Regulation of uterine and umbilical amino acid uptakes by maternal amino acid concentrations

We tested the hypothesis that decreased fetal amino acid (AA) supply, produ ced by maternal hypoaminoacidemia (low AA) during hyperglycemia (HG), is re versible with maternal AA infusion and regulates fetal insulin concentratio n ([I]). We measured net uterine and umbilical AA uptakes during maternal H G/low AA concentration ([AA]) and after maternal intravenous infusion of a mixed AA solution. After 5 days HG, all maternal [AA] except glycine were d ecreased >50%, particularly essential [AA] (P < 0.00005). Most fetal [AA] a lso were decreased, especially branched-chain AA (P < 0.001). Maternal AA i nfusion increased net uterine uptakes of Val, Leu, Ile, Met, and Ser and ne t umbilical uptakes of Val, Leu, Ile, Met, Phe, and Arg but did not change net uteroplacental uptake of any AA. Fetal [I] increased 55 +/- 14%, P < 0. 001, with correction of fetal [AA], despite the lack of change in fetal glu cose concentration. Thus generalized maternal hypoaminoacidemia decreases u terine and umbilical uptakes of primarily the essential AA and decreases fe tal branched-chain [AA]. These changes are reversed with correction of mate rnal [AA], which also increases fetal [I].