Whilst epidemiological studies robustly support the relationship between compromised maternal energy homeostasis and poor fetal and postnatal outcome, very little is known about the genetic pathways which control maternal energy allocation to the offspring. In turn, how maternal nutrient partitioning influences the growth and proportionality of the organism is not well understood. Furthermore, bi-directional communication between mother and fetus underlie these events and deciphering the molecular signals involved using genetic tools is now feasible and timely. Late gestation in mammals is accompanied by multiple adaptations of maternal energy homeostasis that are thought to divert maternal resources towards the supply of glucose for the rapidly-growing fetus. These adaptations include peripheral insulin resistance and a reduction in hepatic lipogenesis (1). During pregnancy there is considerable remodelling of the anterior pituitary which causes an increase in somatolactotrophic cells (2). In addition, the syncytiotrophoblast cells of the placenta secrete placental lactogen and a pregnancy-specific version of growth hormone (GH) (2). Since GH and its family members are known to cause insulin resistance and inhibit hepatic lipogenesis (1, 3), increased activity of the pituitary-placental sommatolactotrophic axis may modulate maternal adaptations in late pregnancy. The product of the imprinted Delta-like homologue 1, DLK1, is an endocrine signalling molecule that reaches a high concentration in maternal serum during late pregnancy (4). We have recently discovered that that the conceptus is the source of this molecule. DLK1 may be a novel endocrine signal from fetus to mother. Our studies with genetically-modified mice show that endocrine DLK1 acts to inhibit hepatic lipogenesis (5 and in preparation). Our working hypothesis is that DLK1 produced by the conceptus alters the activity of the pituitary-placental somatolactotrophic axis, thus modulating important metabolic changes in maternal resource allocation during pregnancy. Understanding the function of DLK1 in pregnancy has potential clinical value since failures of growth and timely development occur when maternal resource allocation is disrupted. Moreover, maternal serum DLK1 could be a non-invasive biomarker for complications of pregnancy, and/or genetic variation in Dlk1 sequences in mother or fetus may be indicative of poor pregnancy outcome.