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Atherogenic Diet (atherogenic + diet)
Selected AbstractsHypocholesterolemic and Anti-Obesity Effects of Saponins from Platycodon grandiflorum in Hamsters Fed Atherogenic DietsJOURNAL OF FOOD SCIENCE, Issue 8 2008H.L. Zhao ABSTRACT:, Platycodins, a group of saponin glycosides from Platycodon grandiflorum, are believed to possess anti-obesity and cholesterol-lowering properties. The aim of the present study was to investigate whether dietary platycodins affect plasma, hepatic, or fecal cholesterol concentrations, as well as cholesterol absorption and fractional synthesis rates in a dose-dependent manner. Golden Syrian hamsters (n= 45) were fed atherogenic (0.25% cholesterol) diets enriched with platycodins in the forms of either aqueous extracts (containing 0.3% to 0.5% of platycodins of diet mass) or crude saponins fractions (containing 0.9% to 1.0% of platycodins of diet mass) for 28 d. {3, 4},13C-cholesterol and 2H2O tracers were administered on days 26 and 28 to assess cholesterol absorption and biosynthesis, respectively. After platycodin intervention, total cholesterol concentrations in plasma and liver were reduced (P < 0.05) by 13% to 28% and 41% to 79%, respectively, whereas cholesterol concentrations in feces were increased (P < 0.05) up to 2.5-fold compared to controls. Platycodin feeding increased (P < 0.001) cholesterol absorption up to 60%, but not cholesterol synthesis. These results suggest that platycodin-enriched diets can lower circulating and whole body cholesterol contents, and thus reduce the risk of cardiovascular diseases through mechanisms independent from cholesterol absorption or synthesis. [source] High dietary methionine plus cholesterol stimulates early atherosclerosis and late fibrous cap development which is associated with a decrease in GRP78 positive plaque cellsINTERNATIONAL JOURNAL OF EXPERIMENTAL PATHOLOGY, Issue 3 2009Anthony Zulli Summary The role of homocysteine, or its precursor methionine, in the formation of fibrous caps and its association with endoplasmic reticulum (ER) stress is unclear. Homocysteine can stimulate collagen accumulation and upregulate the ER stress chaperone glucose regulated protein 78 (GRP78). The aim of this study was to determine if high dietary methionine would increase fibrous caps, and that removal of an atherogenic diet would decrease the amount of ER stressed cells. New Zealand white rabbits were fed for 2, 4, or 12 weeks an atherogenic diet [1% methionine + 0.5% cholesterol (2MC, 4MC or 12MC)]; for 4 or 12 weeks a 0.5% cholesterol diet (4Ch, 12Ch); and to study plaque regression, an MC diet for 2 or 4 weeks accompanied by 10 weeks of a normal diet (2MCr, 4MCr). Endothelial function, atherosclerosis and GRP78 positive cells were studied. Endothelial function was abolished in 4MC and atherosclerosis increased 17-fold (P < 0.05) compared with 4Ch. Fibrous caps composed 48% of total plaque area in 12MC vs. 10% in 12Ch (P < 0.01), and 12MC expressed less GRP78 plaque cells vs. 12Ch (P < 0.01). Four MCr had less plaque GRP78 cells than 12MC (P < 0.05) and less endothelial GRP78 cells (P < 0.01). In addition, GRP78 positive cells were the highest in 4MC, but decreased in all other groups (P < 0.01). GRP78 positive cells within the fibrous cap inversely correlated with cap size (r2 = 0.9). These studies suggest that high dietary methionine could be beneficial for plaque stabilisation, and a normal diet also stabilises plaque and decreases the number of stressed plaque cells. [source] Quercetin and Ethanol Attenuate the Progression of Atherosclerotic Plaques With Concomitant Up Regulation of Paraoxonase1 (PON1) Gene Expression and PON1 Activity in LDLR,/, MiceALCOHOLISM, Issue 9 2010Leslie C. Leckey Background:, As moderate wine drinking is atheroprotective, it is clinically relevant to elucidate its possible mechanism/s of action/s. Our objective is to demonstrate the potential benefits of the wine components, quercetin and ethanol, on the development of aortic plaques with parallel changes in antiatherogenic factors. Methods and Results:, The effects of quercetin and ethanol on the development of aortic atherosclerotic lesions, liver PON1 gene expression, and serum PON1 activity were measured in LDLR,/, mice on an atherogenic diet for 4 and 8 weeks. Depending on the duration and dosage of these modulators, 12.5 to 25 mg/dl quercetin (12.5Q to 25Q) and 18 to 25% ethanol, the magnitude of decreases in aortic lesions caused by moderate ethanol and quercetin ranged from 20 to 70% (p < 0.05 to p < 0.001) based on ultrasound biomicroscopy (UBM) analyses, and from 18 to 61% (p < 0.05 to p < 0.001) based on morphometric analyses. The composite plot of all the UBM and morphometric data showed significant correlation between these 2 methods (p = 0.0001, Pearson r = 0.79 for 4-week treatment; p = 0.000004, Pearson r = 0.84 for 8-week treatment). Concomitantly, 4-week treatments with 12.5Q and 18% ethanol up regulated liver PON1 mRNA by 41% (p < 0.05) and 37% (p < 0.05), respectively, accompanied by 92% (p < 0.001) and 61% (p < 0.001) increases in serum PON1 activity, respectively. The corresponding values after 8-week treatment with 12.5Q and 18% ethanol were 23% (p < 0.05) and 40% (p < 0.02) with respect to the up regulation of liver PON1 mRNA expression, while the stimulations of serum PON1 activity were 75% (p < 0.001) and 90% (p < 0.001), respectively. Conclusions:, Based on these findings, we conclude that quercetin and moderate ethanol significantly inhibit the progression of atherosclerosis by up regulating the hepatic expression of the antiatherogenic gene, PON1, with concomitant increased serum PON1 activity. [source] Overexpression of human lecithin:cholesterol acyltransferase in mice offers no protection against diet-induced atherosclerosis,APMIS, Issue 5 2000ANJA MEHLUM Human lecithin:cholesterol acyltransferase (LCAT) is a key enzyme in the metabolism of cholesterol. We have used homozygous transgenic mice overexpressing the human LCAT transgene to study the effect of a "Western-type" atherogenic diet (30% fat, 5% cholesterol and 2% cholic acid) on their LCAT expression, activity, lipoprotein profile and tendency to develop atherosclerosis. The LCAT activity was 35-fold higher in serum of the homozygous transgenic mice than in murine control serum, and decreased 11,20% in the transgenic mice when fed the atherogenic diet. The total cholesterol and high-density lipoprotein cholesterol (HDL-C) concentrations were approximately doubled in the transgenic mice compared with the controls when both groups were fed a regular chow diet. In mice on the atherogenic diet, the triglyceride concentration decreased about 50% to the same level in transgenic and control mice. Total cholesterol and HDL-C concentrations increased and were 60,80% higher in the transgenic mice. The expression of LCAT mRNA in the liver was decreased by 49,60% in the transgenic mice when fed the atherogenic diet. The development of atherosclerosis was similar in transgenic and control mice. Thus, the 14- to 27-fold higher LCAT activity and the higher HDL-C concentrations in the homozygous LCAT transgenic mice had no significant protective influence on the development of diet-induced atherosclerosis. [source] Alcohol Inhibits the Progression as Well as the Initiation of Atherosclerotic Lesions in C57Bl/6 Hyperlipidemic MiceALCOHOLISM, Issue 9 2000Eugene E. Emeson Background: Evidence that a moderate consumption of alcohol is associated with a reduced incidence of and mortality due to coronary artery disease continues to accumulate. Despite recent evidence that substances in red wine confer resistance to coronary artery disease, it is clear that at least a substantial proportion of the protective effect is due to the alcohol content of the beverage. We have previously shown that the chronic ingestion of alcohol incorporated into a total liquid diet during a 24-week period inhibits the development of fatty streak lesions in hyperlipidemic C57Bl/6 mice. We have now repeated this study and demonstrated that alcohol continues to markedly inhibit atherogenesis during a 48-week period. Methods: Mice were fed a high fat atherogenic liquid diet with 0% or 6% alcohol or a high fat atherogenic pelleted diet with 0% or 15% alcohol in their drinking water. After 24 and 48 weeks on these diets, subgroups of mice were euthanized and the aortas were studied for extent of atherosclerosis. Plasma lipid levels were also measured and flow cytometry studies performed to characterize their T and B lymphocyte populations. Additional groups of mice were given the high fat atherogenic diets for 24 weeks to allow lesions to develop and were then treated with alcohol diets to determine whether they inhibit the progression of the lesions. Results: The alcohol diets suppressed the development of atherosclerotic lesions at both 24 and 48 weeks in both the liquid and pelleted diet models. The addition of the alcohol diets after allowing lesions to form for 24 weeks halted the further progression of the lesions. The alcohol treatments also decreased the plasma levels of total cholesterol and high density lipoprotein (HDL) cholesterol at almost all time intervals. Conclusions: We conclude that alcohol not only inhibits the initial development of atherosclerotic lesions but also inhibits the progression of existing atherosclerotic lesions. The alcohol-mediated decrease in HDL cholesterol in these experiments suggests that HDL plays little or no role in amelioration of atherogenesis in this model. [source] | ||||||||||