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首页> 外文期刊>The British Journal of Nutrition >Maternal undernutrition leads to endothelial dysfunction in adult male rat offspring independent of postnatal diet
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Maternal undernutrition leads to endothelial dysfunction in adult male rat offspring independent of postnatal diet

机译：母体营养不良导致成年雄性大鼠后代的内皮功能障碍，与产后饮食无关

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摘要

Increasing evidence suggests a role for prenatal environment in the onset of cardiovascular and metabolic disease in later life. In the rat, undernutrition in utero and a postnatal high-fat diet gives rise to a phenotype similar to the metabolic syndrome. As endothelial dysfunction is a feature of both CVD and the metabolic syndrome we investigated the impact of maternal undernutrition and/or postnatal high-fat on endothelial function. Virgin Wistar rats were mated and randomly assigned to groups to receive food either ad libitum (control) or at 30% of ad libitum intake throughout gestation. At postnatal day 250, a cohort from each group was challenged with a high-fat diet (D12451, 45% energy from fat; Research Diets, Inc., New Brunswick, NJ, USA) for the remainder of the study. At 1 year of age, small mesenteric arteries were dissected and mounted on a wire myograph and responses to phenylephrine, endothelin, acetylcholine, leptin and sodium nitroprusside assessed. Vasoconstriction to endothelin was significantly enhanced in all groups compared with controls (-log effective concentration equal to 50% of the maximal response (pEC50); P < 0.001). Endothelium-dependent vasodilatation to acetylcholine was significantly blunted in all groups compared with controls (% maximum response; P < 0.01), while dilatation to leptin and sodium nitroprusside was similar in all groups. These data demonstrate that both maternal undernutrition and postnatal high fat lead to vascular alterations and suggest that maternal undernutrition alone is at least as detrimental to offspring endothelial function as a long-term exposure to a high-fat diet in the offspring.
机译：越来越多的证据表明，产前环境在以后的生活中会引发心血管疾病和代谢疾病。在大鼠中，子宫内营养不良和产后高脂饮食会产生类似于代谢综合征的表型。由于内皮功能障碍是CVD和代谢综合征的特征，因此我们研究了母亲营养不良和/或产后高脂对内皮功能的影响。将维珍维斯塔（Virgin Wistar）大鼠交配并随机分组，以在整个妊娠期间随意采食（对照组）或随意采食30％的食物。在出生后的第250天，在其余的研究中，每组的一组都接受高脂饮食（D12451，脂肪能量占45％;美国纽约州新不伦瑞克省的Research Diets，Inc.）挑战。在1岁时，解剖小肠系膜动脉并将其安装在钢丝肌电图仪上，并评估对去氧肾上腺素，内皮素，乙酰胆碱，瘦素和硝普钠的反应。与对照组相比，所有组中对内皮素的血管收缩均显着增强（对数有效浓度等于最大应答的50％（pEC50）; P <0.001）。与对照组相比，所有组内皮细胞对乙酰胆碱的血管舒张作用显着减弱（最大应答百分比; P <0.01），而所有组中对瘦素和硝普钠的舒张作用相似。这些数据表明，孕产妇营养不良和产后高脂肪都会导致血管改变，并表明，单独长期使用孕产妇营养不足与长期摄入高脂饮食一样，对后代内皮功能的危害至少相同。

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