| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
| First Page | Previous Page | Next Page | Last Page |
| Effects of family-oriented risk-based prevention on serum cholesterol and blood pressure values of children and adolescents Salminen, M., T. Vahlberg, et al. (2005), Scand J Prim Health Care 23(1): 34-41. Abstract: OBJECTIVE: To describe the effects of family-oriented prevention on total and LDL cholesterol and blood pressure of children. DESIGN: A controlled intervention study. SETTING: Family-oriented prevention of risk factors of coronary heart disease (CHD) in Eastern Finland. The programme consisted of two counselling meetings at children's schools, and three at children's homes. SUBJECTS: In total 388 in the intervention group (IG) with a family history of cardiovascular diseases (CVDs), and 470 in control groups: 151 in control group I (CI) with a family history of CVDs, and 319 in control group II (CII) with no family history. MAIN OUTCOME MEASURES: Serum mean total and LDL cholesterol, and blood pressure. RESULTS: Among the youngest (6-9 years) girls, changes in total (-0.3 vs. +0.2 mmol/l) and LDL cholesterol (-0.3 vs. +0.0 mmol/l) were more favourable in IG than in CI. Diastolic blood pressure increased less among the youngest boys in IG (+3 mm Hg) than among those in CI (+11 mm Hg) or CII (+10 mm Hg). CONCLUSION: Family-oriented health counselling had favourable effects on total and LDL cholesterol among girls aged 6-9 years, and on the development of diastolic blood pressure among boys aged 6-9 years. |
| Effects of fibrillar C-terminal fragment of cleaved alpha1-antitrypsin on cholesterol homeostasis in HepG2 cells Janciauskiene, S. and S. Lindgren (1999), Hepatology 29(2): 434-42. Abstract: Amyloid fibrils of diverse origin are known to disturb vital cellular functions and induce cell death. In this study, the effects of amyloid fibrils from the C-terminal fragment (C-36) of cleaved alpha1-antitrypsin (AAT) on low-density lipoprotein (LDL) metabolism were investigated in HepG2 cells. Treatment of the cells with C-36 fibrils (10 micromol/L) enhanced 125I-LDL binding and uptake 10 to 15 times, and highly up-regulated levels of LDL receptor mRNA, as compared with control cells. Competition experiments using excess of unlabeled LDL and blockage experiments with a monoclonal LDL receptor antibody diminished or completely abolished the stimulatory effects of fibrils on LDL binding and LDL receptor mRNA levels, suggesting that fibrils act via the LDL receptor pathway. However, C-36 fibrils had no significant effect on 2-14Cacetate incorporation into cholesterol biosynthesis and cholesterol ester formation, but inhibited 125I-LDL degradation by 20% and reduced bile acid biosynthesis up to 48% in a dose-dependent manner. Preincubation of the cells with fibrils before the addition of LDL totally abolished the LDL inhibitory effect on unesterified cholesterol synthesis, further confirming the LDL receptors to be the target for C-36 fibrils. Moreover, the expression of sterol regulatory element binding protein-1 (SREBP-1) was found to increase twofold and more after 24 hours of incubation of the cells with several concentrations of C-36 fibrils. Our study suggests that the cytotoxicity of C-36 fibrils on HepG2 cells is associated with perturbed intracellular cholesterol homeostasis, induced through fibril-stimulated expression of the LDL receptors via the sterol-responsive element. |
| Effects of fish oil supplementation on the changes in myocardial cyclic adenosine monophosphate, inositol 1,4,5-triphosphate and mitochondrial calcium levels during acute coronary occlusion-reperfusion in cholesterol-fed rabbits Chen, M. F., H. C. Hsu, et al. (1994), Int J Cardiol 46(1): 23-31. Abstract: We studied the changes in myocardial second messengers and mitochondrial calcium levels during acute coronary occlusion-reperfusion in New Zealand white male rabbits fed a high cholesterol diet with or without fish oil supplementation. Group I, control rabbits, were fed a standard laboratory rabbit chow. In addition to the standard chow, Group II rabbits received a 1% cholesterol-enriched diet for 2 weeks, while Group III rabbits were fed a 1% cholesterol and 10% fish oil supplemented diet for 2 weeks. Acute coronary occlusion for 10 min or 1 h was induced by ligating the marginal branch of the left circumflex coronary artery. The vessel was then reperfused for 1 or 4 h in short- and long-term ischemia studies respectively. In the short-term ischemia study, myocardial samples taken from the cholesterol-fed rabbits had the highest cyclic adenosine monophosphate, inositol 1,4,5-triphosphate and mitochondrial calcium levels among the normal (nonischemic) and the ischemic areas of the three groups. The cholesterol and fish oil treated rabbits significantly suppressed the elevation of cyclic adenosine monophosphate (P < 0.05 compared with the cholesterol-fed rabbits in normal and ischemic areas respectively), but did not significantly attenuate the elevation of inositol 1,4,5-triphosphate and calcium levels. In the long-term ischemia study, the cholesterol-fed rabbits had the highest levels of these three messengers among the normal areas. However, only inositol 1,4,5-triphosphate level reached statistical significance (P < 0.05 compared with control). This group of rabbits had the lowest level of cyclic adenosine monophosphate, but the highest inositol 1,4,5-triphosphate and calcium levels among the ischemic areas.(ABSTRACT TRUNCATED AT 250 WORDS) |
| Effects of fluvastatin and its major metabolites on low-density lipoprotein oxidation and cholesterol esterification in macrophages Tanaka, K., M. Yasuhara, et al. (2001), Jpn J Pharmacol 86(3): 289-96. Abstract: We investigated effects of fluvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, and its major metabolites, M2 and M4, on CuSO4-induced low-density lipoprotein (LDL) oxidation and cholesteryl ester accumulation in mouse peritoneal macrophages. All the test compounds inhibited LDL oxidation, and M2 had the most potent effect comparable to vitamin E. When LDL was previously incubated with the test compounds in the presence of CuSO4, the pre-treatment resulted in a marked reduction of facilitated cholesteryl ester accumulation in macrophages. Supplementation of mevalonate did not overcome the inhibitory effects of fluvastatin and its metabolites on both LDL oxidation and facilitated cholesterol esterification. Pravastatin, another HMG-CoA reductase inhibitor, did not show any inhibitory effect. Consequently, these effects of fluvastatin and its metabolites are considered to be derived from their own unique chemical structures. Moreover, fluvastatin and M2 directly inhibited cholesterol esterification induced by oxidized LDL in macrophages, but pravastatin was also found to have a weak effect. As their inhibitory effects were overcome by addition of mevalonate, the direct inhibitory effect on cholesterol esterification would be a common property of HMG-CoA reductase inhibitors. The inhibitory effects of fluvastatin and its metabolites on both LDL oxidation and cholesterol esterification in macrophages may contribute to the antiatherogenic action in vivo. |
| Effects of fluvastatin in type 2 diabetic patients with hyperlipidemia: reduction in cholesterol oxidation products and VCAM-1 Guan, J. Z., H. Murakami, et al. (2004), J Atheroscler Thromb 11(2): 56-61. Abstract: The purpose of this study was to investigate the lipid-lowering and anti-oxidative effects of fluvastatin, a 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor, in type 2 diabetic patients. Six patients (3 men and 3 women, mean age = 56.2) took 20 mg of fluvastatin once daily (at night) for 12 weeks. Several markers of oxidative stress were then measured in these patients including plasma cholesterol oxidation products, i.e. oxysterols, and the levels of circulating adhesion molecules. Plasma total cholesterol levels were reduced by 12.3% in these individuals after 4 weeks of treatment, with levels remaining below 220 mg/dl for the entire treatment period. LDL levels were significantly reduced at 4 (18.1%) and 12 weeks (16.1%), and triglyceride levels were significantly reduced after 8 (22.5%) and 12 (37.7%) weeks of treatment. HDL-C levels increased from 50.7 +/- 15.4 prior to treatment to 63.8 +/- 24.3 mg/dl after 12 weeks of treatment, though this increase was not statistically significant. Lipid hydroperoxide, thiobarbituric acid-reactive substance (TBARS), and oxysterol levels were also reduced, suggesting that fluvastatin also had anti-oxidative effects. Finally, VCAM-1 levels were similarly reduced by fluvastatin treatment. We conclude that fluvastatin safely improves the plasma lipid profile in type 2 diabetic patients with hyperlipidemia. We speculate that this drug might be doubly effective in reducing atherosclerosis and cardiac events in these patients as a result of its demonstrated anti-oxidative effects and its ability to reduce VCAM-1 levels. |
| Effects of fluvastatin on coronary atherosclerosis in patients with mild to moderate cholesterol elevations (Lipoprotein and Coronary Atherosclerosis Study LCAS) Herd, J. A., C. M. Ballantyne, et al. (1997), Am J Cardiol 80(3): 278-86. Abstract: Despite the potential for reduced morbidity and mortality, aggressive intervention against mild to moderate hypercholesterolemia in patients with coronary heart disease (CHD) remains controversial and infrequently practiced. Eligible patients in the 2.5-year Lipoprotein and Coronary Atherosclerosis Study were men and women aged 35 to 75 years with angiographic CHD and mean low-density lipoprotein (LDL) cholesterol of 115 to 190 mg/dl despite diet. Patients (n = 429; 19% women) were randomized to fluvastatin 20 mg twice daily or placebo. One fourth of patients were also assigned open-label adjunctive cholestyramine up to 12 g/day because prerandomization LDL cholesterol remained > or = 160 mg/dl. The primary end point, assessed by quantitative coronary angiography, was within-patient per-lesion change in minimum lumen diameter (MLD) of qualifying lesions. Across 2.5 years, mean LDL cholesterol was reduced by 23.9% in all fluvastatin patients (+/- cholestyramine) (146 to 111 mg/dl) and by 22.5% in the fluvastatin only subgroup (137 to 106 mg/dl). Primary end point analysis (340 patients) showed significantly less lesion progression in all fluvastatin versus all placebo patients, deltaMLD -0.028 versus -0.100 mm (p <0.01), and for fluvastatin alone versus placebo alone, deltaMLD -0.024 versus -0.094 mm (p <0.02). A consistent angiographic benefit with treatment was seen whether baseline LDL cholesterol was above or below 160 or 130 mg/dl. Beneficial trends with treatment were also consistently seen in clinical event rates but were not statistically significant. Thus, lipid lowering by fluvastatin in patients with mildly to moderately elevated LDL cholesterol significantly slowed CHD progression. |
| Effects of fluvastatin, a new inhibitor of HMG-CoA reductase, and niceritrol on serum lipids, lipoproteins and cholesterol ester transfer activity in primary hypercholesterolemic patients Sasaki, J., K. Yamamoto, et al. (1995), Int J Clin Pharmacol Ther 33(7): 420-6. Abstract: Effects of a combination therapy of fluvastatin, a new inhibitor of HMG-CoA reductase, and niceritrol on lipid metabolism were investigated measuring a wide range of parameters in 42 patients with primary hypercholesterolemia. After a wash-out period patients were randomly allocated to 1 of the 2 groups, the fluvastatin-preceding group (G-1) and the niceritrol-preceding group (G-2). In G-1 fluvastatin monotherapy (30 mg/day) significantly decreased total cholesterol (TC) and LDL-cholesterol (LDL-C). There was no significant change in HDL-cholesterol (HDL-C), triglyceride (TG) and lipoprotein (a) (Lp(a)). Further effect in HDL-C and TG was observed after the addition of niceritrol (750 mg/day). On the other hand, in G-2, while niceritrol alone (750 mg/day) produced no significant change in TC, LDL-C, HDL-C, TG and Lp(a), the addition of fluvastatin (30 mg/day) reduced TC and LDL-C levels significantly. Cholesterol ester transfer (CET) activity was significantly reduced by niceritrol monotherapy. After the concomitant use of the 2 drugs CET activity was significantly reduced only in G-2. No significant change in lipoprotein lipase and hepatic triglyceride lipase activities were observed in the 2 groups at either point in time. No serious adverse effect was observed in this study. It is concluded that fluvastatin is an effective drug for lowering LDL-cholesterol and causes no adverse alteration in lipid metabolism. Combination with niceritrol at a dose of 750 mg/day dose not appear to augment or attenuate beneficial effects of fluvastatin. |
| Effects of four days of regular, moderate consumption of ethanol on high-density lipoprotein cholesterol concentrations in plasma Howes, L. G., H. Krum, et al. (1990), Clin Chem 36(9): 1692. |
| Effects of FR145237, an acyl-CoA:cholesterol acyltransferase inhibitor, on diet-induced hypercholesterolemia in diabetic rats Sakuma, Y., H. Hagihara, et al. (1997), Life Sci 60(6): 351-6. Abstract: Recent studies have shown that acyl-CoA:cholesterol acyltransferase (ACAT) plays an important role in the initiation of diabetes-associated hypercholesterolemia. To confirm this hypothesis, effects of a potent ACAT inhibitor, FR145237, on diet-induced hypercholesterolemia were examined in streptozotocin (STZ)-induced diabetic rats. One-week feeding of 1% cholesterol and 0.5% cholic acid to normal rats and STZ-induced diabetic rats increased plasma cholesterol levels in both groups, and the response was more remarkable in the STZ rats than in the normal ones (1266 +/- 476 mg/dl and 146 +/- 7 mg/dl, respectively). FR145237 dose-dependently reduced the rise in plasma cholesterol levels in the STZ rats and the levels were almost normalized by treatment with 1 mg/kg/day of the compound. These results suggest that hyperresponse to dietary cholesterol was induced in the STZ rats and that ACAT is involved in the hyperresponse. The effects of FR145237 on other plasma lipids such as high density lipoprotein (HDL) cholesterol and triglyceride (TG) levels were also examined. |
| Effects of F-strain Mycoplasma gallisepticum inoculation on serum very low density lipoprotein diameter and fractionation of cholesterol among lipoproteins in commercial egg-laying hens Burnham, M. R., E. D. Peebles, et al. (2003), Poult Sci 82(10): 1630-6. Abstract: Experimental inoculation with the F-strain of Mycoplasma gallisepticum (FMG) at 12 wk of age has been shown to affect the performance, liver, reproductive organs, and yolk lipid characteristics of commercial layers. Therefore, this study was conducted to determine the serum lipoprotein characteristics of commercial egg-laying hens at 16 wk of age and throughout lay after inoculation with FMG at 12 wk of age. Mean diameters of very low density lipoproteins (VLDL) were determined for the 10th, 50th, and 90th percentiles of serum total VLDL of each hen. Percentages of total serum cholesterol recovered in VLDL and low and high density lipoprotein particle classes were also determined. Inoculation of birds with FMG at 12 wk did not change the physical properties or relative concentrations of their circulating lipoproteins. However, the age of the bird had significant differential effects on all the parameters examined. These data demonstrate that FMG-inoculation at 12 wk of age does not affect the lipoproteins of laying hens, but because these birds were housed in biological isolation units, these results do not preclude the possibility that these yolk precursors may be affected in FMG-infected birds that are housed in facilities in which there are increased levels of environmental stress. These data further suggest that alterations in liver, reproductive organs, and yolk lipid characteristics in response to FMG, as noted in previous reports on commercial layers, are not mediated through changes in circulating VLDL diameters. |
| Effects of gamma-irradiated fats on plasma lipid concentrations and hepatic cholesterol metabolism in rats Kim, E., S. M. Jeon, et al. (2001), Ann Nutr Metab 45(4): 152-8. Abstract: Currently, there is a growing need for food irradiation that is effective in food preservation and quality improvement. Accordingly, this study was designed to observe the effects of gamma-irradiated dietary fat on plasma lipid concentrations and hepatic cholesterol metabolism in rats. Male rats were fed 5-kGy-gamma-irradiated beef tallow (gammaBT), corn oil (gammaCO), perilla oil (gammaPO), and nonirradiated fats (BT, CO, and PO) for 6 weeks. The gamma-irradiated fat feeding did not affect the plasma lipid concentrations. However, the hepatic cholesterol content was significantly higher in the rats fed gamma-CO as compared with the rats fed nonirradiated CO (40.0 vs. 28.2 mg/g liver). The hepatic HMG-CoA (3-hydroxy-3-methylglutaryl-coenzyme A) reductase activities were not significantly different between the controls and the gamma-irradiated fat fed groups. However, the hepatic ACAT (acyl-CoA:cholesterol acyltransferase) activity was significantly lower in the gammaPO group as compared with its control group (138.2 vs. 404.5 pmol min(-1) mg(-1)). Among the nonirradiated groups, the ACAT activities of the CO and PO groups were higher than that of the BT group. The amounts of coprostanone, cholesterol, and total fecal neutral sterol were significantly higher in the gammaPO group as compared with the other groups. These results indicate that although slight changes in the lipid metabolism were observed as a result of 5-kGy-gamma-irradiated fat feeding, they were relative to the fat type and had no harmful consequences. |
| Effects of garlic extract consumption on blood lipid and oxidant/antioxidant parameters in humans with high blood cholesterol Durak, I., M. Kavutcu, et al. (2004), J Nutr Biochem 15(6): 373-7. Abstract: Effects of garlic extract supplementation on blood lipid profile and oxidant/antioxidant status were investigated in volunteer subjects with high blood cholesterol. A total of 23 volunteer subjects with high blood cholesterol (>5.98 mmol/L) participated in the study. Of them, 13 patients were evaluated as a hypertensive group and the others a normotensive group. Before (first sample) and after (second sample) garlic extract consumption for 4 months, routine blood analyses including lipid parameters and liver and kidney function tests were performed. Additionally, blood oxidant (malondialdehyde MDA, oxidation resistance OR), and antioxidant (antioxidant potential AOP, nonenzymatic superoxide radical scavenger activity NSSA) parameters were measured. Serum total cholesterol, low-density lipoprotein (LDL) and very-low-density lipoprotein (VLDL) cholesterols, and triglyceride levels were found to be significantly lowered, but HDL high-density lipoprotein cholesterol level increased after the extract use. The total:HDL cholesterol ratio was also found to be significantly decreased after the extract use. There were no meaningful differences with regard to other routine biochemical parameters. Additionally, blood AOP, OR, and NSSA values were found increased and MDA level decreased in the second samples relative to the first ones. Systolic and diastolic blood pressure values were also found to be significantly lowered after extract supplementation in the hypertensive group, but no similar changes were observed in the normotensive group. We conclude that garlic extract supplementation improves blood lipid profile, strengthens blood antioxidant potential, and causes significant reductions in systolic and diastolic blood pressures. It also leads to a decrease in the level of oxidation product (MDA) in the blood samples, which demonstrates reduced oxidation reactions in the body. |
| Effects of gender, apolipoprotein E phenotype and cholesterol-lowering by plant stanol esters in children: the STRIP study. Special Turku Coronary Risk Factor Intervention Project Tammi, A., T. Ronnemaa, et al. (2002), Acta Paediatr 91(11): 1155-62. Abstract: AIM: To evaluate the effects of gender, apolipoprotein E phenotype and cholesterol absorption and synthesis (estimated as serum plant sterol and cholesterol precursor sterol concentrations) on the cholesterol-lowering effect of plant stanol esters in children. METHODS: Eighty-one healthy, normocholesterolaemic 6-y-old children (45 boys) were recruited from the Special Turku Coronary Risk Factor Intervention Project (STRIP), a randomized prospective trial aiming at atherosclerosis prevention in childhood. This placebo-controlled, double-blind, cross-over study comprised two 3-mo study periods and a 6-wk wash-out period. During the study periods, 20 g of the children's daily dietary fat intake was replaced with plant stanol ester margarine or control margarine. RESULTS: In boys, plant stanol esters reduced serum total and low-density lipoprotein cholesterol concentrations by 6% (0.09 to 0.42 mmol/L) and 9% (0.09 to 0.36 mmol/L), respectively (p < 0.01 for both). In girls, the decreases in concentrations were 4% (0.03 to 0.38 mmol/L) and 6% (0.02 to 0.32 mmol/l) (p < 0.05 for both). The response rate did not differ between the genders. Serum total and low-density lipoprotein cholesterol concentrations decreased by 6% and 8% (p < 0.01 for both), respectively, in both children with the apolipoprotein E 3/4 or 4/4 (apoE4+) phenotype and the apolipoprotein E 2/3 or 3/3 (apoE4-) phenotype. Cholesterol absorption decreased both in the apoE4+ children and in the apoE4- children, but cholesterol synthesis consistently increased in the apoE4+ children only. CONCLUSION: Plant stanol esters reduce serum cholesterol concentration in healthy children irrespective of their gender or apoE4 phenotype. |
| Effects of genotype and diet on cholesterol efflux into plasma and lipoproteins of normal, apolipoprotein A-I-, and apolipoprotein E-deficient mice Huang, Y., Y. Zhu, et al. (1997), Arterioscler Thromb Vasc Biol 17(10): 2010-9. Abstract: We investigated the contribution of apoE to cholesterol efflux into plasmas of normal, apoA-I-, and apoE-deficient mice, which were fed with chow- and cholesterol-rich diets. Plasmas of normal and apoA-I-deficient mice contain apoE in pre-beta-migrating VLDL as well as in HDL-like lipoproteins, which have either electrophoretic alpha- or gamma-mobilities. The latter particle resembled gamma-LpE in human plasma also by its mobility on nondenaturing two-dimensional electrophoresis. No apoE-containing lipoproteins were found in plasmas of apoE-deficient mice. When apoA-I- and apoE-deficient mice received both chow- and fat-rich diets, their plasmas released significantly less 3H-cholesterol from radiolabeled fibroblasts than did plasma of normal mice. Removal of apoE from plasmas of normal and apoA-I-deficient mice by anti-apoE immunoaffinity chromatography decreased their cholesterol efflux capacities (per 1 minute/per 1 hour) by 26%/40% (P = 0.0092/0.0007) and 30%/26% (P = 0.0092/0.0003), respectively. Net cholesterol efflux from fibroblasts into apoA-I-deficient plasma was 45% lower compared with plasma of normal mice. Incubation of fibroblasts with apoE-deficient plasma caused net influx of cholesterol. Prior addition of human apoE to or removal of apoB-containing lipoproteins from apoE-deficient plasma restored its ability to cause net cholesterol efflux to 50% of normal plasma. Some of the differences between cholesterol efflux into normal and apoE-deficient plasmas were attributable to the failure of apoE-deficient plasmas to take up cell-derived 3H-cholesterol into gamma-LpE. Compared with normal plasma, both apoA-I-deficient and apoE-deficient plasmas were significantly decreased in their activity to esterify cell-derived 3H-cholesterol. Anti-apoE chromatography decreased significantly cholesterol esterification in normal plasma and apoA-I-deficient plasma but not in apoE-deficient plasma. Taken together, the data provide evidence that apoE is an important contributor to reverse cholesterol transport, partially because of initial uptake of cell-derived cholesterol by gamma-LpE and partially because of the contribution of apoE-containing lipoproteins to esterification of cholesterol in plasma. |
| Effects of Ginkgo biloba extract on the proliferation of vascular smooth muscle cells in vitro and on intimal thickening and interleukin-1beta expression after balloon injury in cholesterol-fed rabbits in vivo Lin, S. J., T. H. Yang, et al. (2002), J Cell Biochem 85(3): 572-82. Abstract: Restenosis may develop in response to cytokine activation and smooth muscle cell proliferation. Ginkgo biloba extract (EGb) has been used to treat cardiovascular and cerebrovascular diseases. In the present study, the effects of EGb on the growth of cultured vascular smooth muscle cells (VSMC), as well as on the expression of interleukin-1beta (IL-1beta) and the intimal response in balloon-injured arteries of cholesterol-fed rabbits, were investigated. Using bromodeoxyuridine incorporation as an index of cell proliferation, EGb was found to inhibit serum-induced mitogenesis of cultured rat aorta VSMC in a dose-dependent manner. In vivo, EGb and probucol (positive control) reduced the atheroma area in thoracic aortas of male New Zealand white rabbits fed a 2% cholesterol diet for 6 weeks with balloon denudation of the abdominal aorta being performed at the end of the third week. Intimal hyperplasia, expressed as the intimal/medial area ratio, in the abdominal aortas was significantly inhibited in the both the EGb group (0.61 +/- 0.06) and the probucol group (0.55 +/- 0.03) compared to the C group (0.87 +/- 0.02). In the balloon-injured abdominal aorta, both EGb and probucol significantly reduced IL-1beta mRNA and protein expression and the percentage of proliferating cells. The inhibitory effects of EGb on the intimal response might be attributed to its antioxidant capacity. EGb may have therapeutic potential for the prevention of restenosis after angioplasty. |
| Effects of ginsenosides on myocardial reperfusion arrhythmia and lipid superoxidation in high cholesterol diet rats Yang, Y., K. He, et al. (1999), Shi Yan Sheng Wu Xue Bao 32(4): 349-52. Abstract: To explore the effects of GSL on myocardial reperfusion arrhythmia and lipid superoxidation in high cholesterol diet rats. Hyperlipidemia model was set up with administered high cholesterol emulsion 15 ml/kg to rats orally for 14 days. In GSL group, rats were given GSL i.p. 75 mg/kg simultaneously when administered high cholesterol emulsion. The experiment of myocardial ischemia reperfusion was performed on all rats. The results showed: (1) After administration of high cholesterol emulsion to rats orally for 14 days, hyperlipidemia model was set up successfully, simultaneously treatment with GSL. It lowered serum lipid; (2) In hyperlipidemia state, serum MDA increased (p < 0.01, SOD and NO decreased markedly (p < 0.01 and p < 0.05 respectively) after 2 h of myocardial reperfusion; the rate of reperfusion arrhythmia (RPAr) increased within 10 min of reperfusion, four out of nine rats died of ventricular fibrillation (VF); and (3) GSL decreased MDA, increased SOD and NO after 2 h of myocardial reperfusion. All changes were significant (p < 0.01); the rate of RPAr decreased, no VF occurred and all rats survived. Hyperlipidemia aggravated myocardial ischemia reperfusion injury and increased the incidence of RPAr. The results suggested that GSL reduced myocardial ischemia reperfusion injury and RPAr in high cholesterol diet state through antiperoxidating and inducing the production of NO. |
| Effects of gliclazide on low-density lipoprotein oxidizability and atherosclerosis in cholesterol-fed rabbits Nomura, H., M. Naito, et al. (2000), J Atheroscler Thromb 7(2): 104-9. Abstract: We studied the effects of a widely-used sulfonylurea, gliclazide, on the oxidizability of low density lipoprotein (LDL) and the development of experimental atherosclerosis in cholesterol-fed rabbits. Daily oral administration of gliclazide (20 mg/kg/day) tended to inhibit the aortic atherosclerosis induced by feeding a 1% cholesterol diet for 10 weeks, although it did not affect diet-induced hyperlipidemia. The administration of gliclazide tended to inhibit the increase of serum thiobarbituric acid-reacting substances (TBARS) by cholesterol feeding and to increase the lag time of the conjugated-diene formation of LDL subjected to in vitro oxidation by copper ion, although without significance. The present study suggests that gliclazide may have antioxidative properties in vivo, and have further beneficial effects for the treatment of diabetes mellitus by inhibiting the oxidation of LDL. |
| Effects of GM1-ganglioside and alpha-sialyl cholesterol on amino acid uptake, protein synthesis, and Na+,K(+)-ATPase activity in superior cervical and nodose ganglia excised from adult rats Ando, M., Y. Nakashima, et al. (1990), Mol Chem Neuropathol 13(1-2): 33-46. Abstract: We examined the effect of GM1-ganglioside in combination with cholera toxin B, and synthetic alpha-sialyl cholesterol (alpha-SC) on neutral amino acid (tritiated alpha-aminoisobutyric acid, 3HAIB) uptake, protein synthesis (3Hleucine incorporation), and Na+,K(+)-ATPase activity in isolated superior cervical ganglia (SCG) and nodose ganglia (NG) from adult rats after aerobic incubation, usually for 2 h at 37 degrees C in vitro. Cholera toxin B, that specifically masks the oligosaccharide chain of GM1-ganglioside, antagonized the GM1-induced changes in 3HAIB uptake, 3Hleucine incorporation, and Na+,K(+)-ATPase activity almost completely in SCG, but partially in NG. Although cholesterol itself had little effect on either 3HAIB uptake and Na+,K(+)-ATPase activity both in SCG and NG, alpha-SC caused considerable reduction of both amino acid uptake and the transport enzyme activity in each ganglia. However, cholesterol was more effective than alpha-SC in decreasing 3Hleucine incorporation in either ganglia. Whereas addition of EGTA markedly reduced either GM1-induced or alpha-SC-induced change in 3Hleucine incorporation into acid-insoluble fraction in both SCG and NG, application of Ca2+ ionophore produced considerable recovery of the protein synthesis from the inhibited level by Ca2(+)-deprivation. ATP and creatine phosphate contents in SCG were elevated by the presence of GM1 or alpha-SC, whereas 3HAIB uptake and Na+,K(+)-ATPase activity were inhibited, suggesting that utilization for membrane transport was diminished as a result of GM1- or alpha-SC-induced decrease of ATPase activity. |
| Effects of graded levels of dietary casein and corn oil on total cholesterol and triacylglycerol in plasma and liver of rats Takeuchi, H., K. Sugiura, et al. (2000), J Nutr Sci Vitaminol (Tokyo) 46(6): 280-4. Abstract: With the intention of examining the effects of dietary protein and oil levels on total cholesterol (T-CHOL) and triacylglycerol (TG) concentrations in the plasma and liver, male Wistar rats, weighing about 170 g, were fed diets containing graded levels of casein and corn oil for 2 wk. At the 5, 20, and 30% levels of dietary corn oil, plasma T-CHOL concentrations were generally enhanced in proportion to the rise of dietary casein level, but plasma TG contents were scarcely influenced by the level. At the 8 to 35% casein levels, plasma T-CHOL and TG concentrations were the highest at the 5% corn oil level, followed in order by the 20 and 30% levels of oil. At the 5 and 20% oil levels, hepatic T-CHOL contents were hardly changed at the 8 to 30% casein levels, but enhanced at the 35% casein level. At the 30% oil level, the T-CHOL contents tended to be changed proportionally to casein levels. At all levels of casein, hepatic T-CHOL contents tended to be relatively high at the 30% corn oil, middle at the 20% oil, and low at the 5% one. At each corn oil level, TG contents in the liver tended to be elevated at the 8 to 15% casein levels and highly preserved at the 15 to 25% ones. Then, the raised TG contents declined at the 5 and 20% levels of corn oil and remained constant at the 30% oil. At each casein level, the contents of hepatic TG were generally high at the 30% oil level, followed in order by the 20 and 5% oil levels. These results indicated that plasma and liver T-CHOL concentrations were proportionately enhnaced by the increase in casein level, and plasma TG contents were hardly affected by the level and hepatic TG ones were lowered by relatively lower or higher casein level, and the rise in corn oil level generally reduced plasma T-CHOL and TG concentrations, but raised hepatic ones. |
| Effects of growth hormone on cholesterol metabolism in the lactating rat mammary gland Shand, J. H., D. W. West, et al. (1997), J Endocrinol 152(3): 447-54. Abstract: Lactating rats were treated for 48 h with bromocriptine (to inhibit prolactin release) or bromocriptine together with an antiserum to rat GH. Animals given the combined treatment were also supplemented concurrently with bovine GH (bGH) or human insulin-like growth factor-I (hIGF-I). The effects of these treatments on the activities of 3-methyl-3-glutaryl-CoA reductase (HMG-CoA reductase), acyl-CoA:cholesterol acyltransferase (ACAT) and neutral cholesteryl ester hydrolase (CEH) and on the microsomal concentrations of non-esterified and esterified cholesterol were measured. Lack of prolactin decreased HMG-CoA reductase but did not affect ACAT, neutral CEH or the concentrations of microsomal cholesterol or cholesteryl esters. In the absence of both hormones, an even greater reduction in HMG-CoA reductase together with increases in ACAT, neutral CEH and both of the microsomal sterols were observed. Concurrent supplementation with either bGH or hIGF-I wholly or partially prevented the effects on HMG-CoA reductase but only bGH was active against the increase in ACAT. Neither bGH nor hIGF-I could prevent the effects of the anti-hormone treatment on neutral CEH, and the changes in ACAT and CEH activities were broadly reflected in the microsomal sterol concentrations. The results indicate that the cessation of lactation brings about rapid changes in the activities of the enzymes involved in cholesterol metabolism within the mammary gland with a definite switch from synthesis to storage. Supplementation with bGH alone was sufficient to maintain cholesterol synthesis at control levels and could also significantly inhibit storage of the sterol as its ester. In the absence of GH, hIGF-I partially supported cholesterol synthesis but had no effect on its conversion to the ester. On a whole-tissue basis, enzyme activities could be correlated with the physiological effects of the anti-hormone treatments. |