Our objective is to establish the importance of glutamine (GLN) nutrition and metabolism during normal pregnancy. We hypothesize that dietary GLN deprivation during pregnancy results in compensatory mechanisms in the mother, fetus, and/or placenta which insure GLN sufficiency. Maternal plasma amino acid profile at term, weight gain during pregnancy, fetal hepatocyte GLN transport (system N), litter size and weight, and fetal weight near term were examined in 5 rat dams which were given a diet lacking GLN (GLN-) and 4 control dams which received an isonitrogenous diet containing a normal amount of GLN (GLN+). Glutamine synthetase (GS) activities in placenta, maternal and fetal, liver, lung, small intestine, and maternal skeletal muscle were also measured near term. Dietary treatment began approximately 5 days prior to ovulation. Results (means ± S.D., * p <0.05): GLN-dams had higher total plasma amino acids (140±75 vs 48±42μMoles·dl-1)*, higher liver GS activities (25.4±6.9 vs 17.0±3.8 μM γ-glutamylhydroxamate·mg-1·h-1)*, and smaller litters (13.2±2.3 vs 16.3)* compared to GLN+ dams. These results suggest that dietary GLN deprivation may cause mobilization of amino acid stores, compensatory increases in maternal liver GS activity, and reduced implantation efficiency. Furthermore, hepatocytes from the fetuses of GLN- dams transported 85% more GLN into cells than did hepatocytes from the fetuses of control dams(234±41 vs 126±23 pmoles·mg protein-1·min-1)*. GLN- dams tended to gain less weight(47.6±8.3 vs 53.6±6.2%) and they may have compensated for smaller litter size by producing larger pups (3.9±1.2 vs 3.3±0.8 g). They may have done so at the expense of their own body weight.

This study was supported by NIH grant RO1 HD29279 to J. Neu.