Proceedings of the Nutrition Society

Research Article

Session 7: Early nutrition and later health Early developmental pathways of obesity and diabetes risk

Symposium on ‘Nutrition in early life: new horizons in a new century’

on 11 – 13 December 2006, The Winter Meeting of the Nutrition Society, an international conference to mark the 100th anniversary of the birth of Elsie Widdowson, was held at Churchill College, Cambridge, hosted by MRC Human Nutrition Research Cambridge jointly with the Neonatal Society supported by the Royal Society of Medicine.

D. B. Dungera1 c1, B. Salgina1 and K. K. Onga1a2

a1 University Department of Paediatrics, University of Cambridge, Addenbrooke's Hospital, Box 116, Cambridge CB2 2QQ, UK

a2 Medical Research Council Epidemiology Unit, Strangeways Research Laboratory, Worts Causeway, Cambridge CB1 8RN, UK

Abstract

Size at birth and patterns of postnatal weight gain have been associated with adult risk for the development of type 2 diabetes in many populations, but the putative pathophysiological link remains unknown. Studies of contemporary populations indicate that rapid infancy weight gain, which may follow fetal growth restriction, is an important risk factor for the development of childhood obesity and insulin resistance. Data from the Avon Longitudinal Study of Pregnancy and Childhood shows that rapid catch-up weight gain can lead to the development of insulin resistance, as early as 1 year of age, in association with increasing accumulation of central abdominal fat mass. In contrast, the disposition index, which reflects the β-cells ability to maintain insulin secretion in the face of increasing insulin resistance, is much more closely related to ponderal index at birth than postnatal catch-up weight gain. Infants with the lowest ponderal index at birth show a reduced disposition index at aged 8 years associated with increases in fasting NEFA levels. The disposition index is also closely related to childhood height gain and insulin-like growth factor-I (IGF-I) levels; reduced insulin secretory capacity being associated with reduced statural growth, and relatively short stature with reduced IGF-I levels at age 8 years. IGF-I may have an important role in the maintenance of β-cell mass, as demonstrated by recent studies of pancreatic β-cell IGF-I receptor knock-out and adult observational studies indicating that low IGF-I levels are predictive of subsequent risk for the development of type 2 diabetes. However, as insulin secretion is an important determinant of IGF-I levels, cause and effect may be difficult to establish. In conclusion, although rapid infancy weight gain and increasing rates of childhood obesity will increase the risk for the development of insulin resistance, prenatal and postnatal determinants of β-cell mass may ultimately be the most important determinants of an individual's ability to maintain insulin secretion in the face of increasing insulin resistance, and thus risk for the development of type 2 diabetes.

Correspondence:

c1 *Corresponding author: Dr D. B. Dunger, fax +44 1223 336996, email dbd25@cam.ac.uk