Lévy-Marchal C, Czernichow P
INSERM Units 457 and 690, Robert Debré Hospital, Paris, France.
Horm Res. 2006;65 Suppl 3:123-30. doi: 10.1159/000091517. Epub 2006 Apr 10.
The metabolic and cardiovascular complications associated with in-utero undernutrition have been identified during the past 10 years. Reduced fetal growth is independently associated with an increased risk of development of cardiovascular diseases, the insulin-resistance syndrome or one of its components (i.e., hypertension, dyslipidaemia, impaired glucose tolerance and type 2 diabetes). Insulin resistance appears to be a key component underlying these metabolic complications. Although the mechanism remains unclear, several pieces of evidence support an active role of adipose tissue in the emergence of insulin resistance (an abnormal growth pattern and repartition, hypersensitivity to catecholamines, regulation of leptin and adiponectin secretion and modulation of peroxisome proliferator-activated receptor gamma). Among individuals born SGA, those who are more at risk of gaining excess adiposity are those who are thin at birth following a period of fetal growth restriction. This period of undernutrition is followed by a neonatal period of catch-up growth and renutrition. This pattern induces important modifications in adipose tissue, with long-term consequences, among which is a high risk of early development of insulin resistance. Not all individuals born SGA will show such modifications in adipose tissue, meaning that not all of those born SGA are at risk of insulin resistance and diabetes. From a broader point of view, several hypotheses have been proposed over the past 10 years to explain this unexpected association between being born SGA and the later development of disease. Each of them points to a detrimental fetal environment, to a genetic susceptibility or to interactions between these two components 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 the most attractive.
过去10年中,人们已经认识到与子宫内营养不足相关的代谢和心血管并发症。胎儿生长受限独立增加了患心血管疾病、胰岛素抵抗综合征或其组成部分(即高血压、血脂异常、糖耐量受损和2型糖尿病)的风险。胰岛素抵抗似乎是这些代谢并发症的关键因素。尽管其机制尚不清楚,但有几条证据支持脂肪组织在胰岛素抵抗的发生中起积极作用(异常的生长模式和分布、对儿茶酚胺的超敏反应、瘦素和脂联素分泌的调节以及过氧化物酶体增殖物激活受体γ的调节)。在小于胎龄儿中,出生时瘦且经历过胎儿生长受限的个体更易出现脂肪过度蓄积。这种营养不足期之后是新生儿期的追赶生长和再营养。这种模式会引起脂肪组织的重要改变,并产生长期后果,其中胰岛素抵抗早期发生的风险很高。并非所有小于胎龄儿都会出现脂肪组织的这种改变,这意味着并非所有小于胎龄儿都有胰岛素抵抗和糖尿病的风险。从更广泛的角度来看,在过去10年中提出了几种假说来解释出生时小于胎龄与后期疾病发生之间这种意外的关联。每种假说都指出有害的胎儿环境、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仍然最具吸引力。