol and cholesteryl esters is commonly seen during the development of both atherosclerosis and glomerulosclerosis. The intracellular cholesterol content is regulated, in part, by the hydrolysis of cholesteryl esters to cholesterol, a reaction catalyzed by cholesterol esterase. Decreased cholesterol esterase has been linked to cholesteryl ester accumulation in vascular cells and has been postulated to be an important factor in the progression of atherosclerosis and, possibly, glomerulosclerosis. In order to determine whether cholesterol esterase regulates glomerular cholesterol accumulation, the effect of cholesterol feeding on the cholesterol content and the activity of cholesterol esterase was examined in rat glomeruli. Cholesterol esterase was measured using a cholesteryl1-14Coleate-lecithin liposome substrate. Total and free glomerular cholesterol was measured spectrofluorometrically. Feeding rats 4% cholesterol for 2 months decreased total glomerular (acid plus neutral) cholesterol esterase activity when compared to glomeruli from similar rats fed a normal chow (1.8 +/- 0.1 versus 1.48 +/- 0.2 nmol/mg protein/h, p < 0.05). Total, free and esterified cholesterol concentrations were higher in glomeruli from cholesterol-fed rats than from controls, consistent with decreased cholesterol esterase activity. Thus, glomerular cholesterol accumulation appears to be regulated by cholesterol esterase. This finding is similar to that in other vascular tissues which have been investigated and which are prone to accumulate cholesterol during the development of atherosclerosis. |
| Effect of dietary cholesterol on the activities of key enzymes of cholesterol metabolism in hyperlipidemia- and atherosclerosis-prone Japanese quail Nagata, J., H. Oku, et al. (1996), J Nutr Sci Vitaminol (Tokyo) 42(4): 287-300. Abstract: The hyperlipidemia- and atherosclerosis-prone (HAP) Japanese quail is a strain developed for the study of atherosclerosis by genetic selection from the commercially available (CA) Japanese quail. To delineate the characteristics of cholesterol metabolism in this strain, concentrations of serum lipids as well as hepatic enzyme activities were compared between HAP and CA quail. The hepatic enzymes studied are involved in the key step reaction in cholesterol metabolism: HMG-CoA reductase, ACAT, and cholesterol 7 alpha-hydroxylase. The animals were fed ad libitum with either 1% cholesterol or cholesterol-free semipurified diet for 28 days. Although a significant increase (p < 0.01) in serum cholesterol was observed in both strains on elapse of cholesterol feeding, formation of atheroma was seen exclusively in HAP quail of the cholesterol-fed group. The serum and liver cholesterol levels of HAP quail fed the cholesterol diet were significantly higher (p < 0.01) than those of CA quail. No significant differences were seen in the rate of cholesterol biosynthesis (HMG-CoA reductase activity), cholesterol ester formation (ACAT activity) and cholesterol catabolism (7 alpha-hydroxylase activity) between CA and HAP quail. Furthermore, the fecal excretions of acidic and neutral sterol showed no significant difference between strains. Although the formation of atheroma in HAP quail may be presumably due to the contribution of the marked increase in serum cholesterol level, the rate of cholesterol catabolism and synthesis in HAP quail compared well with those of CA quail. These observations suggest that the retarded rate of cholesterol biosynthesis or catabolism is not responsible for hypercholesterolemia in HAP quail. |
| Effect of dietary cholesterol on the lipoprotein profile and binding of radioiodinated lipoproteins to hepatic membranes in the cockerel (Gallus domesticus) Loo, G., H. Y. Wong, et al. (1990), Comp Biochem Physiol B 97(1): 83-8. Abstract: 1. Cockerels fed a cholesterol-supplemented diet experienced a marked elevation of lipoprotein particles of density less than or equal to 1.006 g/ml (VLDL) and a diminution of lipoprotein particles of density 1.02-1.05 g/ml (LDL). 2. Unlike VLDL of some cholesterol-fed animals, cholesterol-fed cockerel VLDL did not display beta-mobility on agarose gel electrophoresis. 3. 125ILDL and 125IHDL binding to cockerel liver membranes was not affected by cholesterol feeding. 4. Different lipoprotein types appear to bind to a common site on cockerel liver membranes. 5. The results suggest that liver cells of cockerels may not possess LDL binding sites that are analogous to those of mammalian species. |
| Effect of dietary cholesterol oxidation products on the plasma clearance of chylomicrons in the rat Vine, D. F., K. D. Croft, et al. (2002), Lipids 37(5): 455-62. Abstract: Oxidized cholesterols in the diet have been shown to exacerbate arterial cholesterol deposition and the development of atherosclerosis in animal models. Dietary oxidized cholesterols are absorbed through the intestine and incorporated into lymph chylomicrons. The aim of this study was to investigate the effect of oxidized cholesterols on the metabolism of nascent chylomicrons in vivo. It was shown that oxidized cholesterols markedly delay the clearance of chylomicrons from plasma compared to rats given TG alone. However, there was no difference in the clearance of chylomicrons containing oxidized cholesterols vs. purified cholesterol, although the presence of oxysterols did appear to exacerbate the removal of these particles from circulation. The impaired clearance of chylomicrons containing oxidized cholesterols was not due to impaired lipolysis and slower conversion to the remnant form. Moreover, the incorporation of oxidized cholesterols did not alter the hepatic or splenic uptake of chylomicrons compared to chylomicrons isolated from rats given purified cholesterol or TG alone. Collectively, the results of this study suggest that the exacerbated delay in clearance of chylomicron remnants enriched with oxysterols may be due to impaired uptake by tissues other than the liver and spleen. Apolipoprotein (apo) analysis showed that oxysterol incorporation reduced the apoE content and altered the apoC phenotype of chylomicrons, which may have an impact on the removal of chylomicron remnants from plasma. In conclusion, dietary oxysterols appear to have the potential to adversely affect chylomicron metabolism. Therefore, further investigations in humans are required to determine whether dietary oxidized cholesterols found in cholesterol-rich processed foods delay the clearance of postprandial remnants, which may contribute to and exacerbate the development of atherosclerosis. |
| Effect of dietary cholesterol with or without saturated fat on plasma lipoprotein cholesterol levels in the laboratory opossum (Monodelphis domestica) model for diet-induced hyperlipidaemia Kushwaha, R. S., J. F. VandeBerg, et al. (2004), Br J Nutr 92(1): 63-70. Abstract: Laboratory opossums (Monodelphis domestica) show extreme genetic variability in their responsiveness to dietary lipids; a great proportion of the genetic variability in responsiveness is due to a single major gene. To determine whether the major gene for dietary response detected by genetic analysis in opossums is responsive to dietary cholesterol or dietary saturated fat, or a combination of both, we used males and females of susceptible and resistant lines of laboratory opossums that were 5 to 7 months old. The animals were challenged with three different experimental diets (high-cholesterol diets with or without high saturated fat from lard or coconut oil) and plasma lipoproteins were measured. Plasma and VLDL+LDL-cholesterol concentrations increased several-fold when the animals were fed the diet containing elevated cholesterol (P<0.001) or elevated cholesterol and fat (P<0.001) and differed between the two lines when they were fed high-cholesterol diets with or without fat (P<0.001). Plasma HDL-cholesterol concentrations were higher (P<0.05) in animals of the resistant line than in the susceptible line when they were fed the basal diet (550 (SEM 30) v. 440 (SEM 20) mg/l) and when they were fed the low-cholesterol and high-fat diet (600 (SEM 30) v. 490 (SEM 30) mg/l). Dietary coconut oil and lard had similar effects on plasma lipoprotein cholesterol concentrations in the susceptible line of opossums. A reduction in dietary cholesterol by 50 % with either the lard or coconut oil blunted the plasma cholesterol response. The results from the present studies suggest that the major gene for dietary response previously detected by genetic analysis in laboratory opossums affects the response to dietary cholesterol but not to saturated fat. |
| Effect of dietary cholesterol, trans and saturated fatty acids on serum lipoproteins in non-human primates Idris, C. A. and K. Sundram (2002), Asia Pac J Clin Nutr 11 Suppl 7: S408-15. Abstract: Nine cynomolgus monkeys were rotated randomly through four dietary treatments with each treatment lasting 6 weeks. A wash-out period of 4 weeks was maintained between each dietary rotation. The animals were fed diets containing 32% energy fat derived from palm olein (POL), lauric-myristic-rich oil blend (LM), American Heart Association (AHA) rich oil blend and hydrogenated soybean oil blend (trans). Diets were fed with (phase 1) or without (phase 2) the addition of dietary cholesterol (0.1%). In phase 1, when animals were fed without dietary cholesterol, plasma total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) was significantly raised and high-density lipoprotein cholesterol (HDL-C) was significantly depressed by the trans diets relative to all other dietary treatments. The resulting LDL-C/HDL-C ratio was also significantly increased. The LM diet increased TC significantly relative to the AHA diet while LDL-C was significantly increased compared to both POL and AHA. Apolipoprotein (apo) B was not affected significantly by these dietary treatments. Apo A1 was significantly increased by POL relative to all other dietary treatments. The trans diet reduced apo A1 and the resulting apo B/A1 ratio was increased significantly by trans relative to all other dietary treatments. Addition of 0.1% dietary cholesterol to these diets almost doubled the plasma TC and LDL-C in all dietary treatments. However, HDL-C was only marginally higher with the addition of dietary cholesterol. The LM + C (cholesterol added) diet resulted in the highest TC and LDL-C that was significant compared to all other dietary treatments. Trans + C increased TC compared to POL + C and AHA + C diets while increases in the LDL-C did not attain significance. The addition of dietary cholesterol did not affect HDL-C between treatments whereas plasma triglycerides were significantly increased by the trans + C diet relative to all other treatments. Both the trans + C and LM + C diets increased apo B and decreased apo A1 relative to the POL + C and AHA + C diets. The resulting apo B/A1 ratio was similarly altered. These results affirm that the lauric + myristic acid combination, along with trans fatty acids, increased lipoprotein-associated coronary heart disease risk factors compared to either POL or AHA. |
| Effect of dietary consumption, advanced age and overweight on the physical characteristics of cholesterol gallstones and biliary lipid composition in west Algerian women Lamri-Senhadji, M. Y., K. Mekki, et al. (2002), Ann Nutr Metab 46(3-4): 139-46. Abstract: The aim of this study was to determine the effect of age, overweight and food consumption on the number and size of cholesterol stones and bile composition in west Algerian women undergoing surgery for cholelithiasis. Patients were divided into four groups according to body mass index (BMI, weight/height(2), kg/m(2)) and age. The highest number of patients with cholesterol gallstones was observed in the older women, in particular in those being overweight. In all patients, the stone number and size was approximately similar. The same dietary consumption was observed in older and young patients. Overweight patients were characterized by higher energy consumption (14.5 +/- 2.0 MJ x day(-1)) versus normal-weight patients (10.6 +/- 1.3 MJ x day(-1); p < 0.01) and versus Mediterranean diet (8 MJ x day(-1)). In normal-weight patients, the cholesterol saturation index (CSI) was higher in older patients (+56%) versus young patients while it diminished (-53%) in older overweight versus young patients. In older patients, the CSI was fourfold higher in normal-weight compared to overweight patients (p < 0.001). In conclusion, differences in food consumption were noted in overweight patients compared to normal-weight patients. Advanced age and overweight impaired biliary lipid composition, increased the number of patients with cholesterol gallstones but did not significantly affect the physical characteristics of west Algerian women. |
| Effect of dietary copper supplementation on cell composition and apoptosis in atherosclerotic lesions of cholesterol-fed rabbits Lamb, D. J., T. Y. Avades, et al. (2002), Atherosclerosis 164(2): 229-36. Abstract: We have previously shown that dietary copper supplementation modulates the formation of atherosclerotic lesions in the cholesterol-fed rabbit. In the present study, we have investigated the effects of copper supplementation on the cellular composition and characteristics of atherosclerotic lesions in cholesterol-fed NZW rabbits. Rabbits received a 1% cholesterol diet with or without 0.02% copper acetate (containing 12 and 0.3 mg copper per 100 g diet, respectively) for 12 weeks. The tunica intima was significantly smaller in the animals receiving copper supplements (0.016+/-0.005 vs. 0.068+/-0.019 mm(2), P<0.05) and this was accompanied by a significant increase in aortic copper content (4.0+/-0.8 vs. 1.8+/-0.2 microg/g tissue, P<0.05). The percentage area staining for smooth muscle cells (HHF-35 positive) was significantly lower in the intima of animals receiving copper supplements (7.13+/-1.02 vs. 9.72+/-0.82%, P<0.05). However, there were no significant differences in area staining for macrophages (RAM-11 positive) between groups (22.6+/-7.9 vs. 23.3+/-4.9%). There were also significantly fewer apoptotic cells (0.96+/-0.33 vs. 2.54+/-0.56%, P<0.005) in the aortic intima from animals supplemented with copper, but no difference in the number of proliferating cells. However, there was a reduction in intimal collagen staining (Sirius red positivity) in the animals receiving a copper supplement. Taken together, these data show that dietary copper can significantly affect the composition and progression of atherosclerotic lesions. |