| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
| First Page | Previous Page | Next Page | Last Page |
| Increased contents of phospholipids, cholesterol, and lipid peroxides in decidua basalis in women with preeclampsia Staff, A. C., T. Ranheim, et al. (1999), Am J Obstet Gynecol 180(3 Pt 1): 587-92. Abstract: OBJECTIVES: Accelerated recovery from preeclampsia has been reported after postpartum curettage. Lipid deposition in decidual spiral arteries (acute atherosis) is a histologic feature of preeclampsia. Increased tissue content of lipids is associated with enhanced formation of lipid peroxides, which are compounds that may induce endothelial dysfunction. We hypothesized that the content of lipids and lipid peroxides is elevated in decidua basalis tissues of women with preeclampsia compared with those of women with uneventful pregnancies.Study Design: Decidua basalis tissues were obtained with a vacuum aspiration technique during cesarean delivery from 30 preeclamptic and 34 uneventful pregnancies. Total cholesterol, phospholipids, triglycerides, free fatty acids, and lipid peroxides were quantified. RESULTS: Significantly elevated contents of phospholipids, total cholesterol, and lipid peroxides were found in preeclamptic decidua basalis tissues, whereas the contents of triglycerides and free fatty acids did not differ significantly from those of the control group. CONCLUSIONS: Decidua basalis tissues, with their elevated lipid content, may be a source of lipid compounds that can cause maternal endothelial dysfunction in preeclampsia. |
| Increased cyclic AMP in aortas of cholesterol fed rabbits Langner, R. O., C. L. Bement, et al. (1996), Res Commun Mol Pathol Pharmacol 94(2): 193-202. Abstract: Cyclic Amp (cAMP) levels were measured in the aortas of rabbits fed a cholesterol rich diet for either 24 days (Group I), 86 days (Group II) or 86 days followed by 54 days of a normal diet (Group III). Aortic levels of cholesterol and cholesterol esters, calcium and collagen and noncollagen protein synthetic rates were also measured at each time period. Cyclic AMP levels were unchanged in the Group I animals but were significantly elevated in Groups II & III. Aortic levels of cholesterol and cholesterol esters, calcium and collagen and noncollagen protein synthetic rates were also significantly elevated in Groups II & III but unchanged in Group I. Since cAMP levels were not changed in Group I animals the increase in cAMP appears to be a later, adaptive change in response to the feeding of a cholesterol rich diet. The observation that cAMP levels are increased in response to cholesterol feeding is important since cAMP is known to be involved with a wide range of metabolic functions, which may have a significant effect on the development of vascular disease. |
| Increased density of cortical apolipoprotein E immunoreactive neurons in rabbit brain after dietary administration of cholesterol Sparks, D. L., H. Liu, et al. (1995), Neurosci Lett 187(2): 142-4. Abstract: Rabbits were fed 2% cholesterol diet for 4, 6 and 8 weeks or control diet for 6 weeks. Frontal cortex and hippocampal formation were stained with apolipoprotein E (Apo-E) antibody using standard immunocytochemical methods. The number of neurons expressing the Apo-E epitope and the intensity of Apo-E immunoreactivity increased with increasing time on the cholesterol diet. Because Apo-E chaperones cholesterol in the brain, the data may suggest that elevated circulating levels of cholesterol eventually cause increased cerebral levels. |
| Increased dietary fat content accelerates cholesterol gallstone formation in the cholesterol-fed prairie dog LaMorte, W. W., D. P. O'Leary, et al. (1993), Hepatology 18(6): 1498-503. Abstract: Epidemiological studies have provided conflicting information about the relationship between fat consumption and gallstone formation. We studied cholesterol gallstone formation in prairie dogs after 1 wk of the following diets: (group A) a control diet with no added cholesterol and 5% of calories from corn oil, (group B) 1.2% cholesterol with 5% of calories from corn oil or (group C) 1.2% cholesterol with 40% of calories from corn oil. In controls serum cholesterol was 58.9 +/- 4.5 mg/dl, gallbladder bile was unsaturated with cholesterol (cholesterol saturation index = 0.7 +/- 0.1; cholesterol = 3.8 mmol/L) and none of 12 animals formed cholesterol crystals or stones. The low-fat diet supplemented with cholesterol (group B) increased serum and biliary cholesterol concentrations to 292 +/- 76 mg/dl and 7.5 +/- 1.1 mmol/L, respectively (p < 0.05), but cholesterol saturation index was only modestly increased (1.1 +/- 0.1) and in only one of eight animals did cholesterol monohydrate crystals develop. Group C, animals, which received cholesterol plus high levels of corn oil, had higher serum cholesterol levels (457 +/- 66 mg/dl), higher biliary cholesterol concentrations (16.6 +/- 1.3 mmol/L), higher cholesterol saturation indexes (1.7 +/- 0.1) and increased incidence of cholesterol gallstones (5 of 11). The two cholesterol-supplemented diets increased biliary phospholipid concentrations, decreased the ratio of cholic/chenodeoxycholic acid and increased the proportion of biliary lecithins containing linoleic acid, but these abnormalities were greatest in group C, which was given large amounts of corn oil. These findings suggest that cholesterol gallstone formation in the prairie dog is accelerated by increased dietary omega-6 polyunsaturated triglycerides. |
| Increased esterification of cholesterol and transfer of cholesteryl ester to apo B-containing lipoproteins in Type 2 diabetes: relationship to serum lipoproteins A-I and A-II Jones, R. J., D. Owens, et al. (1996), Atherosclerosis 119(2): 151-7. Abstract: This study examines the activity of two key enzymes of reverse cholesterol transport, cholesterol ester transfer protein (CETP) and lecithin:cholesterol acyl transferase (LCAT) in 21 patients with non-insulin dependent diabetes mellitus (NIDDM) and 21 control subjects. Serum CETP was assessed by measuring plasma-mediated cholesteryl ester transfer between pooled exogenous lipoprotein with endogenous LCAT inhibited--an estimate of CETP mass. CETP activity was determined as cholesteryl ester transfer in the presence of the patients' lipoproteins and LCAT (endogenous assay). LCAT activity was determined in the same assay. There was no significant difference in CETP mass between the diabetic and non-diabetic subjects and there was no correlation between CETP mass and LCAT activity. Using the endogenous lipoprotein assay, CETP was elevated in serum from diabetic patients compared to control subjects (10.05 +/- 1.89 vs. 5.50 +/- 0.53 nmol/ml/h P < 0.05). LCAT was also increased in the diabetic patients (53.63 +/- 4.70 vs. 41.22 +/- 3.40 nmol/ml/h P < 0.05). Serum free cholesterol from diabetic and control subjects correlated with CETP activity measured using endogenous lipoprotein assay (r = 0.77, P < 0.001 and r = 0.82, P < 0.001), and also with LCAT activity (r = 0.76, P < 0.01 and r = 0.79, P < 0.01). There was a negative correlation between CETP activity with the endogenous lipoprotein assay and serum high density lipoprotein (HDL) cholesterol in the diabetic patients (r = -0.38, P < 0.01), but not in control subjects. In a subgroup of 10 control subjects, there was a positive correlation between LCAT activity and apolipoprotein (apo) A-I (r = 0.49, P < 0.05) and apo A-II (r = 0.51, P < 0.05) and also between CETP activity (endogenous assay) and apo A-I (r = 0.87, P = 0.001) and apo A-II (r = 0.63, P < 0.05). No relationship was observed between CETP activity and apo A-I or apo A-II in the diabetic subjects. Thus, serum CETP mass was normal in Type 2 diabetes but CETP activity (endogenous assay) was increased and was related to free cholesterol levels and LCAT activity in both diabetic and non-diabetic subjects. |
| Increased ether lipid cytotoxicity by reducing membrane cholesterol content Diomede, L., B. Piovani, et al. (1991), Int J Cancer 49(3): 409-13. Abstract: Ether-linked glycerophospholipids (ether lipids, EL) are selectively toxic and anti-proliferative agents against cancer cells in vitro. The reason for such selectivity is not completely clear. Their mechanism of action is mediated through an interaction with the plasma membrane and the membrane lipid composition may modulate it. As a continuation of previous reports, we now present data showing that cholesterol concentration modulates EL toxicity in the K562, U937 and MOLT4 leukemic cell lines in vitro. Cells become sensitive to otherwise ineffective doses of EL when their cholesterol content is lowered. Cell cholesterol levels were reduced by exposure to an egg lipid mixture (neutral glycerides, phosphatidylcholine and phosphatidylethanolamine, AL721). The data contribute to an understanding of the EL mechanism of action on membranes and suggest that the cellular cholesterol concentration must be considered a major factor in modulating the cytotoxic effects of EL. |
| Increased experimental atherosclerosis in cholesterol-fed rabbits exposed to passive smoke: taking issue with study design and methods of analysis Wu, J. M. (1993), J Am Coll Cardiol 22(6): 1751-3. |
| Increased expression of gallbladder cholecystokinin: a receptor in prairie dogs fed a high-cholesterol diet and its dissociation with decreased contractility in response to cholecystokinin Kano, M., J. Shoda, et al. (2002), J Lab Clin Med 139(5): 285-94. Abstract: A series of our studies have shown that formation of cholesterol-supersaturated bile in patients with cholesterol gallstone disease is causatively related to decreased gallbladder contractility and mucin hypersecretion by the gallbladder. Supersaturated bile may modify the composition of gallbladder membranes so that the transduction of smooth muscle regulatory signals is impaired, and it may enhance the inflammation-induced mucin secretion by the gallbladder. To achieve a better understanding of the mechanism by which supersaturated bile impairs the contractility, we studied changes in the expression levels of gallbladder cholecystokinin (CCK-A) receptor messenger ribonucleic acid (mRNA) in prairie dogs fed a high-cholesterol diet. Levels of pathobiological determinants in arachidonate metabolism which are important for mucin secretion were also measured in their bile. Adult male prairie dogs were randomly assigned to receive either a semisynthetic diet (SSD) or an SSD plus 1.2% cholesterol (a high-cholesterol diet) for 2-, 4-, and 6-week periods. The contractile force in response to CCK-octapeptide (CCK-8) was measured by using gallbladder muscle strips. The mRNA levels of the CCK-A receptor were determined by reverse-transcription polymerase chain reaction (RT-PCR). Parallel to the increase in the cholesterol saturation index, the contractile responses to CCK-8 decreased in the animals fed a high-cholesterol diet for 4 weeks and markedly decreased in the animals with gallstone formation. However, in contrast to the decreased contractility, the steady-state mRNA levels of the gallbladder CCK-A receptor were significantly increased in the animals fed a high-cholesterol diet in comparison with the corresponding control animals. In the bile, a high-cholesterol diet caused an increase in the proportion of arachidonyl-phosphatidylcholine species, where phospholipase A(2) activity, prostaglandin E(2), and mucin concentrations were increased parallel to the feeding period. Up-regulation of the CCK-A receptor mRNA in the gallbladder of animals fed a high-cholesterol diet associated with decreased contractility may be due to an impairment of CCK signaling related to increased membrane cholesterol contents and its related reaction of biological compensation in order to increase the receptor concentration. The results of the present study suggest that in prairie dogs fed a high-cholesterol diet both a decrease in gallbladder contractility related to impairment of CCK signaling and phospholipase A(2) (PLA(2))-induced mucosal inflammation in the gallbladder with associated biliary alterations favoring cholesterol crystal formation pathogenetically contribute to the formation of cholesterol gallstones. |
| Increased gap junction assembly between cultured cells upon cholesterol supplementation Meyer, R., B. Malewicz, et al. (1990), J Cell Sci 96 (Pt 2): 231-8. Abstract: Novikoff hepatoma cells provide an excellent model system for the study of gap junction assembly, a process that could be influenced by lipids and other factors at numerous points. Since it is possible to alter the cellular levels of cholesterol in these cells, it was added to the cells in serum-supplemented medium and changes in gap junction assembly were evaluated. Cells were dissociated and reaggregated following exposure to a range of cholesterol concentrations for 24 h. A five- to sixfold increase in the number of aggregated gap junction particles and a 50% increase in cellular cholesterol content were observed with 20 microM added cholesterol. A 1-h exposure to added cholesterol, during cell reaggregation, resulted in a fourfold increase in the number of aggregated gap junction particles, demonstrating that the effect was rapid. The number of aggregated gap junction particles and formation plaque areas were used as measures of junction assembly and assayed by quantitative freeze-fracture and electron microscopy. Junctional permeabilities were evaluated by means of dye transfer times following the intracellular microinjection of Lucifer Yellow. Increased dye transfer was observed between cholesterol-treated cells, which suggested that the increase in assembly was accompanied by an increase in junction permeability. Cells were treated with cycloheximide (100 micrograms ml-1) and actinomycin D (10 micrograms ml-1) to determine whether protein and RNA syntheses were involved in the enhanced gap junction assembly. Cycloheximide but not actinomycin D blocked the increased junction assembly observed with added cholesterol. These results suggested that protein synthesis, but not RNA synthesis, is necessary for the increased gap junction formation observed.(ABSTRACT TRUNCATED AT 250 WORDS) |
| Increased HDL-cholesterol level improves the prognosis in patients with coronary vasospasm Miwa, K., Y. Miyagi, et al. (1994), J Cardiol 24(5): 373-7. Abstract: Cardiovascular events were analyzed in the subset of 49 consecutive patients with vasospastic coronary artery disease who underwent diagnostic coronary arteriography from December, 1987 to March, 1991 to confirm coronary artery spasm during anginal attacks. During the follow-up period (30 +/- 14 months, mean +/- SEM), seven patients had cardiovascular accidents including acute myocardial infarction, unstable angina, and stroke (group A), while the remaining 42 patients were event-free (group B). Current smokers at the end of the follow-up period were more common in group A (71%) than in group B (12%) (p < 0.01). Serum total-cholesterol, low density lipoprotein cholesterol, and triglyceride levels were not significantly different between the two groups before or after the follow-up period. The baseline high-density lipoprotein cholesterol (HDL-C) level also did not differ between group A (32.5 +/- 8.3 mg/dl) and group B (41.0 +/- 12.9 mg/dl). However, the HDL-C level significantly increased during the follow-up period in group B (delta HDL-C 6.1 +/- 9.4 mg/dl) (p < 0.01), but not in group A (delta HDL-C -3.3 +/- 7.2 mg/dl). The HDL-C level at the end of the follow-up period in group A (29.2 +/- 9.0 mg/dl) was significantly lower than in group B (47.1 +/- 11.5 mg/dl) (p < 0.01). Cardiovascular accidents were significantly more common in current smokers (50%) (p < 0.01) than in current nonsmokers (5%) after the follow-up.(ABSTRACT TRUNCATED AT 250 WORDS) |
| Increased hepatic cholesterol accumulation in transgenic mice overexpressing human secretory phospholipase A2 group IIA Eckey, R., M. Menschikowski, et al. (2004), Inflammation 28(2): 59-65. Abstract: It has been demonstrated in transgenic mice that the overexpression of human phospholipase A2 group IIA (sPLA2), an acute-phase reactant, is associated with depressed plasma cholesterol levels, altered lipoprotein compositions, and increased lipid depositions in aortic walls. It was the aim of the present study to investigate whether the reduced plasma cholesterol levels in sPLA2-transgenic mice may be due to an increased transfer of lipids from sPLA2-modified lipoproteins to the liver and/or other nonvascular tissues. Ten sPLA2-transgenic mice and an equal number of nontransgenic littermates were fed a cholesterol-enriched (1%) diet for 13 weeks. After autopsy, cholesterol and triglyceride concentrations were measured in homogenates of liver, spleen, kidney, and myocardial tissues. Compared to the nontransgenic controls, the sPLA2-transgenic mice exhibited significantly lower plasma cholesterol levels, which was due to a reduction in both HDL and beta-lipoprotein (LDL + beta-VLDL) cholesterol. Liver tissues from the transgenic mice were found to contain significantly increased concentrations of free and esterified cholesterol, which was not associated with increased triglyceride concentrations. Spleen, kidney, and heart tissues of the two animal groups showed no significant differences in cholesterol or triglyceride concentrations. The findings suggest that the overexpression of human secretory phospholipase A2 group IIA leads to an enhanced delivery of cholesterol from phospholipolysed lipoproteins to the liver. This mechanism is likely to contribute to the development of hypocholesterolemia observed in patients with inflammatory diseases. |
| Increased hepatobiliary and fecal cholesterol excretion upon activation of the liver X receptor is independent of ABCA1 Plosch, T., T. Kok, et al. (2002), J Biol Chem 277(37): 33870-7. Abstract: The ATP-binding cassette transporter ABCA1 is essential for high density lipoprotein (HDL) formation and considered rate-controlling for reverse cholesterol transport. Expression of the Abca1 gene is under control of the liver X receptor (LXR). We have evaluated effects of LXR activation by the synthetic agonist T0901317 on hepatic and intestinal cholesterol metabolism in C57BL/6J and DBA/1 wild-type mice and in ABCA1-deficient DBA/1 mice. In wild-type mice, T0901317 increased expression of Abca1 in liver and intestine, which was associated with an approximately 60% rise in HDL. Biliary cholesterol excretion rose 2.7-fold upon treatment, and fecal neutral sterol output was increased by 150-300%. Plasma cholesterol levels also increased in treated Abca1(-/-) mice (+120%), but exclusively in very low density lipoprotein-sized fractions. Despite the absence of HDL, hepatobiliary cholesterol output was stimulated upon LXR activation in Abca1(-/-) mice, leading to a 250% increase in the biliary cholesterol/phospholipid ratio. Most importantly, fecal neutral sterol loss was induced to a similar extent (+300%) by the LXR agonist in DBA/1 wild-type and Abca1(-/-) mice. Expression of Abcg5 and Abcg8, recently implicated in biliary excretion of cholesterol and its intestinal absorption, was induced in T0901317-treated mice. Thus, activation of LXR in mice leads to enhanced hepatobiliary cholesterol secretion and fecal neutral sterol loss independent of (ABCA1-mediated) elevation of HDL and the presence of ABCA1 in liver and intestine. |
| Increased high density lipoprotein cholesterol in adult nephrotic syndrome in Nigeria Adigun, M. O., E. O. Agbedana, et al. (1999), Afr J Med Med Sci 28(1-2): 97-100. Abstract: Forty-eight adult subjects consisting of 28 patients with nephrotic syndrome and 20 control subjects were studied. The plasma levels of high density lipoprotein (HDL) cholesterol, low density lipoprotein (LDL) cholesterol and very low density lipoprotein (VLDL) cholesterol were all significantly elevated in the patients with nephrotic syndrome. The elevations in plasma total cholesterol and triglyceride concentrations and the ratio of LDL cholesterol/HDL cholesterol were also significant. On the other hand, there was a significant reduction in the ratio of HDL cholesterol to total cholesterol in the nephrotics. Our results suggest altered lipid and lipoprotein metabolism in adult nephrotic syndrome. The significant increase in low density lipoprotein cholesterol and the reduction in the ratio of HDL cholesterol to total cholesterol, despite the high HDL cholesterol, probably suggests an increased risk for developing coronary heart disease in Nigerian adults suffering from nephrotic syndrome. It is therefore suggested that patient-management strategies for nephrotic syndrome should include lowering of cholesterol by dietary and/or pharmacological therapies. |
| Increased high-density lipoprotein cholesterol concentration in alcoholics is related to low cholesteryl ester transfer protein activity Savolainen, M. J., M. Hannuksela, et al. (1990), Eur J Clin Invest 20(6): 593-9. Abstract: Cholesteryl ester transfer protein (CETP) facilitates the transfer of cholesteryl esters from HDL to apoB-containing lipoproteins. Since alcoholics have high HDL cholesterol and low LDL cholesterol levels, a defect in cholesteryl ester transfer could be responsible for the alcohol-induced alteration in cholesterol distribution between lipoproteins. To test this hypothesis, we compared CETP activity in plasma from 30 alcoholics without severe liver damage and 16 control subjects. Plasma CETP activity was 28% lower in the alcoholics compared with the controls (P less than 0.001), while the teetotallers among the latter had slightly higher CETP activity than those who consumed alcohol in moderation. CETP activity increased slowly after ethanol withdrawal, but did not reach the control level within the 7-day observation period. A positive correlation was observed between plasma CETP activity and the LDL cholesterol HDL cholesterol ratio (r = 0.480, P less than 0.002), whereas CETP activity showed a negative correlation with HDL cholesterol level (r = -0.467, P less than 0.001). The results indicate that defective transfer of cholesteryl esters from HDL to LDL contributes to the high HDL cholesterol levels in alcoholics. |
| Increased high-density lipoprotein cholesterol in patients with epilepsy treated with carbamazepine: a gender-related study Duggal, H. S., R. Jain, et al. (1999), Epilepsia 40(11): 1674-5. |
| Increased high-density lipoprotein cholesterol in patients with epilepsy treated with carbamazepine: a gender-related study Sudhop, T., J. Bauer, et al. (1999), Epilepsia 40(4): 480-4. Abstract: PURPOSE: Long-term treatment with carbamazepine (CBZ) may alter serum lipoprotein concentrations. Gender-related examinations, however, are rare and inconsistent in their results. METHODS: To examine possible sex differences, serum lipoproteins were analyzed in 127 clinic outpatients (56 women and 71 men) with epilepsies with focal or secondarily generalized tonic-clonic seizures (or both) treated with a CBZ monotherapy. Results were compared with a control group of 177 blood donors (67 women and 110 men) matched for age and weight. RESULTS: Total cholesterol, low-density lipoprotein (LDL) cholesterol and high-density lipoprotein (HDL) cholesterol were higher in both male and female patients treated with CBZ compared with controls. The known sex difference in serum lipoprotein concentrations (i.e., higher LDL cholesterol and triglycerides but lower HDL cholesterol in men) was confirmed in controls and patients treated with CBZ, with the exception of LDL cholesterol. The HDL as well as the LDL differences were significantly more pronounced in women treated with CBZ than in men when compared with their controls. These results were independent of the dose of CBZ and plasma concentrations. Lathosterol, a cholesterol precursor, and its ratio to cholesterol, an indicator of cholesterol synthesis, were not different, when compared between gender and different HDL groups. CONCLUSIONS: The observed increase in HDL cholesterol in patients with CBZ, especially in women, might correlate with the previously reported diminished rate of death from coronary heart disease in patients with epilepsy as HDL exerts an antiatherogenic effect. |
| Increased immunogenicity of human renal carcinoma cells following treatment with cholesterol derivatives Ludes, B., C. Staedel, et al. (1990), Eur Urol 17(2): 166-72. Abstract: Tumor cells isolated from human renal cell carcinoma biopsies were treated with cholesteryl hemisuccinate or 25-hydroxycholesterol and the subsequent changes in their membrane fluidity and capacity to induce skin reactivity in the homologous patient were investigated. Both cholesterol derivatives were found equally efficient in decreasing membrane fluidity when measured by fluorescence polarization of diphenylhexatriene. Using trimethylammonium-diphenylhexatriene, a specific cell surface probe, 25-hydroxycholesterol, appeared much more efficient than cholesteryl hemisuccinate in inducing a membrane rigidification in the carcinoma cells. Cells treated with cholesteryl hemisuccinate induced a strong positive skin reaction compatible with delayed-type hypersensitivity in 54% of the patients, whereas 25-hydroxycholesterol-treated cells were less potent (36% positive skin reactions). Thus, manipulation of the physicochemical state of the membrane of human renal carcinoma cells could increase their immunogenicity in the autologous patient, although this seemed not to be related only to membrane rigidification. |
| Increased intestinal ABCA1 expression contributes to the decrease in cholesterol absorption after plant stanol consumption Plat, J. and R. P. Mensink (2002), Faseb J 16(10): 1248-53. Abstract: The hypocholesterolemic effect of plant stanols is explained by a decreased intestinal cholesterol absorption due to a competition between plant stanols and cholesterol for incorporation into mixed micelles. Earlier we had suggested that plant stanols have a so far unknown action inside the enterocytes. The recent discovery of the involvement of ATP binding cassette (ABC) transporters in cholesterol absorption was a lead to further explore the hypocholesterolemic mechanism of plant stanols. We found that mixed micelles enriched with sitostanol or with cholesterol plus sitostanol were potent inducers of ABCA1 expression in caco-2 cells, an accepted model to study human intestinal lipoprotein metabolism. Based on these findings, we now hypothesize that plant stanols--and possibly plant sterols--increase ABCA1-mediated cholesterol efflux back into the intestinal lumen. We further hypothesize that intracellular levels of plant stanols are monitored by the same sensors (SREBP-2 and LXR) as those that monitor cholesterol. Consequently, increased plant stanol levels within the enterocyte activate cholesterol efflux through ABCA1- but not SREBP-2-mediated endogenous cholesterol synthesis even if intracellular cholesterol concentrations are lowered through consumption of plant stanols. If our hypothesis is correct, then the LXR pathway may be a target for dietary regulation of intestinal lipid metabolism. |
| Increased intestinal contents viscosity reduces cholesterol absorption efficiency in hamsters fed hydroxypropyl methylcellulose Carr, T. P., D. D. Gallaher, et al. (1996), J Nutr 126(5): 1463-9. Abstract: This study was conducted to test the hypothesis that increased intestinal contents viscosity lowers plasma cholesterol concentrations by decreasing cholesterol absorption. Male Golden Syrian hamsters were fed for 4 wk diets containing 0.12% cholesterol, and either 4% cellulose or four different viscosity grades of hydroxypropyl methylcellulose (HPMC). Dietary HPMC confers viscosity in the small intestine but is resistant to fermentation. Cholesterol absorption efficiency was measured using the dual isotope ratio method, and plasma and liver cholesterol concentrations were determined enzymatically. Ex vivo viscosity of intestinal contents supernatants was measured using a Wells-Brookfield cone/plate viscometer, and the means of treatment groups ranged from 6 to 6532 mPa.s. Relative to dietary cellulose, all viscosity grades of HPMC resulted in significantly lower cholesterol absorption efficiency, lower plasma cholesterol concentration, and lower liver cholesteryl ester content. The logarithm of intestinal contents ex vivo viscosity was inversely correlated with dietary cholesterol absorption (r2 = 0.84, P = 0.028). Furthermore, dietary cholesterol absorption was positively correlated with plasma cholesterol concentration (r2 = 0.89, P = 0.017) and liver cholesteryl ester content (r2 = 0.96, P = 0.0031). Thus, the data suggest an independent role of intestinal contents viscosity in lowering plasma cholesterol concentration and liver cholesteryl ester content by reducing cholesterol absorption efficiency. |
| Increased iron staining in the cerebral cortex of cholesterol fed rabbits Ong, W. Y., B. Tan, et al. (2004), Mech Ageing Dev 125(4): 305-13. Abstract: The link between hypercholesterolemia and neuronal damage is not clear. In the present study, we studied some of the possible effects of hypercholesterolemia on the brain, using the cholesterol fed New Zealand White rabbit as a model. An increase in the number of iron positive cells (i.e. oligodendrocytes) was observed in the brain parenchyma, in rabbits treated with a high cholesterol diet for 8 weeks. At this time, no neuronal death was observed, indicating that the increased iron did not occur as a consequence of neuronal injury. No heme oxygenase-1 (HO-1) or bilirubin immunoreactivity was observed in the brains in these rabbits, indicating that the iron accumulation did not occur as a consequence of increased breakdown of heme. It is postulated that cholesterol could have subtly damaged brain endothelial cells, resulting in increased iron transport across brain endothelial cells. Hypercholesterolaemia is known to be associated with increased plasma lipid peroxidation which might contribute to such damage. |