Pregnancy is a state of high metabolic demand. Fasting diverts metabolism to fatty acid oxidation, and the fasted response occurs much more rapidly in pregnant women than in the non-pregnant state. The product of the imprinted Delta-like homologue 1 gene (DLK1) is an endocrine signaling molecule that reaches a high concentration in the maternal circulation during late pregnancy. By utilising murine models with deleted Dlk1 we show that the fetus is the source of maternal circulating DLK1. In the absence of fetally-derived DLK1, the maternal fasting response is impaired. Furthermore, we found that maternal circulating DLK1 levels predict embryonic mass in mice and can differentiate healthy small for gestational age (SGA) from pathologically small infants in a human cohort. Therefore measurement of DLK1 in maternal blood may be a valuable method for diagnosing human disorders associated with impaired DLK1 expression, and to predict poor intrauterine growth and complications of pregnancy.

Genomic imprinting is an epigenetic process causing expression of a subset of genes in a parent-of-origin-specific manner. Among vertebrates, only therian mammals have been demonstrated to imprint, indicating that placentation and imprinting arose at similar time points in evolution and that imprinting may be involved in key mammal-specific processes. However, although several theories have been posited to explain the evolution of imprinting, each has shortcomings and none fully explains the wide variety of genes regulated by imprinting. In this review, we catalog the phenotypes associated with genetic mutation and overexpression at particular imprinted loci in order to consider the wide impact of imprinted genes on development. In addition to the well-described roles of imprinted genes in prenatal growth and placentation, more recent data emphasize that imprinted genes are critical for specific aspects of postnatal mammalian development involving adaptive processes, metabolism, and behavior.

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Introduction Developmental coordination disorder is a neurodevelopmental disorder affecting motor ability, with an estimated prevalence of between 2% and 6% in school-aged children. It is associated with considerable psychosocial impact. However, the financial cost this poses to families and society has never been assessed. We aimed to estimate the direct, indirect and out-of-pocket costs associated with developmental coordination disorder in United Kingdom school-aged children in the 6 months prior to our survey. Method Parents/guardians answered an online questionnaire adapted from the Client Service Receipt Inventory. Results Mean direct healthcare costs were approximately £700 in the 6 months prior to the survey. Almost all children were in mainstream education, but many received additional support. Among children who received therapy, the average indirect cost was £574 in the 6 months prior to the survey. However, this did not include changes to employment made to accommodate caring for the child. Notably, respondents commented that they frequently struggled to access services for their children. Thus, these figures may be a marked underestimation of true need. Conclusion This study represents the first cost-of-illness study for developmental coordination disorder. It demonstrates that developmental coordination disorder incurs a significant cost to society but particularly to families. Improvements to diagnostic pathways and post-diagnosis service provision are much needed.