GC that are not inactivated by the fetoplacental 11β-hydroxysteroid dehydrogenase-unequivocally reduce morbidity in preterm neonates but have a mildly detrimental effect on growth ( 5– 8). Repeated antenatal courses of betamethasone or dexamethasone- i.e. IGFBP-1 acts as a growth-inhibitory factor ( 2, 3), presumably because the formation of IGF-I:IGFBP-1 complexes reduces free IGF-I concentrations ( 4). Intrauterine growth is driven by the availability of oxygen and nutrient substrates (glucose, FFA, and AA), and by the endocrine and intratissue effects of insulin, IGF-I and IGF-II, and the IGF-binding proteins (IGFBP) ( 1). Future research should clarify the role of IGF-I in the protein-catabolic response to GC. These changes may explain the growth-inhibitory effects of repeated antenatal GC administration. In conclusion, an antenatal course of GC elicited a transient catabolic state encompassing all nutrient substrates, and a temporary drop in IGF-I concentrations. Shorter duration since GC administration and lower IGF-I concentrations independently predicted AA levels. Although all AA were transiently increased, the increment was most robust for glutamine and alanine. The AA surge was greater in newborns with a birth weight z score 0. We found that recent GC exposure (≤48 h) raised glucose, FFA, and AA concentrations, and the homeostasis model assessment of insulin resistance (HOMA-IR) index, but lowered IGF-I concentrations. We analyzed umbilical vein (UV) plasma obtained at birth from 91 preterm newborns that received one course of GC (last exposure 1–1358 h before birth) and 49 newborns that did not. Here we explored the effect of antenatal GC on nutrient substrates, and on IGF-I and IGF-binding protein-1 (IGFBP-1). Glucocorticoid (GC) administration before preterm birth reduces neonatal morbidity but may restrain growth.
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