Early Programming of Appetite, Type 2 Diabetes, Breast Cancer and Ageing (Reported at http://www.bbc.co.uk/news/health-12668519, on 8 March 2011)
‘The major focus of our research is to understand the mechanistic basis of the relationships between poor early growth and subsequent increased risk of type 2 diabetes, obesity, breast cancer and premature death. There are a large number of epidemiological studies suggesting that such relationships exist, however the molecular mechanisms mediating such phenomena are not understood.’ Susan Ozanne *
The Cambridge University Institute of Metabolic Science is seeking mechanisms by which early environment and poor early growth correlate with type 2 diabetes and insulin resistance. Insulin-signaling defects in humans may provide early indications of metabolic disease, as may early defects in adults who had a low birth weight. Ongoing studies in placenta will relate the expression of insulin signaling molecules to the nutritional status of both mother and baby.
Molecular markers for prediction of risk of type 2 diabetes in later life are being studied in a rodent model of early nutritional growth restriction. Defects in the pancreas, muscle, liver and adipose tissue in growth restricted rats are studied to determine the molecular mechanisms underlying these changes such as the role of epigenetic alterations.
Appetite is shown to be programmed by maternal nutrition during lactation. Down-regulation of appetite is seen to be secondary to poor maternal nutrition and so powerful that it prevents diet-induced obesity in mice. Restriction of growth during suckling increases life-span, during fetal life decreases life-span, changes that are associated with differences in kidney telomere length. They are examining telomere length, and expression of stress response proteins, that underlie the ageing process.