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母体营养不良会降低子代大鼠的主动脉壁厚度和弹性蛋白含量,而不会改变内皮功能。

Maternal undernutrition reduces aortic wall thickness and elastin content in offspring rats without altering endothelial function.

作者信息

Skilton Michael R, Gosby Alison K, Wu Ben J, Ho Lisa M L, Stocker Roland, Caterson Ian D, Celermajer David S

机构信息

Department of Medicine, University of Sydney, Sydney, NSW 2006, Australia.

出版信息

Clin Sci (Lond). 2006 Oct;111(4):281-7. doi: 10.1042/CS20060036.

Abstract

Epidemiological studies suggest a link between fetal/early infant nutrition and adult coronary artery disease. In the present study, we examined the effects of altering nutrition during gestation, lactation and juvenile life on aortic structure and function in rats. Wistar rat dams were fed either a control or low-protein diet throughout pregnancy, or a low-protein diet for the final 7 days of gestation only. At 21 days post-partum, male pups were weaned on to a control, low-protein or high-fat diet. At 12 weeks, the offspring rats were killed. In 46 rats, aortic sections were mounted and stained to assess media thickness and elastin content. In a further 38 rats, aortic rings were suspended in an organ bath and vascular reactivity was tested with dose-response curves to the endothelium-dependent dilator acetylcholine and the endothelium-independent dilator sodium nitroprusside. Rats exposed to maternal protein restriction while in utero had a significantly decreased aortic wall thickness compared with control rats (P=0.005). Total elastin content of the aorta was also decreased by both maternal low-protein (P=0.02) and early postnatal low-protein (P=0.01) diets. Neither maternal nor postnatal low-protein or high-fat diets, however, resulted in any significant changes in arterial dilator function. In conclusion, fetal undernutrition in rats, induced via a maternal low-protein diet, causes a decrease in aortic wall thickness and elastin content without altering aortic dilator function. These changes in vascular structure may amplify aging-related changes to the vasculature and contribute to the pathophysiology of the putative link between impaired fetal growth and adult cardiovascular disease.

摘要

流行病学研究表明,胎儿期/婴儿早期营养与成人冠状动脉疾病之间存在联系。在本研究中,我们研究了孕期、哺乳期和幼年时期营养改变对大鼠主动脉结构和功能的影响。Wistar大鼠母鼠在整个孕期要么喂食对照饮食,要么喂食低蛋白饮食,或者仅在孕期的最后7天喂食低蛋白饮食。产后21天,雄性幼鼠断奶后分别喂食对照饮食、低蛋白饮食或高脂肪饮食。12周时,将后代大鼠处死。对46只大鼠的主动脉切片进行固定和染色,以评估中膜厚度和弹性蛋白含量。另外38只大鼠的主动脉环悬挂在器官浴槽中,通过对内皮依赖性舒张剂乙酰胆碱和非内皮依赖性舒张剂硝普钠的剂量反应曲线来测试血管反应性。与对照大鼠相比,子宫内暴露于母体蛋白质限制的大鼠主动脉壁厚度显著降低(P=0.005)。母体低蛋白饮食(P=0.02)和出生后早期低蛋白饮食(P=0.01)均使主动脉的总弹性蛋白含量降低。然而,母体或产后的低蛋白或高脂肪饮食均未导致动脉舒张功能发生任何显著变化。总之,通过母体低蛋白饮食诱导的大鼠胎儿期营养不足会导致主动脉壁厚度和弹性蛋白含量降低,而不会改变主动脉舒张功能。血管结构的这些变化可能会放大与衰老相关的血管变化,并促成胎儿生长受限与成人心血管疾病之间假定联系的病理生理学过程。

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