Levy-Marchal Claire, Jaquet Delphine
INSERM U457, Robert Debré Hospital, Paris, France.
Pediatr Diabetes. 2004 Sep;5(3):147-53. doi: 10.1111/j.1399-543X.2004.00057.x.
This review highlights the evidence of linking small for gestational age (SGA) with metabolic/cardiovascular disturbances (dysmetabolic syndrome) in later life. The metabolic and cardiovascular complications associated with in utero undernutrition have been identified during the past 10 yr. Reduced fetal growth is independently associated with an increased risk of the development of cardiovascular diseases, the insulin-resistance syndrome, or one of its components: hypertension, dyslipidemia, impaired glucose tolerance, or type 2 diabetes. All of them appear to result from the initial development of insulin-resistance which appears as a key component underlying the metabolic complications. Although the mechanism remains unclear, there is some evidence that argues in favor of an active contribution of the adipose tissue in the emergence of insulin-resistance associated with in utero undernutrition, but this hypothesis remains to be further documented. From a broader point of view, several hypotheses have been proposed over the past 10 yr to understand this unexpected association. Each of them points to either a detrimental fetal environment or genetic susceptibilities or interactions between these two components as playing a critical role in this context. Although not confirmed, the hypothesis suggesting that this association could be the consequence of genetic/environmental interactions remains at the moment the most attractive.
本综述强调了小于胎龄儿（SGA）与成年后代谢/心血管紊乱（代谢综合征）之间存在关联的证据。过去10年中，已明确了与子宫内营养不良相关的代谢和心血管并发症。胎儿生长受限与心血管疾病、胰岛素抵抗综合征或其组成部分之一（高血压、血脂异常、糖耐量受损或2型糖尿病）发生风险增加独立相关。所有这些似乎都源于胰岛素抵抗的最初发展，而胰岛素抵抗似乎是代谢并发症的关键潜在因素。尽管其机制尚不清楚，但有证据表明，脂肪组织在与子宫内营养不良相关的胰岛素抵抗出现过程中起到了积极作用，但这一假说仍有待进一步证实。从更广泛的角度来看，在过去10年中提出了几种假说，以解释这种意外的关联。每种假说都指出，不利的胎儿环境或遗传易感性，或这两个因素之间的相互作用在这种情况下起着关键作用。尽管尚未得到证实，但认为这种关联可能是遗传/环境相互作用结果的假说目前最具吸引力。
