| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Evidence that peroxisome proliferator-activated receptor delta influences cholesterol metabolism in men Skogsberg, J., K. Kannisto, et al. (2003), Arterioscler Thromb Vasc Biol 23(4): 637-43. Abstract: OBJECTIVE: The objective of this work was to explore the role of peroxisome proliferator-activated receptor delta (PPARD) in lipid metabolism in humans. METHODS AND RESULTS: PPARD is a nuclear receptor involved in lipid metabolism in primates and mice. We screened the 5'-region of the human gene for polymorphisms to be used as tools in association studies. Four polymorphisms were detected: -409C/T in the promoter region, +73C/T in exon 1, +255A/G in exon 3, and +294T/C in exon 4. The frequencies of the rare alleles were 4.2%, 4.2%, 1.2% and 15.6%, respectively, in a population-based group of 543 healthy men. Only the +294T/C polymorphism showed significant association with a metabolic trait. Homozygotes for the rare C allele had a higher plasma LDL-cholesterol concentration than homozygotes for the common T allele, which was verified in an independent cohort consisting of 282 healthy men. Transfection studies showed that the rare C allele had higher transcriptional activity than the common T allele. Electrophoretic mobility shift assays demonstrated that the +294T/C polymorphism influenced binding of Sp-1. An interaction with the PPAR alpha L162V polymorphism was also detected for several lipid parameters. CONCLUSIONS: These findings suggest that PPARD plays a role in cholesterol metabolism in humans. |
| Evidence that polyunsaturated lecithin induces a reduction in plasma cholesterol level and favorable changes in lipoprotein composition in hypercholesterolemic rats Jimenez, M. A., M. L. Scarino, et al. (1990), J Nutr 120(7): 659-67. Abstract: For 30 d adult rats were fed a hypercholesterolemic (H) diet (25% saturated fat, 1% cholesterol and 0.5% cholic acid) containing different amounts of saponins (1% or 0.2%) and/or purified polyunsaturated lecithin (2.5% or 0.7%). Lecithin induced a striking reduction in the plasma levels of very low density lipoprotein (VLDL), intermediate density lipoprotein (IDL) and low density lipoprotein (LDL) cholesterol as well as an increase in the level of high density lipoprotein (HDL) cholesterol. Saponins had only a very slight effect in lowering the level of VLDL cholesterol. Apoprotein A-I was unexpectedly present in VLDL, IDL and LDL after feeding rats the H diet and disappeared only after lecithin feeding. The activity of plasma lecithin-cholesterol acyltransferase was higher when the two lecithin diets were fed than when the other diets were fed. Fecal excretion of neutral sterols was unmodified by the various diets whereas acid steroid excretion increased after lecithin feeding. Saponins, when added with lecithin to the diet, reduced the beneficial effect of lecithin. The results indicate that polyunsaturated lecithin induced a reduction in plasma cholesterol, possibly through an increased formation of HDL particles. |
| Evidence that reverse cholesterol transport is stimulated by lipolysis of triglyceride-rich lipoproteins Miller, N. E. and M. N. Nanjee (1991), FEBS Lett 285(1): 132-4. Abstract: The hypothesis that reverse cholesterol transport by high density lipoprotein (HDL) is augmented by lipolysis of triglyceride-rich lipoproteins received support from experiments in rabbits whose tissue cholesterol had been pre-labeled with 3Hcholesterol several weeks earlier. When lipolysis was stimulated by intravenous heparin (which releases lipoprotein lipase from vascular endothelium), reciprocal changes in plasma triglyceride and HDL cholesterol concentrations were accompanied by a rise in the specific radioactivity of HDL cholesterol, indicative of increased transfer of cholesterol into HDL from slowly exchanging cholesterol pools in extra-hepatic tissues. |
| Evidence that the initial up-regulation of phosphatidylcholine biosynthesis in free cholesterol-loaded macrophages is an adaptive response that prevents cholesterol-induced cellular necrosis. Proposed role of an eventual failure of this response in foam cell necrosis in advanced atherosclerosis Tabas, I., S. Marathe, et al. (1996), J Biol Chem 271(37): 22773-81. Abstract: Macrophages in atherosclerotic lesions accumulate free cholesterol (FC) as well as cholesteryl ester and appear to have high rates of phospholipid (PL) synthesis and increased PL mass. Previous short term (i.e. |
| Evidence that the major membrane lipids, except cholesterol, are made in axons of cultured rat sympathetic neurons Vance, J. E., D. Pan, et al. (1994), J Neurochem 62(1): 329-37. Abstract: Membrane lipids and proteins required for axonal growth and regeneration are generally believed to be synthesized in the cell bodies of neurons and transported into the axons. However, we have demonstrated recently that, in cultured rat sympathetic neurons, axons themselves have the capacity to synthesize phosphatidylcholine, sphingomyelin, and phosphatidylethanolamine. In these experiments, we employed a compartment model of neuron culture in which pure axons grow in a fluid environment separate from that containing the cell bodies. In the present study, we again used compartmented cultures to confirm and extend the previous results. We have shown that three enzymes of phosphatidylcholine biosynthesis via the CDP-choline pathway are present in axons. We have also shown that the rate-limiting step in the biosynthesis of phosphatidylcholine by this route in neurons, and locally in axons, is catalyzed by the enzyme CTP:phosphocholine cytidylytransferase. The biosynthesis of other membrane lipids, such as phosphatidylserine, phosphatidylethanolamine derived by decarboxylation of phosphatidylserine, phosphatidylinositol, and fatty acids, also occurs in axons. However, the methylation pathway for the conversion of phosphatidylethanolamine into phosphatidylcholine appears to be a quantitatively insignificant route for phosphatidylcholine synthesis in neurons. Moreover, our data provided no evidence for the biosynthesis of another important membrane lipid, cholesterol, in axons. |
| Evidence that the major oxysterols in human circulation originate from distinct pools of cholesterol: a stable isotope study Meaney, S., M. Hassan, et al. (2001), J Lipid Res 42(1): 70-8. Abstract: The major oxysterols in human circulation are 7 alpha-, 27-, and (24S)-hydroxycholesterol. Two unique experiments were performed to elucidate their origin and kinetics. A volunteer was exposed to (18)O(2)-enriched air. A rapid incorporation of (18)O in both 7 alpha- and 27-hydroxycholesterol and disappearance of label after exposure were observed. The half-life was estimated to be less than 1 h. Incorporation of (18)O in (24S)-hydroxycholesterol was not significant. In the second experiment a volunteer was infused with liposomes containing 10 g of (2)H(6)cholesterol. This resulted in an enrichment of plasma cholesterol with (2)H of up to 13%, and less than 0.5% in cerebrospinal fluid cholesterol. The content of (2)H in circulating 7 alpha-hydroxycholesterol remained approximately equal to that of plasma cholesterol and decreased with a half-life of about 13 days. The (2)H content of circulating 27-hydroxycholesterol was initially lower than that of cholesterol but in the last phase of the experiment it exceeded that of cholesterol. No significant incorporation of (2)H in (24S)-hydroxycholesterol was observed.It is evident that 7 alpha-hydroxycholesterol must originate from a rapidly miscible pool, about 80% of 27-hydroxycholesterol from a more slowly exchangeable pool, and more than 90% of (24S)-hydroxycholesterol from a nonexchangeable pool, presumably the brain. The results are discussed in relation to the role of oxysterols in cholesterol homeostasis and their use as markers for pathological conditions. - Meaney, S., M. Hassan, A. Sakinis, D. Lutjohann, K. von Bergmann, A. Wennmalm, U. Diczfalusy, and I. Bjorkhem. Evidence that the major oxysterols in human circulation originate from distinct pools of cholesterol: a stable isotope study. J. Lipid Res. 2001. 42: 70;-78. |
| Evolution of cholesterol concept of atherogenesis from Anitchkov to our days Klimov, A. N. and V. A. Nagornev (2002), Pediatr Pathol Mol Med 21(3): 307-20. Abstract: Our review addresses the development of the cholesterol concept of atherogenesis from the classical investigations of Anitchkov and Chalatov (1913), who induced experimental cholesterol atherosclerosis in rabbits, to the present time. We conclude that based on data obtained to date relating to the presence of different classes of lipoproteins in blood, on the role of peroxidatively modified low density lipoproteins in atherogenesis, and on the involvement of various arterial and blood cells and other factors, the cholesterol concept of atherogenesis has not lost its significance. Moreover, cholesterol-lowering therapy has a leading role in the primary and secondary prevention of coronary heart disease events and other clinical manifestations of atherosclerosis. |
| Evolution of methods for measurement of HDL-cholesterol: from ultracentrifugation to homogeneous assays Warnick, G. R., M. Nauck, et al. (2001), Clin Chem 47(9): 1579-96. Abstract: BACKGROUND: Adoption of automated homogeneous assays for HDL-cholesterol (HDL-C) is increasing, driven by the need of clinical laboratories to cope with increasing workloads while containing costs. However, performance characteristics of homogeneous assays often differ in important aspects from those of the earlier precipitation methods. This review provides an overview of the new generation of homogeneous assays for HDL-C within the historical context of the evolution of methods and the efforts to standardize measurements of the lipoproteins. APPROACH: This is a narrative review based on method evaluations conducted in the laboratories of the authors as well as on relevant publications, especially comparative evaluation studies, from the literature. Publications considered here have been collected by the authors over the past 30 years of involvement as methods for HDL-C made the transition from their early use in lipid research laboratories to clinical laboratories and the recent emergence of homogeneous assays. CONTENT: The presentation includes descriptions of methodologies, including homogeneous, precipitation, electrophoresis, and ultracentrifugation assays. Reference methods and recommended approaches for assessing accuracy are described. Accuracy and imprecision are summarized in the context of the National Cholesterol Education Program (NCEP) standards for analytical performance. The effects of interfering substances and preanalytical sources of variation are presented. SUMMARY: Homogeneous assays have been shown to be reasonably well suited for use in routine clinical laboratories, generally meeting the NCEP criteria for precision, accuracy, and total error. However, discrepant results compared with the reference methods have been observed with some of the assays, and the sources of discrepancies are not well characterized. Some homogeneous reagents have not been thoroughly evaluated. At least three of the reagents have experienced successive adjustments in formulation; hence, the reagents may not yet be fully optimized. For these reasons, the homogeneous assays cannot be confidently recommended for use in long-term clinical trials and other research applications without thorough validation. |
| Evolution of NCEP guidelines: ATP1-ATPIII risk estimation for coronary heart disease in 2002. National Cholesterol Education Program Conti, C. R. (2002), Clin Cardiol 25(3): 89-90. |
| Evolution, cholesterol, and low-fat diets Baschetti, R. (1999), Circulation 99(1): 166. |
| Exaggerated blood pressure response to exercise in children with increased low-density lipoprotein cholesterol Kavey, R. E., D. A. Kveselis, et al. (1997), Am Heart J 133(2): 162-8. Abstract: Arterial vascular responses are characteristically altered with hypercholesterolemia: conduit vessels manifest increased stiffness, and conduit and resistance vessels demonstrate impaired endothelium-dependent dilation and augmented vasoconstriction to neurohumoral stimulation. These changes should be reflected in an exaggerated blood pressure increase in response to exercise. To evaluate this hypothesis, we compared the blood pressure response to treadmill exercise in children with hypercholesterolemia and children with normal lipid levels. In a preliminary retrospective study, 15 hypercholesterolemic boys 10 to 18 years old underwent treadmill exercise testing, and their blood pressure results were compared with those of 32 normolipidemic children in the same age group who had undergone treadmill exercise electively in the same time period. In the second phase, 10 hypercholesterolemic boys and 10 normolipidemic age-matched boys were evaluated prospectively according to the same protocol. Treadmill exercise involved a modified Bruce protocol with heart rate and blood pressure measured before exercise, immediately after exercise, and throughout recovery. Office blood pressures were normal in all children, with no significant difference between groups. With treadmill exercise, all subjects achieved >95% of predicted maximum heart rate and endurance times, maximum oxygen consumption, and maximum respiratory ratio did not differ between groups. Results of the retrospective and prospective groups were similar and were therefore combined. Children with increased low-density lipoprotein (LDL) cholesterol had significantly higher systolic and diastolic blood pressures immediately before treadmill exercise (systolic 120 +/- 13 mm Hg vs 113 +/- 13 mm Hg, p < 0.03; diastolic 68 +/- 8 mm Hg vs 63 +/- 9 mm Hg, p < 0.01). After exercise, blood pressures were again significantly higher in the subjects with high LDL cholesterol (systolic 182 +/- 20 mm Hg vs 160 +/- 23 mm Hg, p < 0.0003; diastolic 77 +/- 12 mm Hg vs 72 +/- 9 mm Hg, p < 0.03). At the end of recovery, systolic blood pressures remained significantly higher in subjects with high LDL cholesterol (120 +/- 9 mm Hg vs 112 +/- 12 mm Hg, p < 0.005). In this study, children with severely increased LDL cholesterol had an exaggerated blood pressure response to exercise when compared with normolipidemic control subjects. The study findings suggest that control of arterial vascular tone may already be altered in children with hypercholesterolemia. |
| Examination of the relation between periodontal health status and cardiovascular risk factors: serum total and high density lipoprotein cholesterol, C-reactive protein, and plasma fibrinogen Wu, T., M. Trevisan, et al. (2000), Am J Epidemiol 151(3): 273-82. Abstract: Using data from the Third National Health and Nutrition Examination Survey (1988-1994), the authors examined the relation between periodontal health and cardiovascular risk factors: serum total and high density lipoprotein cholesterol, C-reactive protein, and plasma fibrinogen. A total of 10,146 participants were included in the analyses of cholesterol and C-reactive protein and 4,461 in the analyses of fibrinogen. Periodontal health indicators included the gingival bleeding index, calculus index, and periodontal disease status (defined by pocket depth and attachment loss). While cholesterol and fibrinogen were analyzed as continuous variables, C-reactive protein was dichotomized into two levels. The results show a significant relation between indicators of poor periodontal status and increased C-reactive protein and fibrinogen. The association between periodontal status and total cholesterol level is much weaker. No consistent association between periodontal status and high density lipoprotein cholesterol was detectable. Similar patterns of association were observed for participants aged 17-54 years and those 55 years and older. In conclusion, this study suggests that total cholesterol, C-reactive protein, and fibrinogen are possible intermediate factors that may link periodontal disease to elevated cardiovascular risk. |
| Examination stress: changes in serum cholesterol, triglycerides and total lipids Agarwal, V., B. Gupta, et al. (1997), Indian J Physiol Pharmacol 41(4): 404-8. Abstract: Serum cholesterol, triglycerides and total lipids were estimated in twelve students exposed to varying degree of examination stress. Serum cholesterol and triglycerides exhibited a rise proportional to degree of examination stress whereas total lipids exhibited an initial rise followed by a fall. Values of all these parameters attained control level when the stress was over. The rise in serum cholesterol and triglycerides seems to be due to stress induced changes in hormonal levels and peripheral lipolysis respectively. |
| Excess body weight. An underrecognized contributor to high blood cholesterol levels in white American men Denke, M. A., C. T. Sempos, et al. (1993), Arch Intern Med 153(9): 1093-103. Abstract: BACKGROUND: The influence of body weight on serum lipids is often overlooked in clinical practice. METHODS: The association between body weight adjusted for height as calculated by body-mass index (BMI) and serum lipid and lipoprotein levels in white men was examined using the second National Health and Nutrition Examination Survey (NHANES II). Lipid results were categorized into six different levels of BMI: (1) 21.0 kg/m2 or lower, (2) 21.1 to 23.0 kg/m2, (3) 23.1 to 25.0 kg/m2, (4) 25.1 to 27.0 kg/m2, (5) 27.1 to 30.0 kg/m2, and (6) greater than 30.0 kg/m2, and three age groups: (1) young men (20 through 44 years), (2) middle-aged men (45 through 59 years), and (3) older men (60 through 74 years). RESULTS: Using linear trend analysis, changes in BMI from categories 2 to 5 in young men were associated with a total cholesterol level 0.59 mmol/L (23 mg/dL) higher (P <.01), a non-high-density lipoprotein (non-HDL) cholesterol level 0.70 mmol/L (27 mg/dL) higher (P <.01), and a low-density lipoprotein (LDL) cholesterol level 0.59 mmol/L (23 mg/dL) higher (P =.03). For middle-aged men and older men, the same change in BMI was associated with smaller but still significant differences in total cholesterol levels (higher by 0.31 mmol/L 12 mg/dL P <.01 and 0.28 mmol/L 11 mg/dL P <.01, respectively) and non-HDL cholesterol levels (higher by 0.37 mmol/L 14 mg/dL P <.01 and 0.25 mmol/L 10 mg/dL P <.01, respectively), whereas the LDL cholesterol levels were unchanged. Although advancing age may blunt the BMI-associated differences in total and LDL cholesterol levels, the BMI-associated differences in triglyceride levels (higher by 0.70 to 1.33 mmol/L 62 to 118 mg/dL P <.001) and HDL cholesterol levels (lower by 0.18 to 0.39 mmol/L 7 to 15 mg/dL P <.001) were of similar magnitude in all age groups. CONCLUSION: Excess body weight is associated with deleterious changes in the lipoprotein profile. Higher BMI was associated at all ages with higher plasma triglyceride level, lower HDL cholesterol level, and higher total and non-HDL cholesterol levels. In young men, the higher total cholesterol level was reflected mainly in the LDL cholesterol level; in middle-aged and older men, in the non-HDL fraction. Programs to reduce coronary heart disease by improving lipid levels should include more emphasis on achieving and maintaining ideal body weight. |
| Excess membrane cholesterol alters calcium movements, cytosolic calcium levels, and membrane fluidity in arterial smooth muscle cells Gleason, M. M., M. S. Medow, et al. (1991), Circ Res 69(1): 216-27. Abstract: The relations between membrane cholesterol content, basal (unstimulated) transmembrane 45Ca2+ movements, cytosolic calcium levels, and membrane fluidity were investigated in cultured rabbit aortic smooth muscle cells (SMCs) and isolated SMC plasma membrane microsomes. SMCs were enriched with unesterified (free) cholesterol (FC) for 18-24 hours with medium containing human low density lipoprotein and FC-rich phospholipid (PL) liposomes. This procedure increased cholesterol mass without affecting PL mass, resulting in an increase in the FC/PL molar ratio compared with controls in cells (67% FC increase, p less than 0.001; 43% FC/PL ratio increase, p less than 0.01) and in SMC microsomes (52% FC increase, p less than 0.05; 43% FC/PL ratio increase, p less than 0.05). Cholesterol enrichment also increased unstimulated 45Ca2+ influx (p less than 0.001) and efflux (p less than 0.05). Cellular cholesterol content correlated in a linear fashion with these changes (influx: r = 0.722, p less than 0.01; efflux: r = 0.951, p less than 0.05). In addition, cytosolic calcium levels increased approximately 34% (p less than 0.01) with cholesterol enrichment. The cholesterol-induced increase in 45Ca2+ influx was reversible with time and demonstrated sensitivity to the channel blockers. Fluorescence anisotropy measured from 5 degrees C to 40 degrees C using the fluorophore diphenylhexatriene showed decreased membrane fluidity in microsomal membranes obtained from cholesterol-enriched SMCs compared with controls (p less than 0.02). These results suggest that the SMC plasma membrane is very sensitive to cholesterol enrichment with liposomes or human low density lipoprotein and that increases in membrane cholesterol content increase cytosolic calcium levels in SMCs, are associated with a decrease in membrane fluidity, and unmask a new, or otherwise silent, dihydropyridine-sensitive calcium channel that may be involved in altered arterial wall properties with serum hypercholesterolemia. |
| Excess membrane cholesterol alters human gallbladder muscle contractility and membrane fluidity Chen, Q., J. Amaral, et al. (1999), Gastroenterology 116(3): 678-85. Abstract: BACKGROUND & AIMS: The relationship between muscle contractility, plasma membrane cholesterol, and fluidity was investigated in human gallbladders with gallstones. METHODS: Isolated gallbladder muscle cells were used to measure contraction. Plasma membranes of gallbladder muscle were purified in a sucrose gradient and measured for cholesterol content and cholesterol/phospholipid mole ratio. Membrane fluidity was determined by using fluorescence polarization and was expressed as the reciprocal of anisotropy. RESULTS: The maximal contraction induced by cholecystokinin octapeptide was significantly less in gallbladders with cholesterol stones than in those with pigment stones. The membrane cholesterol content and cholesterol/phospholipid mole ratio were significantly higher in gallbladders with cholesterol stones than in those with pigment stones. Membrane anisotropy was also higher than in gallbladders with pigment stones, reflecting lower membrane fluidity in gallbladders with cholesterol stones. After muscle cells from cholesterol stone gallbladders were incubated with cholesterol-free liposomes for 4 hours, cholecystokinin octapeptide-induced contraction, membrane cholesterol content and cholesterol/phospholipid ratio, and membrane fluidity returned to normal levels. CONCLUSIONS: Gallbladder muscle from patients with cholesterol stones has increased membrane cholesterol/phospholipid mole ratio and decreased membrane fluidity resulting in impaired muscle contractility. These abnormalities are corrected by removing the excess cholesterol from the plasma membranes. |
| Excess membrane cholesterol is not responsible for metabolic and bioenergetic changes in AS-30D hepatoma mitochondria Dietzen, D. J. and E. J. Davis (1994), Arch Biochem Biophys 309(2): 341-7. Abstract: Using mitochondria isolated from normal rat liver and AS-30D hepatoma in addition to cholesterol-enriched mitochondria, we have evaluated the ability of membrane cholesterol to induce changes in mitochondrial function, specifically, the preferential export of citrate (i.e., truncation of the Krebs cycle). Two in vitro cholesterol-enrichment procedures failed to produce mitochondria with any physiologically significant increases in free membrane cholesterol. Alternatively, male Wistar rats were maintained on a 2% cholesterol diet to elevate mitochondrial cholesterol. This treatment resulted in liver mitochondria which contained 70% of the cholesterol levels found in AS-30D hepatoma mitochondria, yet only minor metabolic and bioenergetic alterations. Subfractionation of the various mitochondrial preparations revealed that cholesterol was located primarily in outer membranes of both the cholesterol-enriched and AS-30D preparations. We therefore conclude that an increase in membrane cholesterol is not sufficient to induce "truncation" of the citric acid cycle or any other mitochondrial abnormality in tumor cells. |
| Excessive cholesterolemic response in analbuminemic rats fed a cholesterol-rich diet containing casein Zhang, X., J. A. Joles, et al. (1992), J Nutr 122(3): 520-7. Abstract: Female Nagase analbuminemic rats and Sprague-Dawley rats were fed purified diets with or without 1% cholesterol and containing either soybean protein or casein. After consuming the cholesterol-free diets, the analbuminemic rats had significantly higher plasma cholesterol and triglyceride concentrations than the Sprague-Dawley rats. The higher plasma cholesterol levels were essentially in the low density and high density lipoproteins. Based on the fact that the analbuminemic rats excreted more bile acids in feces it is possible that the higher baseline plasma cholesterol concentrations in Nagase analbuminemic rats were partly caused by overproduction of cholesterol. The Nagase analbuminemic rats displayed a greater cholesterolemic response to cholesterol feeding than Sprague-Dawley rats, but only if casein was the protein source in the diet. Casein vs. soybean protein in either cholesterol-free or high cholesterol diets reduced bile acid excretion in Sprague-Dawley but not in Nagase analbuminemic rats. The increased sensitivity to casein plus cholesterol feeding in Nagase analbuminemic rats may be caused by a lack of inhibition of de novo cholesterol synthesis. |
| Excessive salt or cholesterol intake alters the balance among endothelium-derived factors released from renal arteries in spontaneously hypertensive rats Kagota, S., A. Tamashiro, et al. (1999), J Cardiovasc Pharmacol 34(4): 533-9. Abstract: We investigated the vasorelaxation in renal arteries isolated from spontaneously hypertensive rats (SHRs) fed a basal, a high-salt, or a high-cholesterol diet for 8 weeks. In renal arterial rings from the control group, acetylcholine (ACh)-induced endothelium-dependent relaxations were markedly increased by indomethacin (IND) and ONO-3708, a prostaglandin H2/thromboxane A2-receptor antagonist, but not affected by OKY-046, a thromboxane A2 synthetase inhibitor. These increased relaxations were partially inhibited by either NG-nitro-L-arginine methyl ester (L-NAME) or charybdotoxin (CTX), and almost completely abolished by the combination of L-NAME plus CTX. The ACh-induced endothelium-dependent relaxations in the absence of IND were significantly attenuated by the high-salt intake but not affected by the high-cholesterol intake. The degrees of relaxations in the presence of IND were approximately equal among the three diet groups. On the other hand, the relaxations in the presence of IND plus L-NAME were significantly augmented by a high-cholesterol intake and abolished by a high-salt intake, and the relaxations in the presence of IND plus CTX were slightly reduced by a high-cholesterol intake and significantly augmented by a high-salt intake. The production of cyclic guanosine monophosphate (cGMP) in response to ACh was significantly decreased by a high-cholesterol intake and tended to be increased by a high-salt intake. These findings indicate that in the renal artery of SHRs, ACh causes production of a sufficient amount of nitric oxide (NO), together with a relaxing factor resembling endothelium-derived hyperpolarizing factors (EDHFs) and also endothelium-derived contracting factors (EDCFs), probably prostaglandin H2. Our results also suggest that excessive salt intake increases the release of EDCF and NO and decreases that of an EDHF-like factor, whereas excessive cholesterol intake increases release of an EDHF-like factor and decreases that of NO. |
| Exchange of free cholesterol between plasma and erythrocytes from hyperthyroid and hypothyroid rats in vitro Ruggiero, F. M., F. Cafagna, et al. (1990), Lipids 25(9): 529-33. Abstract: In our previous studies, we found that circulating thyroid hormone levels alter cholesterol partition between plasma and erythrocytes by changing the phospholipid content of erythrocytes (Ruggiero, F. M., et al. (1984) Horm. Metabol. Res. 16, 37-40; Ruggiero, F. M., et al. (1987) Lipids 22, 148-151). As an extension of this work, we now followed the exchange of free cholesterol between plasma and erythrocytes in control, hyperthyroid and hypothyroid rats under various experimental conditions in vitro. In control rats, erythrocytes incubated with plasma at 37 degrees C for 4 hr lose 10% of cholesterol which was esterified by lecithin:cholesterol acyltransferase (LCAT) present in the plasma. In hyperthyroid rats, erythrocytes incubated with plasma lose 30% of cholesterol within the same time. By contrast, in the case of hypothyroid rats incubation for 4 hr was necessary to transfer 24% of free cholesterol from plasma to erythrocytes. Inhibition of cholesterol esterification did not affect the loss of erythrocyte cholesterol in control and in hyperthyroid rats. Ca2+ increased the LCAT activity in the plasma of these rats. The findings shed light on the role of thyroid hormones in regulating cholesterol levels in plasma through active cholesterol transfer between plasma and erythrocytes. |