Hales C N
Department of Clinical Biochemistry, University of Cambridge, UK.
Acta Paediatr Suppl. 1997 Nov;423:184-7; discussion 188. doi: 10.1111/j.1651-2227.1997.tb18410.x.
Epidemiological studies have revealed strong and reproducible links between indices of poor fetal, and possibly infant, growth and susceptibility to the development of glucose intolerance and insulin resistance syndrome in adult life. The 'thrifty phenotype' hypothesis has been proposed to explain these associations. Key features of the hypothesis are: (i) intrauterine growth retardation has a nutritional basis and the resulting altered fetal environment permanently alters the development and metabolic functions of organs: (ii) these alterations are beneficial to survival in a poor nutritional environment, but may lead to diseases such as non-insulin-dependent diabetes mellitus if nutrition is abundant and obesity occurs in adult life. Tests of this hypothesis in an animal model in which pregnant and/or lactating rats were fed a diet with a reduced protein content have shown that liver metabolism in the offspring is permanently altered despite their being weaned onto a normal diet. The longevity of male offspring may be significantly increased or decreased depending on whether growth retardation is restricted to the period of suckling or pregnancy, respectively. The latter finding raises questions about potentially detrimental effects of 'catch-up' growth.
流行病学研究表明，胎儿生长不良（可能还有婴儿生长不良）的指标与成年后发生糖耐量异常和胰岛素抵抗综合征的易感性之间存在着强有力且可重复的联系。有人提出了“节俭表型”假说来解释这些关联。该假说的主要特点是：（i）宫内生长迟缓有营养基础，由此导致的胎儿环境改变会永久性地改变器官的发育和代谢功能；（ii）这些改变有利于在营养不良的环境中生存，但如果成年后营养丰富且出现肥胖，可能会导致诸如非胰岛素依赖型糖尿病等疾病。在一个动物模型中对该假说进行了测试，在这个模型中，给怀孕和/或哺乳期的大鼠喂食蛋白质含量降低的饮食，结果表明，尽管后代断奶后食用正常饮食，但其肝脏代谢仍发生了永久性改变。雄性后代的寿命可能会显著增加或减少，这分别取决于生长迟缓是仅限于哺乳期还是孕期。后一个发现引发了关于“追赶”生长潜在有害影响的问题。
