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Influence of Maternal Cholestyramine Treatment on Cholesterol and Bile Acid Metabolism in Adult Offspring¹

Centre for Developmental Medicine, The University of British Columbia, 811 West 10th Avenue, Vancouver, British Columbia, Canada V5Z 1L7

To reduce ileal reabsorption of bile acids and to deplete hepatic cholesterol pools, female rats were fed a diet containing 5% (wt/wt) cholestyramine from 4 days prior to mating. Control rats were fed the same diet without cholestyramine. In one group on day 20 of gestation diet-fed dams and their fetuses were investigated. Additional pups were raised in litters of eight and nursed by their mothers for 30 days at which time they were weaned to the control diet. All dams were given the control diet from day 14 of lactation; at no time did neonates have access to cholestyramine. Offspring were raised until 3 months of age then fed the control, cholestyramine or a high fat, high cholesterol diet for 5 days. Maternal cholestyramine produced significant elevation of fetal hepatic 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase; fetal 7-hydroxylase (7-OH) activity, plasma cholesterol and triglyceride levels, however, were not significantly altered. The elevated HMG-CoA reductase activity persisted in liver and in addition was present in jejunum of 3-month-old male offspring challenged with the control or cholestyramine diet for 5 days. When challenged with the high fat, high cholesterol diet, male offspring from cholestyraminetreated dams had significantly higher plasma cholesterol levels but HMG-CoA reductase and 7-OH activity similar to controls. Maternal treatment had no apparent effect on plasma triglyceride or hepatic 7-OH in 3-month-old male offspring. Changes observed in females were generally similar, although far less pronounced than in the male. These studies demonstrate that maternal cholesterol status during gestation and early lactation can permanently influence cholesterol metabolism in adult offspring.

KEY WORDS: • maternal nutrition • long-term effects • plasma cholesterol • bile acids

¹ Supported by a grant from the Medical Research Council of Canada. S. M. I. supported by a Medical Research Council of Canada scholarship.

Manuscript received 9 May 1983.

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