| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Effects of diet and sexual maturation on low-density lipoprotein cholesterol during puberty: the Dietary Intervention Study in Children (DISC) Kwiterovich, P. O., Jr., B. A. Barton, et al. (1997), Circulation 96(8): 2526-33. Abstract: BACKGROUND: The Dietary Intervention Study in Children (DISC) is a multicenter, randomized, controlled clinical trial designed to examine the efficacy and safety of a dietary intervention to reduce serum LDL cholesterol (LDL-C) in children with elevated LDL-C. METHODS AND RESULTS: The effects of dietary intake of fat and cholesterol and of sexual maturation and body mass index (BMI) on LDL-C were examined in a 3-year longitudinal study of 663 boys and girls (age 8 to 10 years at baseline) with elevated LDL-C levels. Multiple linear regression was used to predict LDL-C at 3 years. For boys, LDL-C decreased by 0.018 mmol/L for each 10 mg/4.2 MJ decrease in dietary cholesterol (P<.05). For girls, no single nutrient was significant in the model, but a treatment group effect was evident (P<.05). In both sexes, BMI at 3 years and LDL-C at baseline were significant and positive predictors of LDL-C levels. In boys, the average LDL-C level was 0.603 mmol/L lower at Tanner stage 4+ than at Tanner stage 1 (P<.01). In girls, the average LDL-C level was 0.274 mmol/L lower at Tanner stage 4+ than at Tanner stage 1 (P<.05). CONCLUSIONS: In pubertal children, sexual maturation, BMI, dietary intervention (in girls), and dietary cholesterol (in boys) were significant in determining LDL-C. Sexual maturation was the factor associated with the greatest difference in LDL-C. Clinicians screening for dyslipidemia or following dyslipidemic children should be aware of the powerful effects of pubertal change on measurements of lipoproteins. |
| Effects of dietary 27-hydroxycholesterol on cholesterol metabolism and bile acid biosynthesis in the hamster Souidi, M., S. Dubrac, et al. (2003), Can J Physiol Pharmacol 81(9): 854-63. Abstract: 27-hydroxycholesterol (27OH-Chol) is an important endogenous oxysterol resulting from the action of sterol 27-hydroxylase (CYP27A1) on cholesterol in the liver and numerous extrahepatic tissues. It may act as a modulator of cholesterol and bile acid metabolism. The effects of 27OH-Chol on the main enzymes and receptors of cholesterol metabolism were investigated by feeding male hamsters a diet supplemented with 27OH-Chol (0.1% w/w) for 1 week. Intestinal scavenger class B, type I (SR-BI) protein level was decreased (-65%), but hepatic expression was increased (+34%). Liver 3beta-hydroxy-3beta-methyl glutaryl coenzyme A reductase (-58%), cholesterol 7alpha-hydroxylase (-54%), oxysterol 7alpha-hydroxylase (-44%), and sterol 12alpha-hydroxylase (-70%) activities were all decreased. Bile acid composition was changed (fourfold increase in the chenodeoxycholic/cholic acid ratio). This study demonstrates that dietary 27OH-Chol modulates major enzymes of cholesterol metabolism and alters the biliary bile acid profile, making it more hydrophobic, at least at this level of intake. Its effects on SR-BI protein levels are organ dependent. The properties of 27OH-Chol or its metabolites on cholesterol metabolism probably result from the activation of specific transcription factors. |
| Effects of dietary alpha linolenic acid on cholesterol metabolism in male and female hamsters of the LPN strain Morise, A., C. Serougne, et al. (2004), J Nutr Biochem 15(1): 51-61. Abstract: N-3 polyunsaturated fatty acids and estrogens are recognized as protective factors of atherosclerosis, however their interactions on cholesterol metabolism remain unclear. Male and female hamsters were fed for 9 weeks diets containing 12.5% lipids and rich in either alpha-linolenic acid ("linseed" diet) or saturated fatty acids ("butter" diet). Hamsters fed the "linseed" diet exhibited lower plasma concentrations of cholesterol (-29%), total LDL (-35%) and HDL (-17%), glucose (-20%), insulin (-40%) and of the LDL-cholesterol/HDL-cholesterol ratio (-27%) than those fed the "butter" diet. In the liver, cholesterol content was 2.7-fold lower in response to the "linseed" diet, whereas the concentration of HDL receptor (SR-BI) and the activities of HMGCoA reductase and cholesterol 7alpha-hydroxylase were 30 to 50% higher than with the "butter" diet. By contrast, the LDL receptor concentration did not vary with the diet. Females exhibited higher concentration of LDL (+24%), lower concentration of plasma triglycerides (-34%), total VLDL (-46%) and VLDL-cholesterol (-37%) and of biliary phospholipids (-19%). Besides, there was also an interaction between gender and diet: in males fed the "butter" diet, plasma triglycerides and VLDL concentration, were 2 to 4 fold higher than in the other groups. These data suggest that gene and/or metabolic regulations by fatty acids could interact with that of sex hormones and explain why males are more sensitive to dietary fatty acids. |
| Effects of dietary canola seed and soy lecithin in high-forage diets on cholesterol content and fatty acid composition of carcass tissues of growing ram lambs Lough, D. S., M. B. Solomon, et al. (1992), J Anim Sci 70(4): 1153-8. Abstract: Phospholipids (soy lecithin) are important in the emulsification of lipids and may escape the rumen and influence the absorption of fatty acids in the small intestine. Our objectives were to determine the influence of dietary canola seed (high in unsaturated fatty acids) and soy lecithin in high-forage diets on total lipid content, cholesterol content, and fatty acid composition of carcass tissues. Forty-three Hampshire or Suffolk-sired ram lambs were weaned at 60 d of age (average 23.6 kg of BW) and assigned to a 2 x 2 factorial arrangement of treatments consisting of 1) basal diet (control = BAS), 2) BAS with 6% whole canola seed (CS), 3) BAS with 4.9% deoiled soy lecithin (SL), and 4) BAS with 6% CS and 4.8% SL (CSSL). The BAS diet consisted of 70% forage and 30% concentrate and contained 15% CP and 2.2 Mcal of ME/kg. Lambs were individually fed and given ad libitum access to feed to an average final BW of 52.1 kg. Longissimus muscle (LM) from the left side of each carcass posterior to the 13th rib (12 to 15 cm in length) was excised and the lean (LM) and corresponding subcutaneous (s.c.) adipose tissue were separated, frozen, and later used for lipid analysis by gas-liquid chromatography. In lean tissue, feeding lambs CS reduced (P less than.01) the proportion of total polyunsaturated fatty acids (PUFA) and feeding SL increased (P less than.01) the proportion of total PUFA. In s.c. adipose tissue, lambs fed CS had lower (P less than.01) saturated fatty acids (SFA) and lambs fed SL had increased (P less than.03) PUFA.(ABSTRACT TRUNCATED AT 250 WORDS) |
| Effects of dietary cholesterol and fasting on hamster plasma lipoprotein lipids Weingand, K. W. and B. P. Daggy (1991), Eur J Clin Chem Clin Biochem 29(7): 425-8. Abstract: Hamsters are commonly utilized for comparative study of cholesterol metabolism. The present study was conducted to assess the effects of fasting on the plasma lipoprotein cholesterol concentrations of hamsters. Over a period of 3 weeks, adult male Golden Syrian hamsters (n = 32) were fed chow with or without the addition of 2 g/kg cholesterol. Half of the animals consuming each diet were fasted for 18 hours prior to blood sampling. Comparison of diets showed the following increases in those animals receiving cholesterol: total plasma cholesterol (180%) and triacylglycerols (75%), high density (75%), low density (250%), and very low density (560%) lipoprotein cholesterol. Compared with fasted animals, total plasma triacylglycerols were higher in both non-fasted diet groups. Compared with fasted hamsters that had received cholesterol, total plasma cholesterol (mean +/- SE mmol/l) was greater (6.36 +/- 0.18 vs 5.43 +/- 0.21; p less than or equal to 0.05) in the non-fasted group, due primarily to higher VLDL cholesterol (2.07 +/- 0.18 vs 1.58 +/- 0.18; p less than or equal to 0.05). There were no differences in HDL cholesterol (2.07 +/- 0.05 vs 2.17 +/- 0.08) or LDL cholesterol (1.29 +/- 0.08 vs 1.37 +/- 0.05) between fasted and non-fasted hamsters fed cholesterol. Fasting is not necessary for the study of the plasma HDL cholesterol and LDL cholesterol of hamsters fed cholesterol. |
| Effects of dietary cholesterol and fat saturation on plasma lipoproteins in an ethnically diverse population of healthy young men Fielding, C. J., R. J. Havel, et al. (1995), J Clin Invest 95(2): 611-8. Abstract: The individual effects of dietary cholesterol and fat saturation on plasma lipoprotein concentrations were determined in an ethnically diverse population of normolipidemic young men (52 Caucasian, 32 non-Caucasian). The experimental diets contained approximately 200 or 600 mg/d of cholesterol, 36-38% of calories as fat, and high or low proportions of saturated and polyunsaturated fat (polyunsaturated/saturated fat ratio approximately 0.8 vs 0.3). At the lower cholesterol intake, the high saturated fat diet had only a modest effect on LDL cholesterol in Caucasians (+ 6 mg/dl-1) and none in non-Caucasians. 600 mg cholesterol with high saturated fat led to a substantial mean increase in LDL cholesterol, which was significantly greater in Caucasian than in non-Caucasian subjects (+ 31 mg/dl vs 16 mg/dl, P < 0.005). 600 mg cholesterol with increased polyunsaturated fat gave a mean LDL increase of 16 mg/dl, lower than found when the same high cholesterol intake was coupled with increased saturated fat. Variation in cholesterol rather than the proportions of saturated and polyunsaturated fat had the most influence on LDL-cholesterol levels. Among non-Caucasians it was the only significant factor. |
| Effects of dietary cholesterol and fatty acids on plasma cholesterol level and hepatic lipoprotein metabolism Ohtani, H., K. Hayashi, et al. (1990), J Lipid Res 31(8): 1413-22. Abstract: The effects of dietary cholesterol and fatty acids on the plasma cholesterol level and rates of very low density lipoprotein (VLDL) cholesterol secretion and low density lipoprotein (LDL) transport through LDL receptors in the liver of the hamster were investigated. Increases of plasma VLDL- and LDL-cholesterol levels and VLDL-cholesterol secretion from hepatocytes were observed in animals fed a diet enriched with 0.1% cholesterol for 2 weeks in comparison with animals fed a control diet. The addition of dietary palmitic acid accelerated the effect of dietary cholesterol on plasma VLDL- and LDL-cholesterol levels and VLDL-cholesterol secretion from hepatocytes. Dietary linoleic acid accelerated the effect of dietary cholesterol on VLDL-cholesterol secretion from hepatocytes and diminished the effect on the plasma LDL-cholesterol level. Hepatic LDL receptor activity was considerably suppressed by a control diet containing 0.05% cholesterol and a further small suppression was induced by a diet enriched with 0.1% cholesterol with or without 5% palmitic acid. However, dietary linoleic acid diminished the effect of dietary cholesterol on the suppression of hepatic LDL receptor activity. These results suggest that dietary palmitic acid augments the effect of dietary cholesterol in elevating the plasma LDL-cholesterol level through acceleration of VLDL-cholesterol secretion from the liver, and that dietary linoleic acid diminishes the effect of dietary cholesterol in elevating the plasma LDL-cholesterol level by preventing the suppression of hepatic LDL receptor activity induced by cholesterol. |
| Effects of dietary cholesterol and phytosterol overload on Wistar rat plasma lipids Laraki, L., X. Pelletier, et al. (1991), Ann Nutr Metab 35(4): 221-5. Abstract: To study the effects of dietary phytosterols on plasma cholesterol, Wistar rats were fed diets containing a cholesterol overload (24 mg/day), to which phytosterols were added or not (24 or 96 mg/day). The cholesterol overload led to a marked increase in cholesterol, mainly linked to very-low-density and low-density lipoproteins. Phytosterols reduced those effects, the highest dose being most efficient. No undesirable effect was observed either on body or on liver weights. This shows that low doses of phytosterols are sufficient to significantly decrease a plasma cholesterol enhancement induced by a dietary cholesterol overload. |
| Effects of dietary cholesterol and plant oils on proteinase activity in the jejunal mucosa of rats Kosarev, A. V. (1990), Vopr Pitan(4): 69-70. |
| Effects of dietary cholesterol and triglycerides on lipid concentrations in liver, plasma, and bile Booker, M. L., W. W. LaMorte, et al. (1997), Lipids 32(2): 163-72. Abstract: Dietary cholesterol (CHL) and triglycerides (TG) can influence plasma, hepatic, and biliary lipid composition, but effects on lipids in these three compartments during the early stages of CHL gallstone formation have not been studied in parallel. We fed prairie dogs diets containing one of four test oils (safflower, coconut, olive, or menhaden) at either 5 or 40% of calories, in the presence of 0 or 0.34% CHL, for 3 wk. In the absence of dietary CHL, increases in dietary TG produced 50-200% increases in the concentrations of biliary CHL and hepatic cholesteryl ester (CE), while the concentrations of hepatic free CHL (FC) as well as plasma FC and CE remained relatively unchanged. Increasing dietary CHL to 0.34% resulted in increases in hepatic FC of approximately 50% for all four fats regardless of whether they were supplied at 5 or 40% of calories. CHL supplementation caused more pronounced increases in biliary CHL (200-400%), hepatic CE (50-200%), plasma FC (up to 100%), and plasma CE (up to 150%), and these increases were exacerbated by concurrent supplementation of dietary fat and CHL (biliary CHL: 300-700%; hepatic CE: 100-250%; plasma FC: up to 165%; plasma CE: 100-350%). These results indicate that enhanced secretion of biliary CHL and, to a lesser extent, increased synthesis of hepatic CE, may be primary mechanisms for maintaining the hepatic FC pool. Furthermore, dietary CHL and high levels of fat intake are independent risk factors for increasing biliary CHL concentrations, and adverse effects on lipid concentrations in plasma and bile tend to be exacerbated by ingestion of diets rich in both fat and CHL. |
| Effects of dietary cholesterol on bile formation and hepatic processing of chylomicron remnant cholesterol in the rat Smit, M. J., F. Kuipers, et al. (1993), Hepatology 17(3): 445-54. Abstract: We have studied the coupling between hepatic uptake of chylomicron remnant cholesteryl ester and biliary excretion of cholesterol and bile acids in rats, after feeding them a cholesterol-free (control) or a high-cholesterol diet (1% wt/wt) for 2 wk. We equipped rats with permanent catheters in the bile duct, duodenum and heart to allow experiments in unanesthetized, unrestrained animals. Cholesterol feeding induced a 20% increase in plasma cholesterol concentration, a threefold increase in hepatic bile acid synthesis and a 27% increase in bile acid pool size, whereas biliary excretion of cholesterol was decreased by 50%. The enlarged bile acid pool contained relatively less cholic acid and more chenodeoxycholic acid and muricholic acids. 3Hcholesteryl ester-labeled chylomicron remnants (150 micrograms protein per rat) were injected intracardially, and blood and bile were collected for a period of 22 hr. Plasma disappearance of remnants was significantly delayed by cholesterol feeding, probably caused by competition with diet-induced beta-very low density lipoproteins for hepatic uptake. In control rats biliary excretion of chylomicron remnant-derived radioactivity (50% in free cholesterol and 50% in bile acids) showed an initial peak 1 hr after injection (2.4% dose per hour). A second peak (90% in bile acids), amounting to 1.5% of the dose per hour, appeared 11 hr after injection. Total 22-hr excretion of 3H was 22% of the dose. In cholesterol-fed rats chylomicron remnant-derived radioactivity appeared more rapidly in bile, with a peak 1 hr after injection, amounting to 3.5% of the dose per hour. In this case radioactivity was mainly present as bile acid. Total excretion in 22 hr was 27% of the dose. We conclude that chylomicron remnant uptake by the liver is efficiently coupled to bile acid synthesis and biliary excretion, thus providing an efficient pathway for removal of intestine-derived cholesterol. After cholesterol feeding, chylomicron remnant cholesteryl ester is more efficiently converted to bile acids, a mechanism which may contribute to the resistance of rats to diet-induced elevation of plasma cholesterol. In contrast, biliary excretion in the form of free cholesterol, the second main excretory pathway, is significantly decreased by a high-cholesterol diet. |
| Effects of dietary cholesterol on cholesterol and bile acid homeostasis in patients with cholesterol gallstones Kern, F., Jr. (1994), J Clin Invest 93(3): 1186-94. Abstract: We examined changes in cholesterol and bile acid metabolism produced by dietary cholesterol in gallstone subjects and matched controls. Healthy women were recruited and, after confirming the presence or absence of radiolucent gallstones, they were studied on regular diets and again on the same diet supplemented with five eggs daily for 15-18 d. Studies included plasma lipids, lipoproteins and apolipoproteins, dietary records, cholesterol absorption, cholesterol synthesis, plasma clearance of chylomicron remnants, biliary lipid composition, and secretion and bile acid kinetics. On low cholesterol, gallstone subjects absorbed a slightly lower fraction of dietary cholesterol, synthesized more cholesterol, and had smaller bile acid pools and faster fractional turnover rate (FTR) of bile acids. On high cholesterol, the fraction of cholesterol absorbed decreased in both groups and cholesterol synthesis decreased, especially in the gallstone group. Biliary cholesterol secretion increased in the gallstone group only. FTR of bile acids did not change in either group. Bile acid synthesis and pool tended to increase (P = NS) in the controls, but in gallstone subjects, synthesis and pool size decreased. We concluded that in gallstone subjects cholesterol and bile acid homeostasis is significantly altered, and that increasing dietary cholesterol increases biliary cholesterol secretion and decreases bile acid synthesis and pool, changes associated with cholesterol gallstone formation. |
| Effects of dietary cholesterol on hepatic metabolism of free fatty acid and secretion of VLDL in the hamster Fungwe, T. V., L. M. Cagen, et al. (1994), Biochem Biophys Res Commun 200(3): 1505-11. Abstract: We reported previously that dietary cholesterol produces hepatic steatosis, increased secretion of the VLDL, and hypertriglyceridemia in the rat, the result of reduced oxidation of fatty acids, stimulation of fatty acid synthesis, and increased incorporation of fatty acid into hepatic triglyceride. The present study was conducted to determine whether these regulatory actions of dietary cholesterol on fatty acid metabolism also occur in the Golden Syrian hamster. In the hamster, dietary cholesterol (0.5%) induced hypertriglyceridemia and hypercholesterolemia. Incorporation of 1-14C oleate into plasma and hepatic triglyceride was enhanced by dietary cholesterol. Experiments with perfused livers confirmed the stimulatory effect of dietary cholesterol on synthesis and secretion of VLDL-triglyceride and other lipids. These data indicate that increased formation of triglyceride in response to dietary cholesterol is not confined to the rat but may be a more general phenomenon. |
| Effects of dietary cholesterol on hepatic production of lipids and lipoproteins in isolated hamster liver Chen, J., W. Song, et al. (1996), Hepatology 24(2): 424-34. Abstract: The effect of 2-week 2% cholesterol vs. chow feeding on regulation of hepatic lipoprotein, lipids and apoprotein (Apo), and biliary lipids production was evaluated by the isolated perfused hamster liver model. Cholesterol feeding did not change very-low-density lipoprotein (VLDL), low-density lipoprotein (LDL), and high-density lipoprotein (HDL) particle size but significantly increased the hepatic production of VLDL-cholesterol fourfold, VLDL-triglyceride two and one-half-fold but not phospholipid in VLDL. It also increased LDL-cholesterol fourfold but not triglyceride or phospholipid in LDL, whereas lipids in HDL remained unchanged. Gradient sodium dodecyl sulfate-polyacrylamide gel electrophesis (SDS-PAGE) and Western blot analysis (density of apoprotein/density of albumin/g liver) indicated that cholesterol feeding enhanced Apo B tenfold, Apo A-I fivefold but not Apo E in VLDL. Apo E and Apo B did not change in LDL. Apo E but not Apo A-I increased (threefold) in HDL by cholesterol feeding. Cholesterol feeding decreased bile salt secretion 28% but increased cholesterol secretion 118% in bile, whereas phospholipid and bile volume remained unchanged. Increased Apo A-I in VLDL suggested that Apo A-I is involved in enhanced hepatic export of cholesterol and triglyceride. Different patterns of lipid and Apos in VLDL and LDL after cholesterol feeding also suggested separate VLDL and LDL export mechanisms. Elevated Apo E but not lipids in HDL after cholesterol feeding suggests that hepatic HDL may function as a carrier of newly synthesized hepatic Apo E into the circulation for transfer to other lipoproteins (chylomicron CM, CMr) to facilitate hepatic cholesterol uptake and clearance. |
| Effects of dietary cholesterol on plasma lipoproteins and their subclasses in IDDM patients Romano, G., M. K. Tilly-Kiesi, et al. (1998), Diabetologia 41(2): 193-200. Abstract: To compare the effects of dietary cholesterol supplementation in insulin-dependent diabetic (IDDM) patients and normal subjects, 10 male IDDM patients in good glycaemic control (HbA1c 7.3+/-0.9%) (mean+/-SD) and normal plasma lipid levels, and 11 control male subjects of similar age, body mass index and lipid plasma levels underwent a double blind, cross-over, sequential study. Cholesterol supplementation of 800 mg/day or placebo were given for consecutive periods of 3 weeks. The concentration of plasma total cholesterol increased significantly with the dietary cholesterol supplementation compared to placebo in IDDM patients by 6% (p < 0.05) and in control subjects by 9% (p < 0.05). No changes were observed in the concentration of plasma triglycerides in either group. The LDL cholesterol level increased by 12% (p < 0.01) in patients and by 7% (p < 0.05) in control subjects. In patients plasma HDL cholesterol concentration remained the same, while in control subjects it tended to increase after cholesterol supplementation (from 1.14+/-0.26 to 1.23+/-0.27 mmol/l, p = 0.06). During the cholesterol intake period the mean concentration of LDL1, LDL2 and LDL3 subclasses in patients showed a significant increase by 21.0 (p < 0.05), 20.4 (p < 0.001) and 11.1% (p < 0.05), respectively, resulting in an 18.0% increase in mean total LDL mass (p < 0.001) without major changes in LDL composition. In the control subjects the changes in the concentrations of LDL subclasses during cholesterol intake were less and not significant. In the IDDM patients the cholesterol intake did not affect the concentration or composition of HDL subclasses or total HDL mass. In contrast, in control subjects cholesterol intake increased the mean concentration of HDL2a by 12.2.% (p < 0.05) and this increase was significantly different if compared to changes obtained in the patients. In conclusion, compared to normal subjects, in IDDM patients, dietary cholesterol intake increased the LDL particle mass significantly and had no positive effect on HDL. |
| Effects of dietary cholesterol on plasma lipoproteins in Smith-Lemli-Opitz syndrome Merkens, L. S., W. E. Connor, et al. (2004), Pediatr Res 56(5): 726-32. Abstract: Smith-Lemli-Opitz syndrome is a condition of impaired cholesterol synthesis that is caused by mutations in DHCR7 encoding 7-dehydrocholesterol-Delta7 reductase. Birth defects and mental retardation are characteristic. Deficient plasma and tissue cholesterol and excess cholesterol precursors 7 and 8 dehydrocholesterol (7DHC and 8DHC) contribute to the pathogenesis. Cholesterol is transported to tissues via lipoproteins. We measured the effect of dietary cholesterol (egg yolk) on plasma lipoproteins to evaluate this potential treatment. We used the enzymatic method to measure total sterols in lipoproteins (n=12) and plasma (n=16). In addition, we analyzed individual plasma sterols by a gas chromatographic method. Samples were evaluated after 3 wk of a cholesterol-free diet and after 6-19 mo of dietary cholesterol. We also analyzed the distribution of sterols in lipoproteins and the apolipoprotein E genotype. Dietary cholesterol significantly increased the total sterols in plasma (2.22 +/- 0.13 to 3.10 +/- 0.22; mean +/- SEM; p < 0.002), in LDL (0.98 +/- 0.13 to 1.52 +/- 0.17 mM), and in HDL (0.72 +/- 0.04 to 0.92 +/- 0.07). Plasma cholesterol increased (1.78 +/- 0.16 to 2.67 +/- 0.25 mM; p < 0.007) and plasma 7DHC decreased in 10 children, but the mean decrease was not significant. The distribution of individual sterols in each lipoprotein fraction was similar to the distribution in plasma. The baseline cholesterol and the response to dietary cholesterol was the same in children with 3/3 and 3/4 apolipoprotein E genotypes. Dietary cholesterol increased total sterols in plasma, LDL, and HDL in children with Smith-Lemli-Opitz syndrome. These favorable increases in the lipoproteins are potentially therapeutic for this condition. |
| Effects of dietary cholesterol on pyroglutamyl aminopeptidase activity in mouse frontal cortex, pituitary, and adrenal glands Ramirez-Exposito, M. J., M. J. Garcia, et al. (2002), Horm Metab Res 34(8): 431-4. Abstract: Pyroglutamyl aminopeptidase (pGluAP) is an omega peptidase that hydrolyzes biologically active peptides, such as thyrotropin-releasing hormone (TRH), with neuronal and extraendocrine functions. We analyzed the effects of a cholesterol-enriched diet on soluble and membrane-bound pGluAP activity in frontal cortex, pituitary and adrenal glands of male and female mice using fluorimetric assays. Significant increases were observed in soluble pGluAP activity in the frontal cortex and adrenal glands in males and in the pituitary in females. Membrane-bound pGluAP activity was increased in the frontal cortex and pituitary of males and females after the mice were fed a cholesterol-enriched diet. These increases may produce changes in the metabolism of endogenous substrates, including TRH, which may be related to alterations in its neuromodulator functions and to the possible relationship between TRH and other neurotransmitter systems. |
| Effects of dietary cholesterol on serum cholesterol: a meta-analysis and review Hopkins, P. N. (1992), Am J Clin Nutr 55(6): 1060-70. Abstract: Attempts to estimate the effects of dietary cholesterol on serum cholesterol by meta-analysis have not previously included baseline together with added dietary cholesterol in a mathematical model. Mean reported changes in serum cholesterol from 27 studies in which controlled diets were supplied by a metabolic kitchen provided 76 data points, each weighted by the number of subjects in nonlinear regression. A good fit to the data (P less than 0.0005, and r = 0.617 between observed and predicted points) was given by the equation y = 1.22(e-0.00384 chi 0) (1-e-0.0136 chi) where y is the change in serum cholesterol (in mmol/L), chi is added dietary cholesterol, and chi 0 is baseline dietary cholesterol (both in mg/d). Possible reasons for the hyperbolic shape of the relationship between change in serum cholesterol and added dietary cholesterol, mechanisms for individual responsiveness to dietary cholesterol, and important implications regarding interpretation of prior studies and public health issues are discussed. |
| Effects of dietary cholesterol restriction in a feline model of Niemann-Pick type C disease Somers, K. L., D. E. Brown, et al. (2001), J Inherit Metab Dis 24(4): 427-36. Abstract: A feline model of Niemann-Pick disease type C (NPC) was employed to evaluate the effect of dietary cholesterol restriction on progression of disease. Two NPC-affected treated cats were fed a cholesterol-restricted diet beginning at 8 weeks of age; the cats remained on the diet for 150 and 270 days respectively. The study goal was to lower the amount of low density lipoprotein (LDL) available to cells, hypothetically reducing subsequent lysosomal accumulation of unesterified cholesterol and other lipids. Neurological progression of disease was not altered and dietary cholesterol restriction did not significantly decrease storage in NPC-affected treated cats. One NPC-affected treated cat had decreased serum alkaline phosphatase activity (ALP) and decreased serum cholesterol concentration. Liver lipid concentrations of unesterified cholesterol, cholesterol ester and phospholipids in NPC-affected treated cats were similar to those seen in NPC-affected untreated cats. Ganglioside concentrations in the NPC-affected treated cats and NPC-affected untreated cats were similar. Histological findings in liver sections from NPC-affected treated cats showed a diffuse uniform microvacuolar pattern within hepatocytes and Kupffer cells, in contrast to a heterogeneous macro/microvacuolar pattern and prominent nodular fibrosis in NPC-affected untreated cats. Similar differences in vacuolar patterns were seen in splenic macrophages. Although some hepatic parameters were modified, dietary cholesterol restriction did not appear to alter disease progression in NPC-affected kittens. |
| Effects of dietary cholesterol, type of fat, and sex on bile lipid composition of adult baboons Mott, G. E., E. M. Jackson, et al. (1992), Am J Clin Nutr 56(3): 511-6. Abstract: We measured the effects of dietary cholesterol (0.24 vs 0.0024 mg/kJ), type of dietary fat saturated, a ratio of polyunsaturated to saturated fatty acids (P:S) of 0.37, vs unsaturated (P:S of 2.2), and sex on biliary lipid and bile acid conjugate composition of 80 adult pedigreed baboons. From these data we calculated the bile cholesterol saturation index and the bile acid hydrophobicity index. Dietary cholesterol significantly increased the bile cholesterol concentration by 25% and the bile cholesterol saturation index by 15%, but did not significantly affect the bile acid conjugate composition or the bile acid hydrophobicity index. Diets high in saturated fatty acid compared with unsaturated fatty acid significantly decreased the bile cholesterol concentrations by 26% and the saturation index by 23%. Saturated fatty acid also decreased the proportion of hydrophobic bile acids and lowered the bile hydrophobicity index. Male baboons had a higher cholesterol saturation index and a lower hydrophobicity index than females. Dietary cholesterol and saturated fatty acid independently influence the bile lipid composition and the cholesterol saturation index. |