Low density lipoprotein oxidation, antioxidants, and atherosclerosis

Catapano, Alberico L.; Maggi, F.M.; Tragni, Elena

doi:10.1097/00001573-200009000-00008

Cited by 91 publications

(61 citation statements)

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“…Increased oxidative stress appears to play an important role in the chronic inflammatory responses to hypercholesterolemia [9]. Although the precise mechanism of atherogenesis is not fully understood, oxidative modification of LDL is considered to be an essential process in the activation of the inflammatory pathway leading to atherosclerosis [10].…”

Section: Discussionmentioning

confidence: 99%

The protective effect of processed cheese against hyperlipidemia in rats

El-Salam

Mohamed

2009

Dairy Sci. Technol.

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-The purpose of this study was to examine the effects of intake of processed cheeses containing different types of fats on plasma lipid profile and lipid peroxidation using hypercholesterolemic rats as an experimental model. This study included three types of processed cheeses: the first two contained vegetable oils and the third contained milk fat only. Five groups of rats (8 animals each) were fed balanced diet (normal), hypercholesterolemic diet (control), and hypercholesterolemic diet containing one of the tested processed cheeses, respectively, for 8 weeks. The body weight and the food intake were recorded and the gain in body weight and food efficiency ratio were also calculated. Blood analysis was carried out at the end of the experiment for total lipids and cholesterol, low density lipoprotein, high density lipoprotein (HDL), triglycerides, and plasma malondialdehyde. Feeding the different processed cheeses with hypercholesterolemic diet showed variable reductions in the plasma lipids, except for HDL, which was increased as compared to control. The highest and significant reduction was observed in the group that received processed cheese containing milk fat only. Also, this group showed significant reduction in lipid peroxidation. These results suggest that consumption of processed cheeses may improve the markers of cardiovascular diseases, particularly processed cheeses containing milk fat only. Further studies on human subjects are needed to verify the present results and to elucidate the possible mechanisms behind the differential effects on serum cholesterol of cheeses containing different types of fats.processed cheese / rat / hyperlipidemia / hypercholesterolemia / lipid profile / conjugated linoleic acid Résumé -Effet protecteur du fromage fondu contre l'hyperlipidémie chez le rat. Le but de cette étude était d'examiner les effets de la consommation de fromages fondus contenant différents types de matière grasse sur le profil lipidique du plasma et la peroxydation des lipides sur le rat hypercholestérolémique comme modèle experimental. L'étude incluait trois types de fromages fondus ; les deux premiers contenaient des huiles végétales et le troisième uniquement de la matière grasse laitière. Cinq groupes de rats (de 8 animaux chacun) ont bénéficié pendant 8 semaines d'un régime alimentaire équilibré (normal), hypercholestérolémique (contrôle) ou hypercholestérolémique contenant un des fromages fondus testés. Le poids et la prise alimentaire ont été relevés et le gain de poids et le ratio d'efficacité alimentaire ont été calculés. À la fin de l'expéri-mentation, une analyse du sang a été réalisée pour les lipides totaux et le cholestérol, LDL et HDL, les triglycérides et le malondialdéhyde du plasma. L'apport des différents fromages fondus à un régime hypercholestérolémique a montré des réductions variables des lipides du plasma, à l'exception des HDL qui augmentaient comparativement au contrôle. La réduction significative la plus élevée était observée dans le groupe qui recevait le fromag...

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Section: Discussionmentioning

confidence: 99%

The protective effect of processed cheese against hyperlipidemia in rats

El-Salam

Mohamed

2009

Dairy Sci. Technol.

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“…It is widely believed that the oxidation of low-density lipoprotein cholesterol (LDL-C) plays an important part in atherogenesis, 21 and it is possible that excess circulating glucose may facilitate peroxidation of cholesterol. [22][23][24] It has also been observed that diabetes is associated with oxidative stress, 25 which is in turn associated with atherogenesis.…”

Section: Discussionmentioning

confidence: 99%

Glucose-Cholesterol Interaction Magnifies Coronary Heart Disease Risk for Hypertensive Patients

2004

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Abstract-Elevated cholesterol and glucose are known independent risk factors for coronary heart disease. This study examines whether an adverse synergistic interaction of cholesterol and glucose magnifies coronary heart disease risk among treated hypertensive patients. Subjects were hypertensive patients (nϭ6672) in a worksite treatment program, with entry fasting glucose Ͻ6.99 mmol/L (126 mg/dL) and total cholesterol Ͻ6.72 mmol/L (260 mg/dL) observed for mean 5.6Ϯ4.5 years follow-up (range 0.5 to 21.7 years). Outcome events were incident hospitalization or death due to coronary heart disease. Cox proportional hazard models were constructed for the whole sample to assess interaction and then stratified by fasting glucose categories with thresholds defined either at impaired fasting glucose ( dL] as reference) in the higher fasting glucose stratum were more than double the corresponding hazard ratios in the lower stratum, whether using impaired fasting glucose or upper quartile fasting glucose as the cut point. These results suggest that an adverse synergistic interaction between glucose and cholesterol magnifies coronary heart disease risk associated with total cholesterol among hypertensive patients, raising the possibility that coronary heart disease prevention might be enhanced if cholesterol intervention criteria were modified by glucose status. Key Words: coronary disease Ⅲ risk factors Ⅲ hypercholesterolemia Ⅲ glucose Ⅲ hypertension H ypercholesterolemia and hyperglycemia are well established independent risk factors for coronary heart disease (CHD) and are often observed among hypertensive patients with metabolic syndrome. 1-3 While the confluence of these risk factors has been noted, the question arises whether interaction among them can lead to an adverse synergism that magnifies risk.The pioneering Framingham risk models based on additive effects of independent risk factors have been the prevalent paradigm to explain cardiovascular disease (CVD) risk. 4 -6 While CVD outcome studies typically use regression models that take into account multiple factors, these models usually explain only a fraction of observed events-a discrepancy that continues to inspire searches for novel factors. 7,8 It is possible that the interaction of known factors, with an adverse, synergistic effect, may account for at least part of the difference between the adverse outcomes predicted by multivariate risk models and the larger number that occur.To date, we have reported evidence of such interaction in 2 very different populations. Analysis of the Honolulu Heart Project 9 data on almost 7000 Japanese-American men revealed an interaction of the upper quartile of baseline postprandial serum glucose with total cholesterol (TC) for 10-year CHD mortality and morbidity. 10 A separate study 11 observed a statistically significant association of the interaction of TC/high-density lipoprotein cholesterol (HDL-C) ratio and the upper quartile of hemoglobin A1c (HbA1c) with atherosclerotic raised lesions from autopsy data collected by t...

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“…These products originated in vivo from oxidized lipoproteins and lipid membranes were linked to initiation and propagation of atherosclerosis (Zhang & Salomon, 2005;Mitra et al, 2011;Hulsmans et al, 2010). The effect of dietary oxidized fat as a contributor to the oxidative stress was also investigated by several groups including our group (Catapano et al, 2000;Drüeke et al, 2001;Garelnabi et al, 2008;Mitra et al, 2011). While there is a consensus in understanding of initial oxidative steps in the generation of early fatty streak lesions as well as the role of products of peroxidized lipid decomposition such as aldehydes in atherosclerosis, the role of further oxidation into neutral carboxylic acids is still obscure.…”

Section: Introductionmentioning

confidence: 99%