| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Dietary cholesterol enhances preneoplastic aberrant crypt formation and alters cell proliferation in the murine colon treated with azoxymethane Kendall, C. W., S. A. Janezic, et al. (1992), Nutr Cancer 17(2): 107-14. Abstract: The effect of dietary cholesterol on the development of colonic preneoplastic aberrant crypts, as well as its influence on the proliferative status of the intestinal epithelium, was investigated in mice exposed to the chemical carcinogen azoxymethane. Two strains of mice, C57BL/6J and BALB/cJ, were fed a semisynthetic diet containing 0% (control), 1.25%, or 5.00% cholesterol for eight weeks. During the first four weeks of the experiment, mice were given weekly injections of azoxymethane. Cholesterol supplementation significantly increased the formation of aberrant crypts (p less than 0.0001), enhanced the rate of cell proliferation (p less than 0.0001), altered the cell proliferative pattern, and increased crypt height (p less than 0.05) and the total number of cells per crypt (p less than 0.01) in the colonic epithelium of both mouse strains. C57BL/6J mice developed a greater number of aberrant crypts (p less than 0.0001). However, a diet-strain interaction was not observed. The results of this study indicate that dietary cholesterol enhances colon carcinogenesis in the murine colon and therefore may be an important factor in the etiology of large bowel cancer in humans. |
| Dietary cholesterol enhances pulmonary eosinophilic inflammation in a murine model of asthma Yeh, Y. F. and S. L. Huang (2001), Int Arch Allergy Immunol 125(4): 329-34. Abstract: BACKGROUND: Epidemiological studies have suggested that the dietary pattern may be associated with the prevalence of asthma. We previously reported that an increased intake of foods of animal origin was associated with the occurrence of allergic rhinitis and asthma in adolescents. Here we examined the effect of dietary cholesterol in a murine model of allergic pulmonary inflammation. METHODS: Weanling C57BL/6 mice were fed a control diet containing 0.02% cholesterol or a diet supplemented with 1% or 2% cholesterol. Four weeks later the mice were sensitized with intraperitoneal ovalbumin (OVA) followed by OVA or saline inhalation 2 weeks later. OVA aerosol-induced inflammation was significantly enhanced by dietary supplementation of 1% or 2% cholesterol. RESULTS: Among OVA-challenged mice, leukocyte numbers, particularly those of eosinophils, in the bronchoalveolar space increased by 3- to 5-fold with the cholesterol supplement. Among OVA aerosol-challenged mice, the levels of interleukin-5 and cysteinyl leukotrienes in the bronchoalveolar lavage fluid were significantly higher in those fed the 2% cholesterol diet compared with mice on the control diet. CONCLUSIONS: Dietary cholesterol may enhance pulmonary allergic inflammation. |
| Dietary cholesterol enhances the induction and development of colonic preneoplastic lesions in C57BL/6J and BALB/cJ mice treated with azoxymethane Rao, A. V., S. A. Janezic, et al. (1992), Cancer Lett 63(3): 249-57. Abstract: The effect of dietary cholesterol on the induction and development of colonic precursor lesions was determined in two mouse strains, C57BL/6J and BALB/cJ, which differ in their metabolism of cholesterol. Mice were randomized into four groups and fed a cholesterol-free or a 1.25% cholesterol diet during and/or subsequent to four weekly injections of azoxymethane (5 mg/kg body wt.). Dietary cholesterol significantly increased the number of aberrant crypt foci (P less than 0.0001), enhanced cell proliferation (P less than 0.0001) and induced alterations in the proliferative pattern and crypt morphometrics in the colonic epithelium of both mouse strains. While C57BL/6J mice developed a greater number of aberrant crypt foci than BALB/cJ mice (p less than 0.0001), a significant diet-strain interaction effect was not observed. The present results indicate that dietary cholesterol enhances the induction and development of chemically-induced colonic precancerous lesions but this process is not affected by genetic differences in cholesterol metabolism, as represented by the two strains of mice studied. |
| Dietary cholesterol enhances torpor in a rodent hibernator Geiser, F., G. J. Kenagy, et al. (1997), J Comp Physiol B 167(6): 416-22. Abstract: Dietary cholesterol can affect both body lipid composition and steroid hormone concentration. We investigated whether a diet rich in cholesterol influences torpor patterns of hibernating chipmunks (Tamias amoenus) and, if so, whether these changes are better explained by diet-induced changes in body lipid composition or the concentration of testosterone, which at high levels inhibits torpor. Two groups of chipmunks were maintained either on a cholesterol diet (rodent chow containing 10% cholesterol) or a control diet (rodent chow) during pre-hibernation fattening and throughout the hibernation season. Torpid chipmunks on the cholesterol diet had significantly lower minimum body temperatures (-0.2 +/- 0.2 vs -0.6 +/- 0.2 degree C), lower metabolic rates (0.029 +/- 0.002 ml O2 g-1 h-1 vs 0.035 +/- 0.001 ml O2 g-1 h-1), and longer torpor bouts at -1 degree C (6.8 +/- 0.5 vs 4.1 +/- 1.0 days) than chipmunks on the control diet. Dietary cholesterol resulted in a significant increase in blood plasma cholesterol (sevenfold), liver cholesterol content (6.9-fold) and liver triglyceride content (3.5-fold) in comparison to controls. In contrast, dietary cholesterol had no detectable effect on the concentration of plasma testosterone, which was very low in both groups. Since torpor was deeper and longer in animals on the cholesterol diet our study suggests that torpor patterns of chipmunks were either directly affected by the dietary cholesterol or via changes in body lipid composition. |
| Dietary cholesterol fails to stimulate acylcoenzyme A: cholesterol acyltransferase activity in the liver of hamsters with a spontaneous high level of cholesterol Sicart, R. and R. Sable-Amplis (1992), Ann Nutr Metab 36(2): 61-70. Abstract: The effect of exogenous cholesterol on acylcoenzyme A:cholesterol acyltransferase (ACAT) was investigated in conventional golden hamsters (NH) and in FEC hamsters characterized by a high level of cholesterol esters in the liver. ACAT activity was determined in liver microsomal fractions obtained from control animals, in animals fed 0.1% cholesterol diet or in microsomes preincubated with exogenous cholesterol. NH responded to cholesterol feeding by increasing the rate of cholesterol esterification in the liver, and exposure of the NH microsomes to media containing cholesterol stimulated ACAT activity. By comparison, whatever the conditions, cholesterol failed to alter the rate of cholesterol esterification in FEC hamsters. This finding raises several questions about cholesterol metabolism in the liver of these animals that does not fit into the well-established schemes of hepatic cholesterol metabolism. |
| Dietary cholesterol fails to stimulate the human cholesterol 7alpha-hydroxylase gene (CYP7A1) in transgenic mice Agellon, L. B., V. A. Drover, et al. (2002), J Biol Chem 277(23): 20131-4. Abstract: Dietary cholesterol has been shown to have a stimulatory effect on the murine cholesterol 7alpha-hydroxylase gene (Cyp7a1), but its effect on human cholesterol 7alpha-hydroxylase gene (CYP7A1) expression in vivo is not known. A transgenic mouse strain harboring the human CYP7A1 gene and homozygous for the disrupted murine Cyp7a1 gene was created. Cholesterol feeding increased the expression of the endogenous modified Cyp7a1 allele but failed to stimulate the human CYP7A1 transgene. In transfected hepatoma cells, 25-hydroxycholesterol increased murine Cyp7a1 gene promoter activity, whereas the human CYP7A1 gene promoter was unresponsive. Electrophoretic mobility shift assays demonstrated the interaction of the liver X receptor alpha (LXRalpha): retinoid X receptor (RXR) heterodimer, a transcription factor complex that is activated by oxysterols, with the murine Cyp7a1 gene promoter, whereas no binding to the human CYP7A1 gene promoter was detected. The results demonstrate that the human CYP7A1 gene is not stimulated by dietary cholesterol in the intact animal, and this is attributable to the inability of the CYP7A1 gene promoter to interact with LXRalpha:RXR. |
| Dietary cholesterol feeding suppresses human cholesterol synthesis measured by deuterium incorporation and urinary mevalonic acid levels Jones, P. J., A. S. Pappu, et al. (1996), Arterioscler Thromb Vasc Biol 16(10): 1222-8. Abstract: The objective of this study was to measure the response of cholesterol biosynthesis in subjects to three different amounts of dietary cholesterol: 50 (low), 350 (medium), and 650 (high) mg cholesterol per 2800 kcal. Individuals with low (n = 7), normal (n = 12), and elevated (n = 11) plasma cholesterol concentrations consumed in random order solid-food test diets (15%, 55%, and 30% of energy as protein, carbohydrate, and fat, respectively) at each dietary cholesterol level. The three diets were consumed for 4 weeks each, and each dietary phase was separated by a 4-week washout period. During the final week of each diet, 0.7 g D2O was given per kilogram of body water and deuterium incorporation into the erythrocyte cholesterol pool was measured for 24 hours. Urinary mevalonate levels were also determined in samples obtained during two consecutive 24-hour periods. Both techniques provided measurements of whole-body cholesterol biosynthesis. In all subjects the cholesterol synthesis rate as measured by deuterium incorporation was significantly lower (P <.05) after the transition from low- to medium- and low- to high-cholesterol diets. Urinary mevalonate excretion decreased after the change from the medium- to high- (P <.05) and low- to high- (P <.01) cholesterol diets. Although correspondence between the two methods was poor, they both indicated some suppression of cholesterol synthesis by dietary cholesterol. The response of cholesterogenesis to different amounts of dietary cholesterol was related to the rate of synthesis under depressed conditions of the low-cholesterol diet. These findings indicate modest downregulation of synthesis in response to dietary cholesterol in humans, independent of plasma cholesterol levels. |
| Dietary cholesterol from eggs increases the ratio of total cholesterol to high-density lipoprotein cholesterol in humans: a meta-analysis Weggemans, R. M., P. L. Zock, et al. (2001), Am J Clin Nutr 73(5): 885-91. Abstract: BACKGROUND: Several epidemiologic studies found no effect of egg consumption on the risk of coronary heart disease. It is possible that the adverse effect of eggs on LDL-cholesterol is offset by their favorable effect on HDL cholesterol. OBJECTIVE: The objective was to review the effect of dietary cholesterol on the ratio of total to HDL cholesterol. DESIGN: Studies were identified by MEDLINE and Biological Abstracts searches (from 1974 to June 1999) and by reviewing reference lists. In addition, we included data from a more recently published study. Studies were included if they had a crossover or parallel design with a control group, if the experimental diets differed only in the amount of dietary cholesterol or number of eggs and were fed for > or =14 d, and if HDL-cholesterol concentrations were reported. Of the 222 studies identified, 17 studies involving 556 subjects met these criteria. RESULTS: The addition of 100 mg dietary cholesterol/d increased the ratio of total to HDL cholesterol by 0.020 units (95% CI: 0.010, 0.030), total cholesterol concentrations by 0.056 mmol/L (2.2 mg/dL) (95% CI: 0.046, 0.065 mmol/L; 1.8, 2.5 mg/dL), and HDL-cholesterol concentrations by 0.008 mmol/L (0.3 mg/dL) (95% CI: 0.005, 0.010 mmol/L; 0.2, 0.4 mg/dL). CONCLUSIONS: Dietary cholesterol raises the ratio of total to HDL cholesterol and, therefore, adversely affects the cholesterol profile. The advice to limit cholesterol intake by reducing consumption of eggs and other cholesterol-rich foods may therefore still be valid. |
| Dietary cholesterol increases the susceptibility of low density lipoprotein to oxidative modification Schwab, U. S., L. M. Ausman, et al. (2000), Atherosclerosis 149(1): 83-90. Abstract: Evidence suggests that oxidative modification of low density lipoprotein (LDL) occurs in vivo, increasing the atherogenecity of the particle. A total of 13 subjects (age range 46-78 years) with an LDL cholesterol concentration >3.36 mmol/l consumed each of four diets for 32-day periods. The diets contained 30% energy as fat of which 2/3 was either corn oil or beef tallow with and without 115 mg/4.2 MJ of supplemental cholesterol in the form of cooked egg yolk. The susceptibility of LDL to oxidation was assessed during a challenge with hemin and hydrogen peroxide, and results are expressed as lag time to oxidation in minutes. Addition of moderate amounts of cholesterol to either the corn oil or beef tallow enriched diet resulted in increased susceptibility of LDL to oxidation (decreased lag time): 69+/-22 min versus 96+/-24 min in the corn oil diet with versus without supplemental cholesterol, respectively, P = 0.006; 82+/-20 min versus 96+/-26 min in the beef tallow diet with versus without supplemental cholesterol, respectively, P = 0.025. A stepwise equation indicated that as plasma oleic acid concentrations increased and/or linoleic acid concentrations decreased, lag time increased (decreased susceptibility to oxidation), whereas as dietary cholesterol concentrations increased, lag time decreased (increased susceptibility to oxidation). In conclusion, these data suggest that addition of a moderate amount of dietary cholesterol to a reduced fat diet rich in polyunsaturated or saturated fatty acids increased the in vitro susceptibility of LDL to oxidation. |
| Dietary cholesterol increases transcription of the human cholesteryl ester transfer protein gene in transgenic mice. Dependence on natural flanking sequences Jiang, X. C., L. B. Agellon, et al. (1992), J Clin Invest 90(4): 1290-5. Abstract: To investigate the regulation of expression of the human cholesteryl ester transfer protein (CETP) gene, transgenic mice were prepared using a CETP minigene linked to the natural flanking sequences of the human CETP gene. By using a transgene containing 3.2 kb of upstream and 2.0 kb of downstream flanking sequence, five different lines of transgenic mice were generated. The abundance of CETP mRNA in various tissues was determined on standard laboratory diet or high fat, high cholesterol diets. In three lines of transgenic mice the tissues expressing the human CETP mRNA were similar to those in humans (liver, spleen, small intestine, kidney, and adipose tissue); in two lines expression was more restricted. There was a marked (4-10-fold) induction of liver CETP mRNA in response to a high fat, high cholesterol diet. The increase in hepatic CETP mRNA was accompanied by a fivefold increase in transcription rate of the CETP transgene, and a 2.5-fold increase in plasma CETP mass and activity. In contrast, CETP transgenic mice, in which the CETP minigene was linked to a metallothionein promoter rather than to its own flanking sequences, showed no change in liver CETP mRNA in response to a high cholesterol diet. Thus (a) the CETP minigene or natural flanking sequences contain elements directing authentic tissue-specific expression; (b) a high cholesterol diet induces CETP transgene transcription, causing increased hepatic CETP mRNA and plasma CETP; (c) this cholesterol response requires DNA sequences contained in the natural flanking regions of the human CETP gene. |
| Dietary cholesterol induced changes in lipid profile in patients with nephrotic syndrome and chronic renal failure Jain, P. K., R. C. Arora, et al. (1991), J Assoc Physicians India 39(10): 751-3. Abstract: Fifteen patients with nephrotic syndrome (9 aged below 30 years), 6 patients with chronic renal failure and 26 healthy males (14 below 30 years) were studied. After estimating the basal serum levels of total cholesterol (STC), triglycerides (STG), high density lipoprotein (HDL) and low density lipoprotein (LDL), the patients were given a high cholesterol and high fat breakfast (containing 32 g fat and 527 mg cholesterol) for 7 days. Lipoprotein levels were again estimated on days 8 and 16. In the basal state, all patients with nephrotic syndrome had markedly elevated levels of STC and LDL. In patients aged below 30 years, STG and VLDL levels were also elevated, while HDL levels were similar in both the groups in comparison to their respective age group controls. In patients with renal failure, basal levels of all lipoproteins were similar to levels in controls. After the high cholesterol fat diet, there was an insignificant rise in all lipoprotein values in patients with nephrotic syndrome and renal failure. However, HDL levels rose significantly in patients with nephrotic syndrome aged below 30 years. Patients with nephrotic syndrome and chronic renal failure can safely be given high cholesterol and high fat diet despite abnormalities in lipid lipoprotein metabolism. |
| Dietary cholesterol induced changes in serum lipoproteins in healthy females Arora, R. C., N. Agarwal, et al. (1992), Mater Med Pol 24(1): 17-9. Abstract: We studied the effect of high cholesterol fat breakfast containing approximately 527 mg cholesterol and 33 gm fat given for seven days in 10 healthy females of young age (18 to 21 years) and in healthy older females of age group (48 to 60 years). Serum total cholesterol and low density lipoprotein did not alter significantly after feeding and after withdrawal of high cholesterol fat breakfast. Serum high density lipoprotein increased significantly in young females after feeding and further increased after withdrawal for seven days, while in older females no appreciable change occurred. Serum triglyceride showed a significant decline in young persons after feeding but gradually increased after withdrawal while in older females no significant change occurred. |
| Dietary cholesterol induces changes in molecular species of hepatic microsomal phosphatidylcholine Bernasconi, A. M., H. A. Garda, et al. (2000), Lipids 35(12): 1335-44. Abstract: After 21 days on a diet containing 1 g% cholesterol and 0.5 g% cholic acid, rats had an increased content of cholesterol in liver microsomal lipids. In liver, both cholesterol content and delta9 desaturase activity increased, whereas delta6 and delta5 desaturase activities decreased. These changes correlated with increases in oleic, palmitoleic, and linoleic acids and decreases in arachidonic and docosahexenoic acids in total microsomal lipids. Similar fatty acid changes were found in phosphatidylcholine (PC), the principal lipid of the microsomal membrane. In PC the predominant molecular fatty acid species (67% of the total) in the control rats were 18:0/20:4, 16:0/20:4, and 16:0/18:2; and they mainly determined the contribution of PC to the biophysical and biochemical properties of the phospholipid bilayer. The cholesterol diet decreased specifically the 18:0/20:4 species, and to a lesser extent, 16:0/20:4 and 18:0/22:6. The 18:1-containing species, especially 18:1/18:2 and less so 16:0/18:1 and 18:1/20:4, were increased. A new 18:1/18:1 species appeared. The independent effects of the presence of cholesterol and change of the fatty acid composition of the phospholipid bilayer of liver microsomes on the packing were studied by fluorescence methods using 6-lauroyl-2,4-dimethylaminonaphthalene, 1,6-diphenyl-1,3,5-hexatriene and 1-(4-trimethylammonium phenyl)-6-phenyl-1,3,5-hexatriene, which test different parameters and depths of the bilayer. Data showed that the increase of cholesterol in the membrane, and not the change of the fatty acid composition of phospholipids, was the main determinant of the increased bulk packing of the bilayer. The increase of fluid oleic- and linoleic-containing species almost compensated for the drop in 20:4- and 22:6-containing molecules. But the most important effect was that the general drop in essential n-6 and n-3 polyunsaturated fatty acids meant that this endogenous source for the needs of the animal decreased. |
| Dietary cholesterol induces transient changes in plasma nitrate levels in rabbits that are correlated to microcirculatory changes Freyschuss, A., R. J. Xiu, et al. (1996), Biochem Biophys Res Commun 221(1): 107-10. Abstract: Dietary treatment of rabbits with 1% cholesterol resulted in a transient rise in their plasma nitrate levels. After 3 weeks of treatment the nitrate levels were about 50% higher than those of the controls (p<0.005). After 10 weeks of treatment the nitrate levels were similar to those at the start of the study. In accordance with previous work (Xiu et al., J. Clin. Invest., 1994, 93, 2732-2737), the cholesterol treatment let to a decreased blood flow velocity in arterioli of the third order in the conjunctiva, and a decreased diameter of these arterioli. There was a significant correlation between plasma nitrate levels and the two microcirculatory variables (p<0.0001). Nitrate is the major metabolic end product of nitric oxide (NO), and plasma nitrate levels may be used as an index of the endogenous formation of NO. The present results suggest that dietary cholesterol induces a transient increase in the synthesis of NO. Such an increased synthesis may compensate for part of a cholesterol-induced degradation of NO. |
| Dietary cholesterol influences on various lipid indices and eicosanoid production in rats fed dietary fat desirable for the protection of ischemic heart disease Lee, J. H., I. Ikeda, et al. (1991), J Nutr Sci Vitaminol (Tokyo) 37(4): 389-99. Abstract: Young male Sprague-Dawley rats were fed diets containing 10% fat with P/S and n-6/n-3 ratios of 1.2 and 5.0, respectively, and differing levels of dietary cholesterol (0.05 to 1.0% by weight) for 3 weeks, following which the tissue lipid concentration, fatty acid composition, desaturation of linoleic acid, and eicosanoid production were examined. The composition of dietary fat was that recommended for the prevention of atherosclerosis. Dietary cholesterol did not largely influence the concentration of serum cholesterol, but it markedly increased liver cholesterol in a dose-dependent manner. The delta 6-desaturase activity in liver microsomes, linoleate desaturation index in liver phosphatidylcholine, and the production of prostaglandin by the aorta and thromboxane A2 by platelets all decreased to a similar extent in relation to dietary cholesterol above 0.2%. Thus, dietary cholesterol influenced various lipid parameters characteristically even when dietary fat with a fatty acid composition desirable for the prevention of atherosclerosis was consumed simultaneously. The dietary cholesterol level of 0.2% was the point of maximum influence in rats upon the indices examined. |
| Dietary cholesterol inhibits the development of aberrant crypt foci in the colon el-Sohemy, A., C. W. Kendall, et al. (1996), Nutr Cancer 25(2): 111-7. Abstract: We evaluated the effect of dietary cholesterol and oxidized cholesterol on the promotion of aberrant crypt foci (ACF), which are putative precancerous lesions in the colon. Sixty female C57BL/6J mice were given four weekly injections (ip) of azoxymethane (AOM) then fed either a control AIN-76 diet or the control diet supplemented with 0.3% cholesterol or 0.3% oxidized cholesterol for 100 days. The oxidized cholesterol was prepared by heating cholesterol at 110 degrees C for 48 hours. Gas chromatographic analysis of the oxidized cholesterol showed that 96% of the cholesterol was unchanged and less than 2% of the cholesterol was oxidized. The remaining 2% impurities were unidentified and present in both the cholesterol and heated cholesterol. The number of ACF in the group fed cholesterol was significantly lower than the control group (7.9 +/- 1.0 vs. 12.5 +/- 1.2, p < 0.01). The number of ACF in the group fed oxidized cholesterol (10.1 +/- 1.1) was not different from the control or cholesterol groups. The size of the ACF (no. of crypts per focus) did not differ between the three dietary groups. Serum low-density lipoprotein (LDL) cholesterol was greater in the cholesterol-fed group than the control group (40.5 +/- 4.6 vs. 24.3 +/- 3.6 mg/dl, p < 0.05). LDL cholesterol from the animals fed oxidized cholesterol (37.7 +/- 4.7 mg/dl) was not different from the control or cholesterol-fed animals. Total and high-density lipoprotein (HDL) cholesterol did not differ between the groups. The results show that dietary cholesterol significantly inhibits the promotion of ACF in the colon. The elevated LDL cholesterol may inhibit de novo cholesterol synthesis in the preneoplastic colonic epithelial cells, thereby inhibiting DNA synthesis and cell proliferation. |
| Dietary cholesterol inhibits whole-body but not cerebrum cholesterol synthesis in young pigs Zhang, S., W. W. Wong, et al. (1994), J Nutr 124(5): 717-25. Abstract: We studied the effect of dietary cholesterol on tissue cholesterol synthesis in 10 genetically lean pigs using the 2H2O incorporation method. Five pigs were fed a diet containing 0% cholesterol (controls) and five were fed a diet containing 0.5% cholesterol (cholesterol-fed) from d 1 to d 54 of age. From d 30 to d 54, they received 2H2O and cholesterol synthesis was determined by measuring deuterium enrichment in erythrocyte cholesterol. All pigs were killed on d 54 and liver, ileum, jejunum, kidney, adipose tissue, muscle, and cerebrum were collected for measurement of free and esterified cholesterol and of the deuterium content of tissue free cholesterol. In vivo cholesterol synthesis was inhibited by dietary cholesterol as reflected by a decrease in fractional synthesis rate from 16.8 +/- 1.7%/d in controls to 2.3 +/- 1.1%/d in cholesterol-fed pigs. Cholesterol feeding raised cholesterol ester concentration in plasma, liver, and other tissues. Deuterium enrichment of free cholesterol in tissues, such as liver, was reduced from 11.98 +/- 2.82 milli atom percent excess in controls to 1.83 +/- 1.14 in cholesterol-fed pigs. Greater cholesterol intake did not inhibit cholesterol synthesis in the cerebrum. Deuterium enrichment levels of cholesterol in plasma and liver were similar to those in other tissues except for brain, suggesting an equilibration of cholesterol between the liver and most extrahepatic tissues. The control of cholesterol synthesis in brain appears to be independent of that in liver and other tissues of the body. |
| Dietary cholesterol is secreted in intestinally derived chylomicrons during several subsequent postprandial phases in healthy humans Beaumier-Gallon, G., C. Dubois, et al. (2001), Am J Clin Nutr 73(5): 870-7. Abstract: BACKGROUND: The process of intestinal absorption and chylomicron resecretion of dietary cholesterol in humans is poorly understood. OBJECTIVE: The present study aimed to test the hypothesis that dietary cholesterol ingested during a given meal is resecreted into chylomicrons (and plasma) during several subsequent postprandial periods. DESIGN: Seven healthy subjects ingested 3 comparable mixed test meals (at 0, 8, and 24 h) containing a given amount of fat (49 g) and cholesterol (157 mg); blood samples were taken 3 and 6 h after each test meal and 48 and 72 h after the beginning of the experiment. Heptadeuterated dietary cholesterol was present in the first test meal only, enabling its specific determination with use of gas chromatography-mass spectrometry. Chylomicrons, LDL, and HDL were isolated and lipids were quantified. RESULTS: In apolipoprotein B-48-containing chylomicrons, deuterated cholesterol concentrations were moderate after the first meal (1.3 x 10(-4) mmol/L), reached a maximum after the second meal (2.4 x 10(-4) mmol/L), and were still elevated after the third meal (1.7 x 10(-4) mmol/L). In plasma, LDL and HDL cholesterol enrichment in deuterated cholesterol was lower than in chylomicrons and plateaued after 24--48 h. Estimates of newly secreted exogenous deuterated cholesterol in chylomicrons indicate that 30.7%, 55.2%, and 14.1% of the total was secreted after the first, second, and third meals, respectively. CONCLUSION: Ingested dietary cholesterol is secreted by the small intestine in chylomicrons into the circulation during > or =3 subsequent postprandial periods in healthy humans. This likely results from a complex multistep intestinal processing of cholesterol with dietary fat as a driving force. |
| Dietary cholesterol lowers the activity of butyrylcholinesterase (EC 3.1.1.8), but elevates that of esterase-1 (EC 3.1.1.1) in plasma of rats Van Lith, H. A. and A. C. Beynen (1993), Br J Nutr 70(3): 721-6. Abstract: The question addressed is whether an increased intake of cholesterol affects esterase-1 (EC 3.1.1.1; ES-1) and butyrylcholinesterase (EC 3.1.1.8) activity in plasma. Rats were fed on a purified diet either without or with cholesterol (10 g/kg) added at the expense of the carbohydrate source. Dietary cholesterol significantly decreased plasma butyrylcholinesterase activity, but raised plasma ES-1 activity. Evidence is discussed, suggesting that plasma butyrylcholinesterase is involved in plasma cholesterol metabolism, whereas esterase-1 is involved in intestinal cholesterol absorption. |
| Dietary cholesterol lowers the activity of plasma butyrylcholinesterase in rats Van Lith, H. A. and A. C. Beynen (1992), Nahrung 36(6): 603-4. |