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首页> 外文期刊>The American Journal of Clinical Nutrition: Official Journal of the American Society for Clinical Nutrition >Developmental programming of adult obesity and cardiovascular disease in rodents by maternal nutrition imbalance.
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Developmental programming of adult obesity and cardiovascular disease in rodents by maternal nutrition imbalance.

机译：母营养不平衡啮齿动物成人肥胖和心血管疾病的发育规划。

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摘要

Studies on fetal undernutrition have generated the hypothesis that fetal programming corresponds to an attempt of the fetus to adapt to adverse conditions encountered in utero. These adaptations would be beneficial if these conditions prevail later in life, but they become detrimental in the case of normal or plentiful nutrition and favor the appearance of the metabolic syndrome. In this article, the discussion is limited to the developmental programming of obesity and cardiovascular disorders caused by an early mismatched nutrition, particularly intrauterine growth retardation followed by postnatal catch-up growth. Selected data in humans are reviewed before evoking some mechanisms revealed or suggested by experiments in rodents. A variety of physiologic mechanisms are implicated in obesity programming, 2 of which are detailed. In some, but not all observations, hyperphagia resulting namely from perturbed development of the hypothalamic circuitry devoted to appetite regulation may contribute to obesity. Another contribution may be the developmental changes in the population of fat cell precursors in adipose tissue. Even if the link between obesity and cardiovascular disease is well established, alteration of blood pressure regulation may appear independently of obesity. A loss of diurnal variation in heart rate and blood pressure in adulthood has resulted from maternal undernutrition followed by postnatal overnutrition. Further research should clarify the effect of mismatched early nutrition on the development of brain centers regulating energy intake, energy expenditure, and circadian rhythms.
机译：胎儿损失的研究产生了胎儿编程对应于胎儿的尝试，以适应子宫内遇到的不利条件的试验。如果这些条件在生命后期占上风，这些适应将是有益的，但在正常或丰富的营养和赞成代谢综合征的外观的情况下，它们变得有害。在本文中，讨论仅限于由早期不匹配的营养，特别是宫内生长迟缓引起的肥胖症和心血管障碍的发育规划，然后进行后捕获生长。在唤起啮齿动物的实验揭示或建议之前，在唤起某些机制之前，审查了人类的所选数据。各种生理机制涉及肥胖编程，其中2个是详细的。在某些情况下，但不是所有观察结果，带有患有致力于食欲监管的下丘脑电路的扰动开发的过夜可能有助于肥胖。另一种贡献可能是脂肪组织中脂肪细胞前体群的发育变化。即使肥胖与心血管疾病之间的联系是很好的建立，血压调节的改变也可能出现独立于肥胖症。成年期心率和血压损失的损失由产妇欠育后，后者是产后产量。进一步的研究应阐明不匹配的早期营养对调节能量摄入，能源支出和昼夜节律的脑中中心发展的影响。

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