Many studies have found an inverse association between fetal growth and cardiovascular disease related to the metabolic syndrome in adulthood. Nevertheless, the relative importance of genetics and the intrauterine environment remain unclear. The objective of the study was to test the fetal origins hypothesis and the fetal insulin resistance hypothesis by studying the impact of fetal growth on Body Mass Index (BMI) in young adulthood. In a nationwide cohort study, the Swedish Medical Birth Register for the years 1973–1979 was linked with the Military Service Conscription Register for 1990–1999. In 1998 a questionnaire was mailed to all male twins, included in the two registers, who were alive and still resident in Sweden. The study covers the 923 male twin pairs for which full data were available. Mixed linear models were used to estimate within-pair and between-pair differences in birthweight and their relations to BMI. A weak positive association was found among the monozygotic twins for the withinpair difference in birthweight and BMI. No significant association was found among the monozygotic for the between-pair difference in birthweight and BMI. No significant associations were found for dizygotic twins. These findings do not seem to support either the fetal programming hypothesis or the fetal insulin resistance hypothesis.

Human epidemiological and animal studies have revealed the late consequences of malnutrition during gestation and early life on the health of the offspring. These studies have highlighted the inverse relationship between birth weight and the incidence of insulin resistance and type 2 diabetes later in life. The aim of this paper is to review the different means of achieving foetal malnutrition and its consequences even for a next generation, in animal models and to identify key area for further research. We address the impact of two models of maternal malnutrition (protein restriction and caloric restriction) as well as the impact of maternal diabetes, the three maternal conditions leading to perturbed foetal nutritional environment. Particular emphasis is given to the endocrine pancreas and the insulin sensitive tissues. More specifically, alterations of the foetal nutritional environment perturb the development of the endocrine pancreas and target the ß cell mass at birth. Some adaptations later in life may take place but stress situations such as pregnancy and ageing precipitate the animals to glucose intolerance and insulin resistance. Even the next generation features alterations in the development of the endocrine pancreas. Some mechanisms by which the foetal ß cell mass is altered are approached in this review and specific attention is paid to the amino acid profile. The preventive role of taurine is discussed.

Assisted reproduction is used to resolve infertility problems in human and in breeding programs to generate livestock. Except for gestation length and birth weight, perinatal outcome of children conceived by In Vitro Fertilization is similar to that of spontaneously conceived children. However, large offspring syndrome observed after In Vitro Production in livestock is quite alarming. The distinct parts of assisted reproduction (oocyte maturation, fertilization and culture) have been found to contribute to abnormal fetal growth and development. Genomic imprinting is suggested to be involved in the induction of the aberrant phenotypes observed after assisted reproduction. Furthermore, current knowledge on postnatal health of offspring conceived by assisted reproduction and speculations on potential longterm effects of In Vitro Fertilization will be described.