Abstract

To study the role of undernourishment in the negative effects of ethanol during pregnancy and to determine whether maternal ethanol intake modifies metabolic response to starvation at late gestation, female rats receiving ethanol in their drinking water before and during pregnancy (ethanol group) were compared with animals that received the same amount of solid diet as the ethanol group rats (pair-fed group) and with normal rats fed ad libitum (control group). All animals were killed on the 21st day of gestation, either in the fed state or after 24-hours fasting. The body weight of ethanol rats was lower than that of controls but higher than that of pair-fed rats. When compared with controls, ethanol and pair-fed rats had reduced fetal body weights, whereas fetal body length was reduced only in the former. In the fed state, blood glucose concentration was lower in the ethanol and pair-fed rats and fetuses than in controls. Twenty-four-hour starvation caused a reduction in this parameter only in control and ethanol mothers. In the fed state, maternal liver glycogen concentration was lower in ethanol and higher in pair-fed mothers than in controls. Blood β-hydroxybutyrate levels were higher in ethanol-treated mothers than in the others, and 24-hour starvation increased this parameter in ethanol and control rats to a greater extent than in the pair-fed ones. Liver triacylglyceride concentration was higher in ethanol-treated mothers than in the other two groups, and starvation caused this concentration to increase in ethanol and control groups but not in the pair-fed group. Maternal liver lipoprotein lipase activity did not differ among the groups when fed, but increased significantly with starvation in controls and ethanol-treated rats. Individual values of lipoprotein lipase activity in all the starved groups correlated with liver triacylglyceride concentrations. Results indicate that maternal undernourishment in ethanol-treated rats contributes to the negative effects of ethanol on fetal development in addition to certain other changes, such as the increase in maternal redox state and in circulating and liver triglycerides, directly related to ethanol oxidation. The intense maternal hypoglycemia observed in rats from the ethanol group could impair glucose availability to the fetus, and this situation would worsen with starvation. The higher hepatic glycogen levels in pair-fed mothers and their fetuses in the fed state as compared with the ethanol group, in spite of their similar hypoglycemia, seems to indicate a different metabolic adaptation in the two groups. A relationship is proposed in the starved condition between maternal liver lipoprotein lipase activity and changes in liver triacylglyceride and circulating ketone bodies in the three groups studied. The findings seem to indicate that, in spite of the metabolic disturbances produced by ethanol intake in the mother, the response to starvation in ethanol rats was similar to the one observed in controls, and different from the one in the pair-fed animals.

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