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Ethanol‐Induced Intrauterine Growth Retardation: Correlation with Placental Glucose Transfer
Author(s) -
Snyder Ann K.,
Singh Sant P.,
Pulten Gordon L.
Publication year - 1986
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.1986.tb05066.x
Subject(s) - growth retardation , correlation , chemistry , endocrinology , medicine , pregnancy , biology , mathematics , genetics , geometry
Placental transfer of glucose and alanine analogs was studied at term in ethanol‐fed and control rats. Etnanol was provided as 30% of the caloric intake throughout gestation. Control groups received isocaloric liquid diet without etnanol by pair‐feeding (PF) or ad libitum (AF). On the 22nd day of pregnancy, the rats were injected with a mixture of [ 3 H] 2‐deoxyglucoe and [ 14 C]α‐aittfnoisobutyric acid. The ratios of f etakmatemal plasma radioactivities 1 hr later were used to compare placental transfer between the groups. Mean ± SE body weight of EF fetuses (4.54 ± 0.07 g) was significantly lower than that of PF (4.88 ± 0.06 g) or AF (5.17 ± 0.09 g) fetuses. Maternal etnanol ingestion reduced placental transfer of 2‐deoxyglucose and a‐ami‐noisobutyric acid by 12% and 35%, respectively. Placental transfer of both analogs was not affected in the PF controls. The weight of EF fetuses correlated ( p < 0.001) with transfer of 2‐deoxyglucose to the fetus. This relationship was also found in the control groups. Fetal body weight did not show a strong correlation with a‐aminoiso‐butyric acid transfer. Thus, impaired transfer of glucose to the fetus may play a significant role in the growth retardation observed in fetuses of ethanol‐fed rats.