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Low birthweight and adult insulin resistance: the “catch-up growth” hypothesis
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  1. Stefano Cianfarania,
  2. Daniela Germania,
  3. Francesco Brancab
  1. aLaboratory of Paediatric Endocrinology “Tor Vergata” University via di Tor Vergata 135 00133-Rome Italy, bNational Institute of Nutrition Rome, Italy
  1. Dr S Cianfarani. Email: stefano.cianfarani{at}uniroma2.it

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Fetal origin of adult diseases

Epidemiological studies have shown a close correlation between intrauterine growth retardation (IUGR) and the onset of insulin resistance, non-insulin-dependent diabetes mellitus (NIDDM), hypertension, hyperlipidaemia, and cardiovascular diseases in adult life.1-6 To explain this association, the concept of re-programming has been introduced: intrauterine exposure to insufficient nutrient supply during critical periods of fetal life would permanently affect the development and function of the endocrine system, leading to metabolic changes, including reduced insulin sensitivity.5 6

Although knowledge of the mechanisms involved in the re-programming process might allow new strategies for early prevention of long term metabolic disturbances to be developed, the pathophysiological link between fetal growth impairment and adult diseases is still unclear.

The “thrifty phenotype” and the “fetal salvage” hypotheses

In 1992 Hales and Barker7 proposed the model of the “thrifty phenotype,” suggesting that intrauterine malnutrition would lead to insulin resistance and decreased β cell mass, thus predisposing to NIDDM. According to this hypothesis, the endocrine alterations induced by intrauterine malnutrition are intended to divert the limited nutrient supply to maintain survival and development of vital organs, such as the brain, at the expense of growth.

More recently, the “fetal salvage” hypothesis has been formulated.8 The finding that prepubertal IUGR children show a far greater insulin response than normal birthweight children, challenges the previously proposed β cell hypoplasia. …

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