Université Catholique de Louvain, Life Sciences Institute, Louvain-la-Neuve, Belgium.
Am J Clin Nutr. 2011 Dec;94(6 Suppl):1846S-1852S. doi: 10.3945/ajcn.110.001651. Epub 2011 May 4.
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.
胎儿营养不良的研究提出了这样一种假设，即胎儿编程对应于胎儿试图适应子宫内遇到的不利条件。如果这些条件在以后的生活中持续存在，这些适应是有益的，但如果营养正常或丰富，它们就会变得有害，并有利于代谢综合征的出现。本文的讨论仅限于由早期营养不匹配引起的肥胖和心血管疾病的发育编程，特别是宫内生长迟缓，随后是追赶性生长。在探讨啮齿动物实验所揭示或提示的一些机制之前，先回顾一下人类的一些选定数据。肥胖编程涉及多种生理机制，其中有 2 种机制被详细描述。在一些但不是所有的观察中，由于负责食欲调节的下丘脑回路发育紊乱导致的过度进食可能导致肥胖。另一个贡献可能是脂肪组织中脂肪细胞前体细胞群体的发育变化。尽管肥胖与心血管疾病之间的联系已得到充分证实，但血压调节的改变可能独立于肥胖而出现。母体营养不良随后是产后营养过剩导致成年人的心率和血压昼夜变化消失。进一步的研究应该阐明早期营养不匹配对调节能量摄入、能量消耗和昼夜节律的大脑中枢发育的影响。
