Metabolic consequences of intrauterine growth retardation

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Abstract
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.