Division of Neuroscience, Oregon National Primate Research Center, Oregon Health and Science University, Beaverton, OR 97006, USA.
Int J Obes (Lond). 2013 Feb;37(2):254-62. doi: 10.1038/ijo.2012.42. Epub 2012 Mar 27.
The link between maternal under-nutrition and cardiovascular disease (CVD) in the offspring later in life is well recognized, but the impact of maternal over-nutrition on the offspring's cardiovascular function and subsequent risk for CVD later in life remains unclear. Here, we investigated the impact of maternal exposure to a high-fat/calorie diet (HFD) during pregnancy and early postnatal period on endothelial function of the offspring in a nonhuman primate model.
Offspring, naturally born to either a control (CTR) diet (14% fat calories) or a HFD (36% fat calories) consumption dam, were breast-fed until weaning at about 8 months of age. After weaning, the offspring were either maintained on the same diet (CTR/CTR, HFD/HFD), or underwent a diet switch (CTR/HFD, HFD/CTR). Blood samples and arterial tissues were collected at necropsy when the animals were about 13 months of age.
HFD/HFD juveniles displayed an increased plasma insulin level and glucose-stimulated insulin secretion in comparison with CTR/CTR. In abdominal aorta, but not the renal artery, acetylcholine-induced vasorelaxation was decreased remarkably for HFD/HFD juveniles compared with CTR/CTR. HFD/HFD animals also showed a thicker intima wall and an abnormal vascular-morphology, concurrent with elevated expression levels of several markers related to vascular inflammation and fibrinolytic function. Diet-switching animals (HFD/CTR and CTR/HFD) displayed modest damage on the abdominal vessel.
Our data indicate that maternal HFD exposure impairs offspring's endothelial function. Both early programming events and postweaning diet contribute to the abnormalities that could be reversed partially by diet intervention.
母体营养不足与后代晚年心血管疾病（CVD）之间的联系已得到充分认识，但母体营养过剩对后代心血管功能的影响以及后代晚年 CVD 的发生风险仍不清楚。在这里，我们在非人灵长类动物模型中研究了母体在妊娠和产后早期暴露于高脂肪/高卡路里饮食（HFD）对后代内皮功能的影响。
自然分娩的后代，其母代分别摄入对照（CTR）饮食（14%脂肪卡路里）或 HFD（36%脂肪卡路里），接受母乳喂养至约 8 月龄断奶。断奶后，后代要么继续维持相同的饮食（CTR/CTR，HFD/HFD），要么进行饮食转换（CTR/HFD，HFD/CTR）。当动物约 13 月龄时，在解剖时采集血液样本和动脉组织。
与 CTR/CTR 相比，HFD/HFD 幼崽的血浆胰岛素水平和葡萄糖刺激的胰岛素分泌增加。与 CTR/CTR 相比，HFD/HFD 幼崽的腹主动脉乙酰胆碱诱导的血管舒张明显降低，但肾动脉无此变化。HFD/HFD 动物还表现出较厚的内膜壁和异常的血管形态，同时与血管炎症和纤维蛋白溶解功能相关的几个标志物的表达水平升高。饮食转换动物（HFD/CTR 和 CTR/HFD）的腹侧血管也有轻度损伤。
我们的数据表明，母体 HFD 暴露会损害后代的内皮功能。早期编程事件和断奶后饮食都会导致异常，而饮食干预可部分逆转这些异常。
