It is now apparent that one key factor determining the current obesity epidemic within the developed world is the extent to which adipose tissue growth and function can be reset in early life. Adipose tissue can be either brown or white, with brown fat being characterised as possessing a unique uncoupling protein (uncoupling protein 1) that enables the rapid generation of heat by non-shivering thermogenesis. In large mammals this function is recruited at approximately the time of birth, after which brown fat is lost, not normally reappearing again throughout the life cycle. The origin and developmental regulation of brown fat in large mammals is therefore very different from that of small mammals in which brown fat is retained throughout the life cycle and may have the same origin as muscle cells. In contrast, white adipose tissue increases in mass after birth, paralleled by a rise in glucocorticoid action and macrophage accumulation. This process can be reset by changes in the maternal nutritional environment, with the magnitude of response being further determined by the timing at which such a challenge is imposed. Importantly, the long-term response within white adipocytes can occur in the absence of any change in total fat mass. The present review therefore emphasises the need to further understand the developmental regulation of the function of fat through the life cycle in order to optimise appropriate and sustainable intervention strategies necessary not only to prevent obesity in the first place but also to reverse excess fat mass in obese individuals.
Pregnancy: Growth: Metabolism: Uncoupling proteinsObesity is of immense importance, affecting almost all organ systems, and is a risk factor for hypertension, type 2 diabetes, cardiovascular mortality and renal disease. Ultimately, obesity is associated with an increased relative risk of mortality (1) . Whilst not all obese adults were overweight children, being overweight in childhood is a good predictor of excess fat mass as an adult (2) . Indeed, recent data have demonstrated a 16-fold increase in the prevalence of the metabolic syndrome in overweight adolescents compared with their normal-weight peers (3) . Furthermore, the adverse effects of early obesity appear to be exacerbated in those individuals previously exposed to a suboptimal nutritional environment in utero (4) . The understanding of the impact of early-life events on later susceptibility to obesity needs to include the pronounced changes in adipocyte lineage that commence in utero at critical stages of development. This information needs to be combined with a full appreciation of the substantial differences between the species used in animal investigations of obesity, to inform knowledge not only of fat distribution but also of how the interaction between diet and energy status can vary.
Adipocyte regulation in early lifeThere are at least two key factors in early life that are critical in determining adipose tissue function in the Abbreviations: PRDM, PR-domain-containing; TLR4, toll-like ...