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Use of hamster as a model to study diet-induced atherosclerosis

机译:以仓鼠为模型研究饮食诱发的动脉粥样硬化

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摘要

Golden-Syrian hamsters have been used as an animal model to assess diet-induced atherosclerosis since the early 1980s. Advantages appeared to include a low rate of endogenous cholesterol synthesis, receptor-mediated uptake of LDL cholesterol, cholesteryl ester transfer protein activity, hepatic apoB-100 and intestinal apoB-48 secretion, and uptake of the majority of LDL cholesterol via the LDL receptor pathway. Early work suggested hamsters fed high cholesterol and saturated fat diets responded similarly to humans in terms of lipoprotein metabolism and aortic lesion morphology. Recent work has not consistently replicated these findings. Reviewed was the literature related to controlled hamster feeding studies that assessed the effect of strain, background diet (non-purified, semi-purified) and dietary perturbation (cholesterol and/or fat) on plasma lipoprotein profiles and atherosclerotic lesion formation. F1B hamsters fed a non-purified cholesterol/fat-supplemented diet had more atherogenic lipoprotein profiles (nHDL-C > HDL-C) than other hamster strains or hamsters fed cholesterol/fat-supplemented semi-purified diets. However, fat type; saturated (SFA), monounsaturated or n-6 polyunsaturated (PUFA) had less of an effect on plasma lipoprotein concentrations. Cholesterol- and fish oil-supplemented semi-purified diets yielded highly variable results when compared to SFA or n-6 PUFA, which were antithetical to responses observed in humans. Dietary cholesterol and fat resulted in inconsistent effects on aortic lipid accumulation. No hamster strain was reported to consistently develop lesions regardless of background diet, dietary cholesterol or dietary fat type amount. In conclusion, at this time the Golden-Syrian hamster does not appear to be a useful model to determine the mechanism(s) of diet-induced development of atherosclerotic lesions.
机译:自1980年代初以来,金叙利亚仓鼠已被用作评估饮食诱发的动脉粥样硬化的动物模型。优势似乎包括内源性胆固醇合成速率低,受体介导的LDL胆固醇摄取,胆固醇酯转移蛋白活性,肝载脂蛋白B-100和肠载脂蛋白B-48分泌以及通过LDL受体途径吸收大部分LDL胆固醇。早期工作表明,饲喂高胆固醇和饱和脂肪饮食的仓鼠在脂蛋白代谢和主动脉病变形态方面的反应与人类相似。最近的工作并未一致地重复这些发现。综述了与控制仓鼠喂养研究有关的文献,该研究评估了品系,背景饮食(未纯化,半纯化)和饮食扰动(胆固醇和/或脂肪)对血浆脂蛋白谱和动脉粥样硬化病变形成的影响。饲喂非纯化胆固醇/脂肪补充饮食的F1B仓鼠比其他仓鼠菌株或饲喂胆固醇/脂肪补充半纯化饮食的仓鼠具有更多的动脉粥样硬化脂蛋白谱(nHDL-C> HDL-C)。但是,脂肪类型;饱和(SFA),单不饱和或n-6多不饱和(PUFA)对血浆脂蛋白浓度的影响较小。与SFA或n-6 PUFA相比,补充了胆固醇和鱼油的半纯化饮食产生了高度可变的结果,这与人类观察到的反应相反。饮食中的胆固醇和脂肪对主动脉脂质积累的作用不一致。不论背景饮食,饮食中的胆固醇或饮食中的脂肪类型如何,均未见仓鼠能持续产生病变。总而言之,目前,Golden-Syrian仓鼠似乎并不是确定饮食诱导的动脉粥样硬化病变发展机制的有用模型。

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