Hales C N
Department of Clinical Biochemistry, University of Cambridge, Addenbrooke's Hospital, Cambridge, UK.
Br Med Bull. 1997 Jan;53(1):109-22. doi: 10.1093/oxfordjournals.bmb.a011594.
Non-insulin-dependent diabetes mellitus (NIDDM) occurs predominantly after the age of 50 years but is not easy to distinguish from late onset insulin-dependent diabetes. It is likely that misclassification is rare in a Caucasian population. Whilst NIDDM is widely believed to be genetically determined, recent epidemiological observations have consistently revealed statistical associations between indices of poor fetal and infant growth with susceptibility to loss of glucose tolerance in adult life. A possible explanation of these observations is that environmental constraints on fetal growth lead to permanent changes in organogenesis such that a poor capacity of insulin secretion and insulin resistance result. It is postulated that these adaptive responses serve to preserve the growth of certain organs, such as the brain, at the expense of others, such as the viscera. In addition, alterations in the function of organs, such as the liver, serve to aid survival of the offspring under conditions of poor postnatal nutrition. The results of studies of an animal model in which pregnant rats were fed a reduced protein diet are consistent with these concepts.
非胰岛素依赖型糖尿病(NIDDM)主要发生在50岁以后,但很难与晚发型胰岛素依赖型糖尿病区分开来。在白种人群中,错误分类的情况可能很少见。虽然人们普遍认为NIDDM是由基因决定的,但最近的流行病学观察一致显示,胎儿和婴儿生长不良指标与成年后糖耐量丧失易感性之间存在统计学关联。对这些观察结果的一种可能解释是,胎儿生长的环境限制导致器官发生永久性变化,从而导致胰岛素分泌能力差和胰岛素抵抗。据推测,这些适应性反应有助于某些器官(如大脑)的生长,而以其他器官(如内脏)为代价。此外,肝脏等器官功能的改变有助于后代在出生后营养不良的情况下存活。对怀孕大鼠喂食低蛋白饮食的动物模型的研究结果与这些概念一致。