Regulation of fetal amino acid metabolism: substrate or hormonal regulation?

Insulin is regarded as the primary fetal growth-promoting hormone, but direct in vivo experimental data supporting this conjecture are sparse. Data obtained from studies in in vivo, chronically catheterized fetal lambs under a variety of experimental circumstances demonstrate that glucose availability is the primary modulator of fetal protein accretion, via its ability to diminish amino acid catabolism. The ovine fetus is shown to be resistant to insulin-induced suppression of proteolysis, relative to the adult. Data from studies in the human premature infant show that the findings in the ovine fetus are similar to those in the ex utero premature human.