Since the rediscovery of brown adipose tissue (BAT) in adult human subjects in 2007, there has been a dramatic resurgence in research interest in its role in heat production and energy balance. This has coincided with a reassessment of the origins of BAT and the suggestion that brown preadipocytes could share a common lineage with skeletal myoblasts. In precocial newborns, such as sheep, the onset of non-shivering thermogenesis through activation of the BAT-specific uncoupling protein 1 (UCP1) is essential for effective adaptation to the cold exposure of the extra-uterine environment. This is mediated by a combination of endocrine adaptations which accompany normal parturition at birth and further endocrine stimulation from the mother's milk. Three distinct adipose depots have been identified in all species studied to date. These contain either primarily white, primarily brown or a mix of brown and white adipocytes. The latter tissue type is present, at least, in the fetus and, thereafter, appears to take on the characteristics of white adipose tissue during postnatal development. It is becoming apparent that a range of organ-specific mechanisms can promote UCP1 expression. They include the liver, heart and skeletal muscle, and involve unique endocrine systems that are stimulated by cold exposure and/or exercise. These multiple pathways that promote BAT function vary with age and between species that may determine the potential to be manipulated in early life. Such interventions could modify, or reverse, the normal ontogenic pathway by which BAT disappears after birth, thereby facilitating BAT thermogenesis through the life cycle.

Changes in maternal diet at different stages of reproduction can have pronounced influences on the health and well-being of the resulting offspring, especially following exposure to an obesogenic environment. The mechanisms mediating adaptations in development of the embryo, placenta, fetus and newborn include changes in the maternal metabolic environment. These changes include reductions in a range of maternal counter-regulatory hormones such as cortisol, leptin and insulin. In the sheep, for example, targeted maternal nutrient restriction coincident with the period of maximal placental growth has pronounced effects on the development of the kidney and adipose tissue. As a consequence, the response of these tissues varies greatly following adolescent-onset obesity and ultimately results in these offspring exhibiting all the symptoms of the metabolic syndrome earlier in young adult life. Leptin administration to the offspring after birth can have some long-term differential effects, although much higher amounts are required to cause a response in small compared with large animal models. At the same time, the responsiveness of the offspring is gender dependent, which may relate to the differences in leptin sensitivity around the time of birth. Increasing maternal food intake during pregnancy, either globally or of individual nutrients, has little positive impact on birth weight but does impact on liver development. The challenge now is to establish which components of the maternal diet can be sustainably modified in order to optimise the maternal endocrine environment through pregnancy, thus ensuring feto–placental growth is appropriate in relation to an individual's gender and body composition.

The ability to not only replicate but also extend the findings from both historical epidemiological studies and contemporary cohorts of the developmental programming of later disease are critical if the mechanisms by which early diet impacts on later disease are to be fully understood. To date, a plethora of models have been established, with the range including global changes in dietary input, imbalanced diets and diets deficient in single nutrients. Key factors in translating these findings to the human situation are the pronounced differences in the relative growth and development between large and small mammals from the time of conception through pregnancy, lactation and weaning. This disparity is reflected in the very different nutritional requirements between species and the substantial divergence between rodents and large animals in the ontogeny of many of the organ systems that are nutritionally regulated. For example, hypothalamic circuitry is much more developed in species with a long gestation and offspring are born with a mature hypothalamic–pituitary axis in sheep and man compared with mice and rats. Similarly, nephron number is established towards the end of gestation in large mammals compared with the lactational period in rats. These types of differences will impact on the ability of individual and combined nutritional interventions to reset developmental processes, and may be further compounded by the gender of a fetus. The challenge for future work in this exciting and dynamic area of research is to utilise these marked comparative differences to generate imaginative nutritional interventions in order to improve the viability, health and well-being of the offspring.