Neonatal hypoglycaemia and hyperinsulinism at birth (cord C-peptide)
LGA
LATE PREGNANCY, HYPERINSULINISM, EARLY PREGNANCY, NEONATAL HYPOGLYCAEMIA, NEONATAL HYPOGLYCAEMIA
Neonatal hypoglycaemia and cord C-peptide were both associated with metabolite changes from the first trimester, during the period of fetal pancreatic development. Early pregnancy TAG abundance (maternal lipolysis, maternal diet) was strongly associated with neonatal hypoglycaemia, while both lipids and phenols showed associations with cord C-peptide. Previous work suggested that lipid storage is likely to be prioritised over lipid mobilisation in early pregnancy, with lipid mobilisation more common in late pregnancy [Although LGA is believed to be related to increased fetal insulin production resulting in increased growth, it had a distinct metabolite profile when compared with neonatal hypoglycaemia and cord blood C-peptide, considered an indirect and direct assessment of neonatal hyperinsulinism, respectively. First, neonatal hypoglycaemia and cord C-peptide both showed changes from the first trimester, while LGA did not. Second, neonatal hypoglycaemia and cord C-peptide both showed prominent increases in TAGs in maternal serum (12 weeks in neonatal hypoglycaemia, 34 weeks in cord C-peptide) which was a less prominent feature of LGA. However, cord blood associations in all three analyses featured carnitines, most prominently in cord blood C-peptide analysis. These differences may suggest that these conditions have true pathophysiological differences, but may also reflect the challenges of suitably measuring these complex conditions, with different time periods of interest. In the analysis of cord blood C-peptide, the outcome of interest is being studied at exactly the same time as the metabolites (also in cord blood). However, LGA develops over months, and neonatal hypoglycaemia may not be evident until 4–24 h after birth.