This review will focus on the mechanisms leading to ROP by exploring factors responsible for poor early weight gain and abnormal vascularisation of the eye of the preterm infant.

Abstracts also expressed by the gastric mucosa and pancreatic β-cells) in fetal samples from LGA and appropriate-for-gestational-age-(AGA) pregnancies and study their association with gender, parity, and delivery mode. Methods Cord blood nesfatin-1 concentrations were prospectively measured by enzyme-linked immunosorbent assay in 40 LGA (9 born from diabetic mothers and 31 born from non-diabetic mothers) and 20 AGA singleton full-term infants.Results Cord blood nesfatin-1 concentrations were lower in LGA compared to AGA neonates, after controlling for confounding factors (b= -0.206, p=0.005, SE 0.07). However, cord blood nesfatin-1 concentrations were elevated in infants born from mothers presenting with gestational diabetes mellitus (GDM), compared to those born from non-diabetic mothers, after controlling for group (b=0.190, p=0.050, SE 0.10). Finally, cord blood nesfatin-1 concentrations were lower in cases of vaginal delivery (b=0.11, p=0.042, SE 0.05). Conclusions Down-regulation of nesfatin-1 in LGA fetuses probably represents a negative feedback exerted by adipose tissue on nesfatin-1 production. On the other hand, fetal nesfatin-1 concentrations are higher in cases of GDM, probably indicating the possible involvement of nesfatin-1 in the regulation of insulin secretion from pancreatic β-cells. Finally, vaginal delivery-associated inflammation could probably account for lower cord blood nesfatin-1 concentrations.