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High and low maternal protein intake of pregnant rats reduces incorporation of food derived amino acids into fetal protein
Author(s) -
Petzke Klaus Jürgen,
DaenzerWiedmer Maren,
Günther Jeanette,
Lang Iris,
Kucia Merzena,
Klaus Susanne,
Metges Cornelia
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.869.1
Subject(s) - fetus , medicine , endocrinology , gestation , amino acid , leucine , taurine , metabolism , placenta , weaning , pregnancy , chemistry , biology , biochemistry , genetics
It has been shown that maternal dietary protein (P) intake affects fetal and post weaning growth (Daenzer et al., J. Nutr. 132: 142, 2002). We studied amino acid (AA) metabolism of pregnant mothers and their fetuses. Female rats were pair‐fed isocaloric diets of either low (LP, 10%), adequate (control, CP, 20%) or high casein content (HP, 40%) from start of mating throughout gestation. On gestation d 14 and 19 the plasma AA concentrations and relative incorporation (RI) of orally administered 13 C‐lysine (Lys) and 13 C‐leucine (Leu) in placental and fetal P based on product/precursor relationships was measured. Placental and fetal weights were not different. Maternal plasma AA showed higher concentrations of branched chain AA in HP, whereas taurine concentrations were increased in LP and CP, but not in HP (P < 0.05). Maternal plasma P 13 C‐enrichment decreased with increasing maternal P intake. On d 14 and 19 RI Lys and RI Leu in placental and fetal P were significantly lower (P < 0.05; except P > 0.05 for HP on day 19) in LP and HP fed rats as compared to CP. The data suggest that oxidative losses of AA induced by HP feeding may have consequences for placental and fetal P synthesis. An inadequate maternal P intake alters intrauterine AA metabolism which underlies fetal growth retardation.