| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Intestinal cholesterol absorption: identification of different binding proteins for cholesterol and cholesterol absorption inhibitors in the enterocyte brush border membrane Kramer, W., F. Girbig, et al. (2003), Biochim Biophys Acta 1633(1): 13-26. Abstract: Absorption of cholesterol from the intestine is a central part of body cholesterol homeostasis. The molecular mechanisms of intestinal cholesterol absorption and the proteins mediating membrane transport are not known. We therefore aimed to identify the proteins involved in intestinal cholesterol absorption across the luminal brush border membrane of small intestinal enterocytes. By photoaffinity labeling using photoreactive derivatives of cholesterol and 2-azetidinone cholesterol absorption inhibitors, an 80-kDa and a 145-kDa integral membrane protein were identified as specific binding proteins for cholesterol and cholesterol absorption inhibitors, respectively, in the brush border membrane of small intestinal enterocytes. The 80-kDa cholesterol-binding protein did not interact with cholesterol absorption inhibitors and vice versa; cholesterol or plant sterols did not interfere with the 145-kDa molecular target for cholesterol absorption inhibitors. Both proteins showed an identical tissue distribution and were exclusively found at the anatomical sites of cholesterol absorption-duodenum, jejunum and ileum. Neither stomach, cecum, colon, rectum, kidney, liver nor fat tissue expressed the 80- or 145-kDa binding proteins for cholesterol and cholesterol absorption inhibitors. Both proteins are different from the hitherto described candidate proteins for the intestinal cholesterol transporter,-SR-BI, ABC G5/ABC G8 or ABC A1. Our data strongly suggest that intestinal cholesterol absorption is not facilitated by a single transporter protein but occurs by a complex machinery. Two specific binding proteins for cholesterol (80 kDa) and cholesterol absorption inhibitors (145 kDa) of the enterocyte brush border membrane are probable protein constituents of the mechanism responsible for the intestinal absorption of cholesterol. |
| Intestinal cholesterol metabolism Lichtenstein, A. H. (1990), Ann Med 22(1): 49-52. Abstract: The handling of cholesterol by the intestine involves a balance between absorption, excretion and metabolism by gut microflora. Between 34-57% of dietary cholesterol is absorbed from the human intestine. Variables effecting the efficiency of cholesterol absorption include the absolute amount of cholesterol consumed, the presence of plant sterols, the fiber content of the diet, transit time and possibly the relative proportions of fatty acids in the diet. On average, 150 mg/day of cholesterol is excreted in the feces. Fecal cholesterol derives from biliary secretions into the intestine, sloughing of epithelial cells and unabsorbed dietary cholesterol. The major metabolic products of cholesterol in the gut are coprostanol, coprostanone, cholestanol, cholestanone and epicoprostanol. Bacterial metabolism of cholesterol can be influenced by diet as evidenced by significant variations among different population groups with different dietary habits. Altered patterns of intestinal bacterial metabolism of cholesterol may place persons at a higher risk of developing colonic disorders. Dairy products have been reported to influence the bacterial metabolism of cholesterol and possibly plasma cholesterol levels although the significance of these findings to overall cholesterol balance needs to be further defined. |
| Intestinal cholesterol synthesis and mobilisation to blood in sucrose-feeding and alcohol-intake Pugalendi, K. V. and S. Ramakrishnan (2000), Indian J Exp Biol 38(8): 762-5. Abstract: Small intestines synthesize cholesterol to a greater extent than liver. Between starch-fed and sucrose-fed rats, using (14C) glucose, it was found that the synthesis of cholesterol by the jejunum of small intestines was greater in the sucrose-fed group than starch-fed group. By a novel experimental technique and using (14C) glucose, it was found that the contribution towards buffer representing lymph was greater in the sucrose-fed group (13.3%) than the controls (11%). Hypercholesterolemia on sucrose feeding may be at least partly due to contribution by the small intestines. Regarding alcohol, using (14C) glucose it was found that total synthesis of cholesterol by the small intestines was decreased in alcohol-fed rats. There was no difference in the cholesterol retained by the intestinal tissue between the controls and alcohol-fed animals while, the secretion towards buffer (lymph) was 9% as against 11. This indicates that there is contribution of cholesterol to blood from small intestines in alcohol-intake also but due to overall decrease in the intestinal synthesis of cholesterol, contribution of intestines to hypercholesterolemia may not be substantial as in the case of sucrose feeding. This is because in sucrose-feeding there is increased cholesterol synthesis. |
| Intestinal digestion, absorption, and transport of structured triglycerides and cholesterol in rats Tso, P., M. D. Karlstad, et al. (1995), Am J Physiol 268(4 Pt 1): G568-77. Abstract: We compared the intestinal absorption of trilinolein (1,2,3-tri-1-14Clinoleyl-sn-glycerol) with two different structured triglycerides containing one linoleic acid (C18:2) and two octanoic acids (C8:0), 1,3-dioctanoyl-2-1-14Clinoleyl-sn-glycerol (2-linoleate) and 1,2-di1-14Coctanoyl-3-linoleyl-sn-glycerol (1,2-octanoate), respectively. Lymphatic radioactive lipid output of 2-linoleate resembled that of trilinolein rats but remained significantly lower during the lipid infusion. Radioactive lipid was recovered along the entire small intestinal lumen, with a significantly higher amount of 14Clipid recovered in the lower small intestine and cecum in the 2-linoleate group. Delayed uptake of radioactive 2-linoleate was not due to poor digestion. In contrast, 1,2-octanoate was efficiently digested, and both the free fatty acid (FFA) and the monoacylglycerol (MG) containing octanoate were rapidly absorbed. Irrespective of its position on the triglyceride molecule, 14C-labeled octanoate was poorly transported into lymph. In addition, intestinal luminal and mucosal recovery of 14Coctanoate was significantly lower in the 1,2-octanoate group compared with 14Clinoleate recovery in the 2-linoleate or trilinolein groups. Total recovery of infused radioactive lipid was significantly less in the 1,2-octanoate group than in the 2-linoleate or trilinolein groups. Thus radioactive octanoate in the form of FFA or 2-MG was rapidly absorbed and transported via the portal vein. The infusion of either 2-linoleate or 1,2-octanoate did not affect the absorption and lymphatic transport of cholesterol compared with trilinolein. In summary, the type of the fatty acid on the structured triglyceride molecule affects its digestion, absorption, and lymphatic transport. Structured triglycerides containing octanoic acid in the 1- and 3-positions and linoleic acid in the 2-position may not be advantageous to use as a sole source of dietary lipid, but should be supplemented with long-chain triglycerides. |
| Intestinal ischemic manifestations related to cholesterol emboli? Quilichini, R., T. Benderitter, et al. (1993), Presse Med 22(16): 786. |
| Intestinal microbial conversion of cholesterol to coprostanol in man. Influence of antibiotics Midtvedt, T., E. Lingaas, et al. (1990), Apmis 98(9): 839-44. Abstract: The intestinal microbial conversion of cholesterol to coprostanol has been measured in groups of healthy subjects before, during and after they received the antibiotics ampicillin, bacitracin, clindamycin, co-trimoxazole, doxycycline, erythromycin, metronidazole, nalidixic acid, ofloxacin or vancomycin orally for 6 days. Before they received antibiotics, the subjects demonstrated two distinct patterns of cholesterol conversion. One pattern was characterised by extensive conversion of cholesterol, the other by little or no conversion. Intake of bacitracin, clindamycin, erythromycin, metronidazole and vancomycin significantly reduced the conversion to coprostanol. In the groups receiving ampicillin or doxycycline, marked reductions were found in most of the subjects. No alterations were found in the groups receiving co-trimoxazole, nalidixic acid or ofloxacin. In 6 subjects no conversion of cholesterol to coprostanol was found up to 5 weeks after the end of the antibiotic intake. We conclude that orally given antibiotics may cause alterations in the intestinal conversion of cholesterol, reflecting changes in the anaerobic, Gram-positive component of the gut flora. |
| Intestinal worm burden and serum cholesterol or lipid concentration in a Shipibo population (Peru) Wiedermann, U., H. Stemberger, et al. (1991), Zentralbl Bakteriol 275(2): 279-86. Abstract: Paired samples of stool and serum of 32 members of the Shipibo tribe resident in the rain forest of the Peruvian lowlands were tested for worm egg count and serum lipid parameters, respectively. 90% of the stool samples tested were found to contain eggs or larvae of several worm species, most commonly 3 or 4 different species. Serum lipid levels were found to be relatively low, most probably due to a low proportion of dietary fat ranging from 16-31%. Statistical analysis showed a significant inverse correlation between worm egg excretion and HDL levels which was true for hookworm, strongyloides and trichuris, but not for ascaris. The mechanisms underlying the observed association between intestinal worm load and HDL reduction are not completely understood and may include reduced HDL synthesis in the gut wall due to inflammatory and/or toxic irritation. |
| Intimal lipid accretion and elevated serum cholesterol in Marek's disease virus-inoculated chickens Njenga, M. K. and C. A. Dangler (1996), Vet Pathol 33(6): 704-8. Abstract: In our previous studies of the early pathogenesis of the Marek's disease virus (MDV)-associated model of atherosclerosis, the brachiocephalic arteries and ascending aortas of MDV-inoculated chickens failed to develop lipid accretion and intimal/medial proliferation consistent with atherosclerotic lesions, as described in the original reports of this model. The role of cholesterol supplementation in the formation of MDV-associated atherosclerotic lesions was reexamined. At 3 days of age, 40 chicks were inoculated with the CU-2 strain of MDV. Another 40 chicks were sham inoculated. At 15 weeks postinfection, half of the sham- and MDV-inoculated birds received 2% cholesterol supplementation in the diet for the rest of the experimental period. At 30 weeks postinfection, the aortas and brachiocephalic arteries were evaluated. Several observations were different from the original description of the model. None of the chickens among the four experimental groups developed atherosclerotic lesions, regardless of MDV inoculation or cholesterol supplementation. However, intimal thickening and marked oil red O-positive foam cell accumulation were observed in all 11 MDV-inoculated, cholesterol-supplemented chickens. None of the nine MDV-inoculated, unsupplemented chickens manifested arterial lipid accumulation, despite the presence of an intimal cellular infiltrate. Also in contrast to the original model description, both cholesterol-supplemented and unsupplemented MDV-inoculated chickens manifested significant increases in serum cholesterol in comparison with the respective sham-inoculated groups. |
| Intimal plaque development and oxidative stress in cholesterol-induced atherosclerosis in New Zealand rabbits Heinle, H., U. Brehme, et al. (2002), Acta Physiol Scand 176(2): 101-7. Abstract: Although oxidative stress is well known in atherogenesis, the origin, nature and kinetics of free radicals involved have not been well described till now. Here, we correlated parameters of oxidative stress with cellular components during induction and stabilization of aortic intimal lesions which were induced in rabbits by feeding a cholesterol-enriched diet for 6 weeks and a normal diet for further 68 weeks. Plasma lipids, aortic plaque size and composition (macrophages, smooth muscle cells, oxidized LDL by morphometry), as well as aortic radical production (by luminol-enhanced chemiluminescence and TEMPO-9AC fluorescence) were measured after various time points. The parameters of oxidative stress were correlated with the different cellular components of the aortic plaques. The plaques increased until week 21, no significant regression was found until week 74, plasma cholesterol was maximal at week 6. Macrophages, oxidized LDL and generation of different species of free radicals were increased during plaque development, yet with different time kinetics. Whereas chemiluminescence correlated only weakly with the amount of intimal macrophages, strong correlations were found between TEMPO fluorescence and smooth muscle cells (r = 0.4778, P < 0.001) and between macrophages and oxidized LDL (r = 0.5896, P < 0.0001). Different indicators of oxidative stress were increased during plaque progression and stabilization. However, the various correlations show, that distinct types of reactive species secreted probably from macrophages and smooth muscle cells contribute to oxidative stress in the different phases of plaque development. |
| Intimal retention of cholesterol derived from apolipoprotein B100- and apolipoprotein B48-containing lipoproteins in carotid arteries of Watanabe heritable hyperlipidemic rabbits Proctor, S. D. and J. C. Mamo (2003), Arterioscler Thromb Vasc Biol 23(9): 1595-600. Abstract: OBJECTIVE: The arterial retention of apolipoprotein (apo) B100- and apoB48-containing lipoproteins was simultaneously determined in a rabbit model of human hypercholesterolemia using 3D confocal microscopy. METHODS AND RESULTS: Lipoproteins containing apoB100 (LDL) and apoB48 (chylomicron remnants) were differentially conjugated with fluorophores and simultaneously perfused at equivalent concentrations under physiological conditions in situ through carotid vessels of Watanabe heritable hyperlipidemic rabbits and compared with controls. Retention of lipoproteins was defined as the amount remaining after an extensive washout phase. LDL and chylomicron remnants were both retained, primarily within the subendothelial space. Without a concomitant increase in exposure to lipoproteins, we found a marked increase in the retention of cholesterol within the intima of Watanabe heritable hyperlipidemic rabbits compared with controls, specifically because of increased entrapment of apoB48-containing lipoproteins. CONCLUSIONS: Collectively, our data suggest that hypercholesterolemia induced as a consequence of LDL receptor deficiency differentially influences retention of LDL and of chylomicron remnants. |
| Intimal smooth muscle cells up-regulate beta-very low density lipoprotein-mediated cholesterol accumulation by enhancing beta-very low density lipoprotein uptake and decreasing cholesterol efflux Ishii, I., H. Satoh, et al. (2002), Biochim Biophys Acta 1585(1): 30-8. Abstract: To clarify the mechanism of smooth muscle cell (SMC)-derived foam cell formation, we investigated beta-very low density lipoprotein (beta-VLDL) cholesterol metabolism in vascular medial SMCs (M-SMCs) from normal rabbits compared with intimal SMCs (I-SMCs) from normal rabbits fed a high-cholesterol diet and LDL receptor-deficient rabbits. For both types of I-SMCs, uptake of 3Hcholesteryl oleate labeled beta-VLDL increased 1.6 times and release of 3Hcholesterol decreased 40% compared with M-SMCs. M-SMCs took up part of the beta-VLDL through the LDL receptor but I-SMCs did not. mRNAs for the VLDL receptor and the LDL receptor relative with 11 ligand binding repeats were expressed at similar levels in all SMCs. M-SMCs expressed more LDL receptor-related protein than I-SMCs. Ligand blotting analysis revealed greater 125I-beta-VLDL binding to a 700-kDa protein in I-SMCs compared with M-SMCs. I-SMCs had higher activities of acid cholesterol esterase and acyl-CoA:cholesterol acyltransferase, and lower activity of neutral cholesterol esterase than M-SMCs in both the absence and the presence of beta-VLDL. These results indicate that I-SMCs accumulate more cholesteryl ester than M-SMCs by taking up more beta-VLDL and by effluxing less cholesterol. |
| Intima-media thickness after cholesterol lowering in familial hypercholesterolemia. A three-year ultrasound study of common carotid and femoral arteries Wendelhag, I., O. Wiklund, et al. (1995), Atherosclerosis 117(2): 225-36. Abstract: Patients with familial hypercholesterolemia (FH) (n = 53) were examined with B-mode ultrasound before and after 3 years of cholesterol-lowering therapy with pravastatin, cholestyramine, or a combination. The aim was to measure the progression rate of intima-media thickening during follow-up in the common carotid and common femoral arteries. Since for ethical reasons it was not possible to perform a randomized placebo controlled study in patients with FH, we chose to recruit an untreated control group with lower risk, matched for sex, age, height and weight, and with serum cholesterol below 6.5 mmol/l. At baseline, intima-media thickness was larger in the hypercholesterolemic group than in the control group in both the common carotid and common femoral arteries. The difference between the change over 3 years observed in the control group and the change observed in the hypercholesterolemic group was calculated and defined as 'net difference'. There was a -32% net difference in low density lipoprotein (LDL) in the hypercholesterolemic group during follow-up. The ultrasound investigation showed a concomitant net difference of -0.06 mm in mean carotid intima-media thickness (95% confidence interval, -0.11 to -0.01 mm) and of -0.09 mm in maximum carotid intima-media thickness (P < 0.05, 95% confidence interval, -0.16 to -0.01 mm), with no net change in lumen diameter. No decrease was recorded in common femoral intima-medial thickness. Seventeen of the patients with FH had a positive history of myocardial infarction (MI) and this subgroup had a significantly larger decrease in mean carotid intima-media thickness during follow-up than the subgroup of patients with a negative history of MI (P < 0.01). In conclusion, the results showed a reduction in common carotid intima-media thickness after long-term cholesterol-lowering therapy in patients with FH. This finding may indicate a beneficial effect on atherosclerosis development in these patients. |
| Intima-media thickness after pravastatin stabilizes also in patients with moderate to no reduction in LDL-cholesterol levels: the carotid atherosclerosis Italian ultrasound study Baldassarre, D., F. Veglia, et al. (2000), Atherosclerosis 151(2): 575-83. Abstract: The Carotid Atherosclerosis Italian Ultrasound study (CAIUS), a multicenter, double-blind clinical trial, performed in 305 asymptomatic, moderately hypercholesterolemic patients, clearly demonstrated beneficial effects of pravastatin on the carotid intima-media thickness (IMT) progression. The database of the CAIUS study was examined in order to investigate the presence of a relationship, if any, between the activity of pravastatin on IMT progression rate and its hypocholesterolemic effect. Quantitative B-mode ultrasound imaging was used to quantify the individual mean maximum IMT progression rate in 3 years. In the overall group of patients (placebo and pravastatin) covariance analysis showed that while the variable 'treatment' (0 = placebo, 1 = pravastatin) was significantly related to the reduction of IMT progression (F= 6.6, P = 0.01), the IMT progression did not correlate with the extent of LDL-C lowering (F= 0.00, P = 0.98). To further investigate this issue. the pravastatin treated group was stratified into quartiles of LDL-C reduction. In contrast to what was observed in the placebo group, in which a positive mean IMT progression rate was observed, independent of the extent of LDL-C reduction, no IMT progressionwas observed in any subgroup treated with pravastatin. No significant difference was found among quartiles and no trend could be identified. In conclusion, the effect of pravastatin treatment on carotid IMT progression rate is beneficial; however the CAIUS study demonstrated that lowering LDL-C by itself, does not explain the variability of beneficial changes in IMT. |
| Intra-abdominal fat is a major determinant of the National Cholesterol Education Program Adult Treatment Panel III criteria for the metabolic syndrome Carr, D. B., K. M. Utzschneider, et al. (2004), Diabetes 53(8): 2087-94. Abstract: The underlying pathophysiology of the metabolic syndrome is the subject of debate, with both insulin resistance and obesity considered as important factors. We evaluated the differential effects of insulin resistance and central body fat distribution in determining the metabolic syndrome as defined by the National Cholesterol Education Program (NCEP) Adult Treatment Panel III. In addition, we determined which NCEP criteria were associated with insulin resistance and central adiposity. The subjects, 218 healthy men (n = 89) and women (n = 129) with a broad range of age (26-75 years) and BMI (18.4-46.8 kg/m2), underwent quantification of the insulin sensitivity index (Si) and intra-abdominal fat (IAF) and subcutaneous fat (SCF) areas. The metabolic syndrome was present in 34 (15.6%) of subjects who had a lower Si median: 3.13 vs. 6.09 x 10(-5) min(-1)/(pmol/l) and higher IAF (166.3 vs. 79.1 cm2) and SCF (285.1 vs. 179.8 cm2) areas compared with subjects without the syndrome (P < 0.001). Multivariate models including Si, IAF, and SCF demonstrated that each parameter was associated with the syndrome. However, IAF was independently associated with all five of the metabolic syndrome criteria. In multivariable models containing the criteria as covariates, waist circumference and triglyceride levels were independently associated with Si and IAF and SCF areas (P < 0.001). Although insulin resistance and central body fat are both associated with the metabolic syndrome, IAF is independently associated with all of the criteria, suggesting that it may have a pathophysiological role. Of the NCEP criteria, waist circumference and triglycerides may best identify insulin resistance and visceral adiposity in individuals with a fasting plasma glucose <6.4 mmol/l. |
| Intracalvarial cholesterol granulomas--clinicopathologic correlates of three cases Sze, C. I., W. Huffer, et al. (2003), Clin Neuropathol 22(1): 41-6. Abstract: Cholesterol granulomas (CGs) are tumor-like lesions seldom encountered by neuropathologists. CGs develop in reaction to localized hemorrhage, often occurring in bony sites with possible impaired drainage of blood and blood products. The most common bony location is the petrous apex, although orbital, frontal sinus, and maxillary sinus sites have been reported. We compare and contrast three recent cases seen at our institution that illustrate the spectrum of clinical, radiographic, and pathologic features that can be seen with these mass lesions. One case demonstrated the unique pathological features of Gamma-Gandy body formation, epithelioid histiocytes heavily encrusted with iron pigments, and extensive tophi. The latter most likely represented aggregates of calcium pyrophosphate crystals associated with extensive iron deposition. |
| Intracellular calcium changes in neuronal cells induced by Alzheimer's beta-amyloid protein are blocked by estradiol and cholesterol Kawahara, M. and Y. Kuroda (2001), Cell Mol Neurobiol 21(1): 1-13. Abstract: 1. The elevation of intracellular Ca2+ levels (Ca2+i) in immortalized hypothalamic neurons (GT1-7 cells) after exposure to Alzheimer's beta-amyloid protein (AbetaP25-35) was investigated using a multisite fluorometry system. 2. The marked rise in Ca2+i appeared after exposure to 5-20-microM AbetaP25-35. Analysis of the spatiotemporal patterns of Ca2+i changes revealed that the magnitude and the latency of the response to AbetaP in each cell were highly heterogeneous. 3. The preadministration of 17beta-estradiol, 17alpha-estradiol, phloretin and cholesterol, which influence the properties of membranes, such as membrane fluidity or membrane potential, significantly decreased the rise in Ca2+i. 4. These findings support the idea that disruption of calcium homeostasis by AbetaP channels may be the molecular basis of the neurotoxicity of AbetaP and of the pathogenesis of Alzheimer's disease. It is also suggested that membrane properties may play key roles in the expression of neurotoxicity. |
| Intracellular cholesterol and phospholipid trafficking: comparable mechanisms in macrophages and neuronal cells Schmitz, G. and E. Orso (2001), Neurochem Res 26(8-9): 1045-68. Abstract: During the past ten years considerable evidences have accumulated that in addition to monocytes/macrophages, that are implicated in innate immunity and atherogenesis, neuronal cells also exhibit an extensive cellular metabolism. The present study focuses on the major protein players that establish cellular distribution of cholesterol and phospholipids. Evidences are provided that neuronal cells and monocytes/macrophages are equipped with comparable intracellular lipid trafficking mechanisms. Selected examples are presented that trafficking dysfunctions lead to disease development, such as Tangier disease and Niemann-Pick disease type C, or contribute to the pathogenesis of diseases such as Alzheimer disease and atherosclerosis. |
| Intracellular cholesterol mobilization involved in the ABCA1/apolipoprotein-mediated assembly of high density lipoprotein in fibroblasts Yamauchi, Y., C. C. Chang, et al. (2004), J Lipid Res 45(10): 1943-51. Abstract: Differential regulation has been suggested for cellular cholesterol and phospholipid release mediated by apolipoprotein A-I (apoA-I)/ABCA1. We investigated various factors involved in cholesterol mobilization related to this pathway. ApoA-I induced a rapid decrease of the cellular cholesterol compartment that is in equilibrium with the ACAT-accessible pool in cells that generate cholesterol-rich HDL. Pharmacological and genetic inactivation of ACAT enhanced the apoA-I-mediated cholesterol release through upregulation of ABCA1 and through cholesterol enrichment in the HDL generated. Pharmacological activation of protein kinase C (PKC) also decreased the ACAT-accessible cholesterol pool, not only in the cells that produce cholesterol-rich HDL by apoA-I (i.e., human fibroblast WI-38 cells) but also in the cells that generate cholesterol-poor HDL (mouse fibroblast L929 cells). In L929 cells, the PKC activation caused an increase in apoA-I-mediated cholesterol release without detectable change in phospholipid release and in ABCA1 expression. These results indicate that apoA-I mobilizes intracellular cholesterol for the ABCA1-mediated release from the compartment that is under the control of ACAT. The cholesterol mobilization process is presumably related to PKC activation by apoA-I. |
| Intracellular cholesterol trafficking Sviridov, D. (1999), Histol Histopathol 14(1): 305-19. Abstract: The overall picture of intracellular cholesterol trafficking is very complex. The transfer of cholesterol within the cell depends on the contribution of several trafficking mechanisms. The known elements of cholesterol trafficking machinery include clathrin-coated pits, scavenger receptor type B1, caveolae, phospholipid rafts, Niemann-Pick C disease protein, sterol carrier protein 2, multidrug resistance protein, microsomal triglyceride transfer protein and steroidogenic acute regulation protein. Several pathways of intracellular cholesterol trafficking, for example retroendocytosis and cholesterol absorption in the intestine, are yet to be connected to specific structural elements. The contribution of different pathways depends on cell type, the source and destination of cholesterol and cellular cholesterol content and requirements. Some pathways are found in most, if not all, cell types, while others are associated with the specialized function of a particular cell type, for example, lipoprotein assembly in the liver or intestine and steroid hormone synthesis in steroidogenic tissue. Certain routes of intracellular cholesterol trafficking are heavily backed up by several auxiliary pathways, others entirely depend on a single functional element. In this review we describe the intracellular machinery involved in the intracellular transfer of cholesterol and give an overview of both the general and specialized pathways of intracellular cholesterol trafficking known to date. |
| Intracellular cholesterol trafficking: role of the NPC1 protein Blanchette-Mackie, E. J. (2000), Biochim Biophys Acta 1486(1): 171-83. |