Obesity and type 2 diabetes are serious health issues in the developed world and are becoming increasingly important on a global scale. Furthermore, the marked increases in both childhood obesity and type 2 diabetes will translate to further increases in adult obesity, diabetes and associated co-morbidities in the near future; as such it has been ranked as a critical public health threat. It is a widely held view that the primary cause of obesity is the development of an obesogenic environment, due to ease of access to highly calorific food and reduced energy expenditure in work and leisure activities. In addition there is strong evidence for a genetic component to human obesity with the identification of a number of genes associated with human obesity. However, on its own the genetic component of this condition cannot account for the dramatic increase in the prevalence of obesity in recent years. Of relevance and as highlighted by epidemiological and experimental studies, is the relationship between the periconceptual, fetal and early infant phases of life and the subsequent development of adult obesity. The terms “developmental programming” and the “Developmental Origins of Adult Health and Disease” are preferentially used to describe these relationships. Despite initial controversy when these relationships were first suggested, both prospective clinical and experimental studies have clearly shown that the propensity to develop abnormalities of cardiovascular, endocrine and metabolic homeostasis in adulthood are increased when fetal development has been adversely affected. This pathogenesis is not based on genetic defects but on altered gene expression seen as a result of fetal adaptation to an adverse intrauterine environment. The relative role of genetic versus environmental factors and the mechanisms underlying developmental programming remain speculative. It is generally argued that in response to an adverse intrauterine environment, the fetus adapts its physiological development to maximise its immediate chances for survival. Owing to the plasticity of the fetus, these adaptations may include resetting of metabolic homeostasis and endocrine systems and the down-regulation of growth, commonly reflected in an altered birth phenotype. It is thought that whilst these changes in fetal physiology (i.e. the prenatal environment) may be beneficial for short term survival in utero they may be maladaptive in postnatal life, contributing to poor health outcomes when offspring are exposed to catch-up growth, diet-induced obesity and other factors. The “predictive adaptive response” hypothesis proposes that the degree of mismatch between the pre- and postnatal environments is a major determinant of subsequent disease. This review will address recent work in animal models and observations in the clinical and epidemiological settings on in utero adaptations and subsequent development of obesity and type 2 diabetes.