| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Nifedipine inhibits accumulation of low density lipoprotein and cholesterol in the aorta of normocholesterolaemic rabbits Gorog, P. and G. V. Born (1994), Drugs 48 Suppl 1: 8-10. |
| Nifedipine reduces atherogenesis in cholesterol-fed heterozygous WHHL rabbits Atkinson, J. B. and L. L. Swift (1990), Atherosclerosis 84(2-3): 195-201. Abstract: We have developed a new model to study the interaction between diet and genetics in atherogenesis, the cholesterol-fed heterozygous WHHL rabbit. To determine the effects of calcium blockers on atherosclerosis in this model, two groups of heterozygous WHHL rabbits were fed 0.25% cholesterol and 2% peanut oil with (n = 6) and without (n = 6) oral nifedipine (40 mg/kg/day) for 16 weeks. Body weights, serum cholesterol, triglycerides and calcium, and blood pressures were not significantly different between the 2 groups during the study period. Heterozygous WHHL rabbits in the nifedipine group had less aortic surface area with sudanophilic lesions (23 +/- 15% vs. 62 +/- 18%, P less than 0.01) and fewer segments of coronary arteries with lesions (19 +/- 9% vs. 35 +/- 8%, P less than 0.02). Total aortic cholesterol, phospholipid, and calcium were also reduced in nifedipine-treated rabbits compared with untreated animals. We conclude that nifedipine reduced atherosclerosis in this model. Although the mechanism is unknown, it is apparent that nifedipine acts independently of changes in plasma lipids and blood pressure. |
| Nikolaj Nikolajewitsch Anitschkow (1885-1964) established the cholesterol-fed rabbit as a model for atherosclerosis research Finking, G. and H. Hanke (1997), Atherosclerosis 135(1): 1-7. Abstract: The cholesterol-fed rabbit is a widely used model for experimental atherosclerosis research. In regard to this, one name is periodically mentioned: Nikolaj Nikolajewitsch Anitschkow. Those infrequent reminders of an important name in modern medical history do not pay an adequate tribute to basic findings concerning the pathology and pathogenesis of atherosclerosis. In contrast to research groups at that time conducting experiments with protein enriched diets, Anitschkow demonstrated, in 1913 in St. Petersburg, that it was cholesterol only that caused these atherosclerotic changes in the rabbit arterial intima, which was very similar to human atherosclerosis. By analysing the plaque's development and histology, Anitschkow was able to identify the cell types, on which modern atherosclerosis research is now focussing with a new set of immunohistochemical methods: smooth muscle cells, macrophages and lymphocytes. He noted early (fatty streaks) and advanced (atheromatous plaques) lesions and, by standardizing cholesterol feeding, he discovered that the amount of cholesterol uptake was directly proportional to the degree of atherosclerosis formation. His explanation for this observation was what modern terminology calls 'response-to-injury'. With modern immunohistochemical and molecular-biological methods, the cholesterol-fed rabbit can be used to investigate the pathophysiological aspects which also contribute to human atherosclerosis, such as lipoproteins, diabetes, mitogens, growth-factors, adhesion molecules, endothelial-function, receptor-pathways or platelets. This model can be combined with a number of other methods causing endothelial dysfunction and injury, such as balloon denudation, electric stimulation, cuff implantation, artificial hypertension, diabetes or infection. Bred strains of hereditary hypercholesterolemic rabbits or those resistant to a cholesterol-diet provide further possibilities to expand experimental designs. |
| Nilvadipine protects low-density lipoprotein cholesterol from in vivo oxidation in hypertensive patients with risk factors for atherosclerosis Inouye, M., T. Mio, et al. (2000), Eur J Clin Pharmacol 56(1): 35-41. Abstract: OBJECTIVE: Nilvadipine, a calcium antagonist, has been shown to have antioxidant activity in vitro, but its effect on in vivo oxidation has not been assessed. The aim of this study was to investigate the antioxidant effect of this agent in vivo. The ratios of 7-keto cholestadien to cholesterol are believed to be an available marker of lipid peroxidation. Using these ratios, we have assessed the antioxidant effect of nilvadipine on low-density lipoprotein (LDL) in hypertensive patients with high risk of atherosclerosis. The risk factors of atherosclerosis may involve oxidation of LDL. METHODS: Fifteen healthy subjects (seven females and eight males aged 35-72 years, mean +/- SD = 55.3 +/-13.8 years) and fifteen hypertensive patients (seven females and eight males aged 45-80 years, mean +/- SD = 60.2 +/- 11.8 years) were recruited. Patients were treated orally with nilvadipine (4 mg b.i.d.) for 4 weeks. Cholesterol oxidation levels of LDL in patients before and after nilvadipine therapy and healthy subjects were studied. RESULTS: The ratios of 7-keto cholestadien to cholesterol in LDL of hypertensive patients before and 4 weeks after nilvadipine treatment and in healthy subjects were 6.5 +/- 1.6% (mean +/- SD), 3.8 +/- 1.2%, and 0.2 +/- 0.1%, respectively. There were significantly (P < 0.001) increased levels of cholesterol oxidation in LDL in patients with hypertension both before and after nilvadipine treatment compared with healthy subjects. However, there was a significantly (P < 0.001) decreased level of cholesterol oxidation in LDL in patients after nilvadipine treatment compared with patients before nilvadipine treatment. CONCLUSION: Our data showed that nilvadipine may protect LDL cholesterol from in vivo oxidation in hypertensive patients with high risk of atherosclerosis. |
| Nitric oxide donor molsidomine favors features of atherosclerotic plaque stability during cholesterol lowering in rabbits De Meyer, G. R., M. M. Kockx, et al. (2003), J Cardiovasc Pharmacol 41(6): 970-8. Abstract: Rupture-prone atherosclerotic plaques are characterized by a thin fibrous cap containing numerous macrophage-derived foam cells and few smooth muscle cells (SMC). Decreasing the ratio between macrophages and SMC might favor plaque stabilization. Macrophages expressing inducible nitric oxide (NO) synthase become hypersensitive to killing by exogenous NO donors. Therefore, we investigated in cholesterol-fed rabbits (20 weeks 0.3% cholesterol) the effect of 4 weeks cholesterol withdrawal alone and in combination with the NO donor molsidomine on plaque size, cell composition, superoxide production and extracellular superoxide dismutase (ecSOD) mRNA expression in the atherosclerotic plaques in the aorta. Cholesterol withdrawal alone did not alter atherosclerotic plaque size, the increased superoxide production or the decreased ecSOD mRNA, but led to the formation of a thin subendothelial macrophage-free layer and reduced both vascular cell adhesion molecule-1 expression and cell replication in the luminal part of the plaques. Treatment with molsidomine (1 mg/kg/day) during cholesterol withdrawal did not affect plaque size but increased the thickness of the subendothelial macrophage-free layer consisting of SMC, and normalized both superoxide production and ecSOD mRNA expression. The latter findings demonstrate that molsidomine, when combined with cholesterol lowering, decreases signs of oxidative stress and increases features of stable atherosclerotic plaques. |
| Nitric oxide inhibition of free radical-mediated cholesterol peroxidation in liposomal membranes Korytowski, W., M. Zareba, et al. (2000), Biochemistry 39(23): 6918-28. Abstract: The ability of nitric oxide ((*)NO) to inhibit propagative lipid peroxidation was investigated using unilamellar liposomes (LUVs) constituted with egg phosphatidylcholine (PC) or 1-palmitoyl-2-oleoylphosphatidylcholine (POPC), (14)Ccholesterol (Ch), and a nonregenerable singlet oxygen-derived primer, 5alpha-hydroperoxycholesterol (5alpha-OOH). Exposing LUVs to ascorbate and a lipophilic iron chelate at 37 degrees C resulted in an exponential decay of 5alpha-OOH and accumulation of free radical-derived 7alpha- and 7beta-hydroperoxycholesterol (7alphabeta-OOH), as detected by high-performance liquid chromatography with electrochemical detection. Thiobarbituric acid-reactive species (TBARS) were generated concurrently in egg PC-containing LUVs. Including the (*)NO donor spermine NONOate (SPNO, 5-50 microM) or S-nitroso-N-acetyl-D,L-penicillamine (SNAP, 50-100 microM) in the reaction mixture had no effect on 5alpha-OOH decay (suggesting that iron was not redox-inhibited) but slowed TBARS and 7alphabeta-OOH accumulation in a strongly dose-dependent fashion. Decomposed SPNO or SNAP had no such effects, implying that (*)NO was the responsible agent. Accumulation of several (14)CCh oxidation products, detected by high-performance thin-layer chromatography with phosphorimaging, was similarly diminished by active SPNO or SNAP. Concomitantly, a new band referred to as RCh.4 appeared, the radioactivity of which increased as a function of incubation time and (*)NO donor concentration. RCh.4 material was also generated via direct iron/ascorbate reduction of 7alpha-OOH in the presence of (*)NO, consistent with 7alpha-nitrite (7alpha-ONO) identity. However, various other lines of evidence suggest that RCh.4 is not 7alpha-ONO, but rather 5alpha-hydroxycholesterol (5alpha-OH) generated by reduction of 5alpha-ONO arising from 7alpha-ONO rearrangement. 5alpha-OH was only detected when (*)NO was present in the reaction system, thus providing indirect evidence for the existence of nitrosated Ch intermediates arising from (*)NO chain-breaking activity. |
| Nitric oxide synthase gene therapy rapidly reduces adhesion molecule expression and inflammatory cell infiltration in carotid arteries of cholesterol-fed rabbits Qian, H., V. Neplioueva, et al. (1999), Circulation 99(23): 2979-82. Abstract: BACKGROUND: Hypercholesterolemia reduces nitric oxide bioavailability, manifested by reduced endothelium-dependent vascular relaxation, and also induces vascular adhesion molecule expression and inflammatory cell infiltration. We have previously shown that gene therapy with NO synthase in hypercholesterolemic rabbits substantially reverses the deficit in vascular relaxation. In the present study, we show that NO synthase gene therapy rapidly and substantially reduces vascular adhesion molecule expression, lipid deposition, and inflammatory cell infiltration. METHODS AND RESULTS: Thirty male New Zealand White rabbits were maintained on a 1% cholesterol diet for 11 to 13 weeks, then underwent carotid artery gene transfer with Ad.nNOS or Ad.betaGal (recombinant adenoviruses expressing neuronal NO synthase or beta-galactosidase, respectively), or received medium alone in a sham procedure. Arteries were harvested at 1 and 3 days after gene transfer, and the following parameters were determined by immunohistochemical and image-analysis techniques: intercellular adhesion molecule-1, vascular cell adhesion molecule-1, lipid deposition by oil red O staining, lymphocyte infiltration (CD43-positive cells), and monocyte infiltration (RAM-11-positive cells). In Ad.nNOS-treated arteries, all markers were significantly decreased relative to Ad. betaGal or sham-treated arteries within 3 days after gene transfer. Ad.nNOS had a particularly striking impact on monocyte infiltration; as early as 24 hours after gene transfer, Ad.nNOS-treated arteries had >3-fold fewer monocytes than Ad.betaGal- or sham-treated arteries. CONCLUSIONS: NO synthase gene therapy rapidly ameliorates several markers of atherosclerosis in the cholesterol-fed rabbit. |
| Nitric oxide, cholesterol oxides and endothelium-dependent vasodilation in plasma of patients with essential hypertension Moriel, P., A. Sevanian, et al. (2002), Braz J Med Biol Res 35(11): 1301-9. Abstract: The objective of the present study was to identify disturbances of nitric oxide radical (NO) metabolism and the formation of cholesterol oxidation products in human essential hypertension. The concentrations of.NO derivatives (nitrite, nitrate, S-nitrosothiols and nitrotyrosine), water and lipid-soluble antioxidants and cholesterol oxides were measured in plasma of 11 patients with mild essential hypertension (H: 57.8 +/- 9.7 years; blood pressure, 148.3 +/- 24.8/90.8 +/- 10.2 mmHg) and in 11 healthy subjects (N: 48.4 +/- 7.0 years; blood pressure, 119.4 +/- 9.4/75.0 +/- 8.0 mmHg). Nitrite, nitrate and S-nitrosothiols were measured by chemiluminescence and nitrotyrosine was determined by ELISA. Antioxidants were determined by reverse-phase HPLC and cholesterol oxides by gas chromatography. Hypertensive patients had reduced endothelium-dependent vasodilation in response to reactive hyperemia (H: 9.3 and N: 15.1% increase of diameter 90 s after hyperemia), and lower levels of ascorbate (H: 29.2 +/- 26.0, N: 54.2 +/- 24.9 micro M), urate (H: 108.5 +/- 18.9, N: 156.4 +/- 26.3 micro M), beta-carotene (H: 1.1 +/- 0.8, N: 2.5 +/- 1.2 nmol/mg cholesterol), and lycopene (H: 0.4 +/- 0.2, N: 0.7 +/- 0.2 nmol/mg cholesterol), in plasma, compared to normotensive subjects. The content of 7-ketocholesterol, 5alpha-cholestane-3beta,5,6beta-triol and 5,6alpha-epoxy-5alpha-cholestan-3alpha-ol in LDL, and the concentration of endothelin-1 (H: 0.9 +/- 0.2, N: 0.7 +/- 0.1 ng/ml) in plasma were increased in hypertensive patients. No differences were found for.NO derivatives between groups. These data suggest that an increase in cholesterol oxidation is associated with endothelium dysfunction in essential hypertension and oxidative stress, although.NO metabolite levels in plasma are not modified in the presence of elevated cholesterol oxides. |
| Nitrogen-bisphosphonates block retinoblastoma phosphorylation and cell growth by inhibiting the cholesterol biosynthetic pathway in a keratinocyte model for esophageal irritation Reszka, A. A., J. Halasy-Nagy, et al. (2001), Mol Pharmacol 59(2): 193-202. Abstract: The surprising discovery that nitrogen-containing bisphosphonates (N-BPs) act via inhibition of the mevalonate-to-cholesterol pathway raised the possibility that esophageal irritation by N-BPs is mechanism-based. We used normal human epidermal keratinocytes (NHEKs) to model N-BP effects on stratified squamous epithelium of the esophagus. The N-BPs alendronate and risedronate inhibited NHEK growth in a dose-dependent manner without inducing apoptosis. N-BPs (30 microM) caused accumulation of cells in S phase and increased binucleation (inhibited cytokinesis). Consistent with N-BP inhibition of isoprenylation, geranylgeraniol or farnesol prevented accumulation in S phase. Binucleation was also induced by the 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor lovastatin and by the squalene synthase inhibitor zaragozic acid A and was prevented by adding low-density lipoprotein. At 300 microM, N-BPs reduced expression of cyclin-dependent kinase (cdk) 2 and cdk4 and enhanced expression of p21(waf1) and p27(kip1) and their binding to cdks with corollary hypophosphorylation of retinoblastoma. Lovastatin and zaragozic acid A produced similar effects, except that p21(waf1) expression and binding to cdks was not induced. Growth inhibition, but not binucleation, was also caused by the geranylgeranyl transferase I inhibitor, GGTI-298, which also enhanced cdk2 and cdk4 association with p27(kip1). These findings are consistent with suppression of epithelial cell growth by N-BPs via inhibition of the mevalonate pathway and the consequent reduction in cholesterol synthesis, which blocks cytokinesis, and in geranylgeranylation, which interferes with progression through the cell cycle. |
| N-Myristoylethanolamine-cholesterol (1:1) complex: first evidence from differential scanning calorimetry, fast-atom-bombardment mass spectrometry and computational modelling Ramakrishnan, M., R. Kenoth, et al. (2002), FEBS Lett 531(2): 343-7. Abstract: The interaction of N-myristoylethanolamine (NMEA) with cholesterol is investigated by differential scanning calorimetry (DSC), fast-atom-bombardment mass spectrometry (FAB-MS) and computational modelling. Addition of cholesterol to NMEA leads to a new phase transition at 55 degrees C besides the chain-melting transition of NMEA at 72.5 degrees C. The enthalpy of the new transition increases with cholesterol content up to 50 mol%, but decreases thereafter, vanishing at 80 mol%. The enthalpy of the chain-melting transition of NMEA decreases with an increase in cholesterol; the transition disappears at 50 mol%. FAB-MS spectra of mixtures of NMEA and cholesterol provide clear signatures of the formation of (NMEA+cholesterol+) (NMEA+cholesterol+Na+). These results are consistent with the formation of a 1:1 complex between NMEA and cholesterol. Molecular modelling studies support this experimental finding and provide a plausible structural model for the complex, which highlights multiple H-bond interactions between the hydroxy group of cholesterol and the hydroxy and carbonyl groups of NMEA besides appreciable dispersion interaction between the hydrocarbon domains of the two molecules. |
| NO activity in familial combined hyperlipidemia: potential role of cholesterol remnants Stroes, E., T. de Bruin, et al. (1997), Cardiovasc Res 36(3): 445-52. Abstract: OBJECTIVE: Patients with familial combined hyperlipidemia (FCH) have an increased cardiovascular mortality despite only moderate elevations of LDL-cholesterol. Since endothelial NO release is intimately involved in the anti-atherosclerotic effects of the endothelium, we studied the effect of short-term lipid-lowering therapy on NO-mediated vasodilatation in patients with FCH. In view of only moderate LDL elevations, we evaluated whether alterations in other lipid fractions upon therapy correlated to changes in NO-mediated vasodilatation. METHODS: NO activity was assessed by serotonin-induced, nitric oxide-mediated increase in forearm blood flow (FBF). Measurements were performed 2 weeks off and 4 weeks on lipid-lowering therapy in 12 FCH patients using forearm venous occlusion plethysmography. Control experiments were performed in 12 healthy subjects. RESULTS: Serotonin-induced vasodilatation was impaired in FCH patients (FBF (unit ml/100 ml forearm tissue/min) from 3.0 (0.3) to 4.8 (0.4)) compared to controls (FBF from 2.9 (0.3) to 6.5 (0.6); p < 0.05 vs. FCH). FBF response to serotonin improved significantly upon lipid-lowering therapy (from 3.0 (0.3) to 5.7 (0.5); p < 0.05 treated vs. untreated). The level of improvement in endothelial function was significantly correlated to the absolute reduction of intermediate density lipoproteins upon lipid-lowering therapy (r = -0.64; p < 0.05), whereas it did not correlate to changes in VLDL- or LDL-cholesterol, nor to Lp(a). CONCLUSION: Patients with familial combined hyperlipidemia have impaired NO-mediated vasodilatation, that responds rapidly to lipid lowering medication, and may be related to changes in intermediate density lipoproteins. |
| No association between serum cholesterol and growth in preadolescent American children Lilienfeld, D. E., M. Jacobson, et al. (1992), Am J Prev Med 8(2): 96-9. Abstract: To determine the relation between serum cholesterol level (SCL) and growth in preadolescent children (2-12 years of age) in the United States, we examined the association of SCL and three measures of growth in a national sample of American children from 1971 to 1974. We investigated three parameters: sitting height, standing height, and weight and undertook separate analyses for sex and race. We found no consistent statistically significant associations with any of these three measures of growth. This result did not change when we adjusted the data for age alone or for age, poverty index, serum protein level, and hematocrit. We conclude that growth in this population group is not dependent on SCL. |
| No cholesterol metabolism anomalies detectable in infants with hypertrophic pyloric stenosis Hennekam, R. C., H. R. Waterham, et al. (2001), Am J Med Genet 99(3): 256-7. |
| No correlation of serum cholesterol levels with measures of violence in patients with schizophrenia and non-psychotic disorders Steinert, T., M. Woelfle, et al. (1999), Eur Psychiatry 14(6): 346-8. Abstract: Epidemiological studies, animal studies, and clinical studies yielded conflicting results concerning a supposed association between increased risk for suicide and violence, and low serum cholesterol levels. Until now, no data has been available for patients with schizophrenia, a disorder with a well-known increased risk of violence. Correlations of serum cholesterol levels at admission and measures of violence were investigated in 103 consecutively admitted patients (44 males, 59 females) of a general psychiatric admission unit. Seventy subjects were diagnosed as suffering from schizophrenia or schizoaffective disorder (ICD-10 F 20, F25), and 33 were diagnosed as suffering from non-psychotic disorders (mainly personality disorders). The level of total exhibited violence during the inpatient treatment period was measured in each patient by the Modified Overt Aggression Scale (MOAS), the Social Dysfunction and Aggression Scale (SDAS), the Staff Observation Aggression Scale (SOAS), and the Violence Scale (VS). Correlations of all violence measures were high (0.75-0.90), but no correlation was found with cholesterol levels, neither for psychotic nor for non-psychotic subjects, neither for men nor for women. The hypothesis of associations of violence and cholesterol levels is not supported by the data. |
| No difference in body weight decrease between a low-glycemic-index and a high-glycemic-index diet but reduced LDL cholesterol after 10-wk ad libitum intake of the low-glycemic-index diet Sloth, B., I. Krog-Mikkelsen, et al. (2004), Am J Clin Nutr 80(2): 337-47. Abstract: BACKGROUND: The role of glycemic index (GI) in appetite and body-weight regulation is still not clear. OBJECTIVE: The objective of the study was to investigate the long-term effects of a low-fat, high-carbohydrate diet with either low glycemic index (LGI) or high glycemic index (HGI) on ad libitum energy intake, body weight, and composition, as well as on risk factors for type 2 diabetes and ischemic heart disease in overweight healthy subjects. DESIGN: The study was a 10-wk parallel, randomized, intervention trial with 2 matched groups. The LGI or HGI test foods, given as replacements for the subjects' usual carbohydrate-rich foods, were equal in total energy, energy density, dietary fiber, and macronutrient composition. Subjects were 45 (LGI diet: n = 23; HGI diet: n = 22) healthy overweight body mass index (in kg/m(2)): 27.6 +/- 0.2 women aged 20-40 y. RESULTS: Energy intake, mean (+/- SEM) body weight (LGI diet: -1.9 +/- 0.5 kg; HGI diet: -1.3 +/- 0.3 kg), and fat mass (LGI diet: -1.0 +/- 0.4 kg; HGI diet: -0.4 +/- 0.3 kg) decreased over time, but the differences between groups were not significant. No significant differences were observed between groups in fasting serum insulin, homeostasis model assessment for relative insulin resistance, homeostasis model assessment for beta cell function, triacylglycerol, nonesterified fatty acids, or HDL cholesterol. However, a 10% decrease in LDL cholesterol (P < 0.05) and a tendency to a larger decrease in total cholesterol (P = 0.06) were observed with consumption of the LGI diet as compared with the HGI diet. CONCLUSIONS: This study does not support the contention that low-fat LGI diets are more beneficial than HGI diets with regard to appetite or body-weight regulation as evaluated over 10 wk. However, it confirms previous findings of a beneficial effect of LGI diets on risk factors for ischemic heart disease. |
| No evidence for an association between serum cholesterol and the course of depression and suicidality Deisenhammer, E. A., K. Kramer-Reinstadler, et al. (2004), Psychiatry Res 121(3): 253-61. Abstract: In a number of previous reports, an association of altered, in most cases lower, serum cholesterol levels with depression, suicidal ideation and current or past suicidal behavior has been suggested. In this investigation, the course of serum cholesterol concentrations was measured in depressed patients during treatment. Ninety-two inpatients with a major depressive episode were included. Serum lipid concentrations were assessed at admission, after 1 week and after 4 weeks of antidepressant treatment. Degrees of depression and suicidality were measured with the Hamilton Depression Rating Scale. Although there was a significant reduction in depression and suicidality scores, neither a significant change in serum cholesterol levels nor a correlation between cholesterol levels and clinical improvement was found. Further, there were no significant differences in lipid levels between patients with and without a history of attempted suicide. In patients who had used a violent method, there was a trend for lower total cholesterol levels compared to those who had poisoned themselves. The results of this study do not support the hypothesis of an association of serum cholesterol with the course of depression and suicidal ideation. Cholesterol levels do not appear to be an appropriate biological marker for suicidality during the first 4 weeks of treatment in patients with a major depressive episode. |
| No pathophysiologic relationship of soluble biliary proteins to cholesterol crystallization in human bile Wang, D. Q., D. E. Cohen, et al. (1999), J Lipid Res 40(3): 415-25. Abstract: This study explores the pathophysiologic effects of soluble biliary glycoproteins in comparison to mucin gel and cholesterol content on microscopic crystal and liquid crystal detection times as well as crystallization sequences in lithogenic human biles incubated at 37 degrees C. Gallbladder biles from 13 cholesterol gallstone patients were ultracentrifuged and microfiltered (samples I). Total biliary lipids were extracted from portions of samples I, and reconstituted with 0.15 m NaCl (pH 7.0) (samples II). Portions of samples II were supplemented with purified concanavalin A-binding biliary glycoproteins (final concentration = 1 mg/mL) (samples III), or mucin gel (samples IV), respectively, isolated from the same cholesterol gallstone biles. Samples V consisted of extracted biliary lipids from uncentrifuged and unfiltered bile samples reconstituted with 0.15 m NaCl (pH 7.0). Analytic lipid compositions of samples I through IV were identical for individual biles but, as anticipated, samples V displayed significantly higher cholesterol saturation indexes. Detection times of cholesterol crystals and liquid crystals were accelerated in the rank order of samples: IV > V > I = II = III, indicating that total soluble biliary glycoproteins in pathophysiologic concentration had no appreciable effect. Crystallization sequences (D. Q-H. Wang and M. C. Carey. J. Lipid Res. 1996. 37: 606-630; and 2539-2549) were similar among samples I through V. Crystal detection times and numbers of solid cholesterol crystals were accelerated in proportion to added mucin gel and the cholesterol saturation of bile only.For pathophysiologically relevant conditions, our results clarify that mucin gel and cholesterol content, but not soluble biliary glycoproteins, promote cholesterol crystallization in human gallbladder bile. |
| Nocturnal eating and serum cholesterol of three-shift workers Lennernas, M., T. Akerstedt, et al. (1994), Scand J Work Environ Health 20(6): 401-6. Abstract: OBJECTIVES--The goal of this study was to examine the effect of rotating three-shift work on the circadian distribution of dietary intake and to investigate the relationships between displaced eating and nutritional status variables blood lipids, blood glucose, body mass index (BMI). METHODS--Dietary data were collected by 147 replicate 24-h dietary recalls from 22 male industrial workers in rotating three-shift work. The intakes of energy and nutrients were estimated by the use of a nutrient data base. The BMI was calculated, and blood glucose, serum triglycerides, high-density lipoprotein (HDL) cholesterol and low-density lipoprotein (LDL) cholesterol were measured once. RESULTS--The dietary intakes of energy, protein, total fat, saturated fat, total carbohydrates, sucrose, and dietary fiber did not differ between 24-h periods but did differ between work shifts and were lowest during the night. Correlation analyses between dietary intakes and nutritional status parameters showed that those who redistributed their eating most to the night shift had higher levels of serum total cholesterol and LDL and a higher LDL:HDL ratio; 63% of the LDL cholesterol level was explained by carbohydrate intake during night shifts. In contrast, the total intake for whole 24-h periods or across entire shift cycles was not related to serum variables or BMI. CONCLUSIONS--Dietary intake is lower during night shifts (34-37% of 24-h intake of various nutrients) than during morning shifts (43-47%) and afternoon shifts (47-59%). The redistribution of food intake to the night may be associated with metabolic disturbances in lipid metabolism. |
| Nonalcoholic components in wine reduce low density lipoprotein cholesterol in normocholesterolemic rats Cascon, E., R. Roig, et al. (2001), Lipids 36(4): 383-8. Abstract: Using an experimental model that enables the effects of alcohol to be distinguished from the effects of the nonalcoholic components present in wine, we determined whether wine has effects other than those of alcohol on the metabolism of cholesterol. Male rats were fed a standard diet and had free access to water and either wine or an equivalent alcohol solution for 45 d or 6 mon. Alcohol intake was similar in the two groups of animals. Consumption of the alcohol solution or wine did not influence plasma cholesterol or high density lipoprotein-cholesterol. At 45 d, the consumption both of wine and of alcohol solution reduced low density lipoprotein (LDL)-cholesterol and very low density lipoprotein cholesterol. At 6 mon, only the rats that consumed wine had reduced LDL-cholesterol. After 45 d of consuming alcohol solution, total cholesterol in the aorta was significantly increased mainly as a result of the rise in free cholesterol. In the aorta, the effect of wine consumption was similar to the effect of alcohol solution consumption, although it was less intense. The only clear effect that could be ascribed to the nonalcoholic components in wine was that the LDL-cholesterol was reduced in the long term, although aortic cholesterol was not. |
| Noncalibration as a source of precision in cholesterol testing? Giavarina, D., L. Targa, et al. (1991), Arch Pathol Lab Med 115(9): 861. |