PC43 LONGTERM EFFECTS OF PRE- AND POSTNATAL EXPOSURE TO LOW AND HIGH DIETARY PROTEIN LEVELS: EVIDENCE FROM EPIDEMIOLOGICAL STUDIES AND CONTROLLED ANIMAL EXPERIMENTS

Abstract

Introduction: Epidemiological evidence relates low birth weight to increased risk for syndrome X, coronary heart disease, and high blood pressure in adult age. Methods: This paper reviews evidence on effects of low and high dietary protein in the development of degenerative disease. Results: Low birth weight was linked to maternal and fetal malnutrition and subsequent fetal growth retardation but there are few epidemiological studies analysing the effect in humans. Their outcome is inconclusive in establishing a relationship between dietary protein in pregnancy and birth weight (Metges 2001). A hypothesis was put forward that surviving poor nutrition in utero programs a ‘thrifty phenotype’ offspring prone to poor health in adult life when exposed postnatally to adequate or excess dietary supply (Hales & Barker 1992). An established model to study fetal programming by maternal malnutrition and exploring mechanisms responsible for the development of adult degenerative disease is the maternal low protein (MLP) model in rodents. Usually a 40–50 % protein restricted casein-based diet is compared with an adequate diet of 18–20% protein during pregnancy. In various studies evidence for the above hypothesis was generated. MLP diet throughout pregnancy results in offspring with age-related loss of glucose tolerance, insulin resistance, hypertension, and possibly obesity (e.g. Ozanne & Hales 1999). However, not only MLP diet results in low birth weight in rats, also maternal protein overnutrition was followed by a reduction of body weight at day of life 2 but a higher weight in wk 6 in the offspring (Daenzer et al. 2002). Exposure to high protein diets during pregnancy and lactation resulted in a decreased body weight of pups until weaning. The offspring of maternal high protein feeding had a higher body fatness and a reduced total energy expenditure at wk 9. In contrast, postnatal protein overnutrition only did not lead to an obese phenotype. So far there is no single mechanism identified explaining how maternal factors change the intrauterine environment to increase disease risk in adult offspring. However, it was suggested that due to inadequate maternal nutrient supply the maternal-fetal nutrient (e.g. glucose, amino acids) and hormonal transfer alters the intrauterine environment with parallel changes of the hormonal setpoints in the fetus. This may lead to persistent modifications in the offspring lasting the whole life. In particular the hypothalamo-pituitary-adrenal axis is thought to play a role in fetal programming. Conclusion: There are indications that also other hormonal systems may be involved which needs further study.