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Journal of Nutrition Vol. 110 No. 7 July 1980, pp. 1432-1440
Copyright © 1980 by American Society for Nutrition
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Glucose Homeostasis in Fetuses of Protein-Deprived and Hypothyroid Pregnant Rats1

Denise M. Brown, Ruth E. Shrader and Frances J. Zeman2

Department of Nutrition, University of California, Davis, CA 95616

Blood glucose and hepatic glycogen were compared in 21-day fetal progeny of rats on five dietary regimens. Three diets were fed ad libitum: the control diet (24% casein), the protein-deficient (PD) diet (4% casein) and the propylthiouracil (PTU) diet (24% casein + 0.2% PTU). In addition, one group of pregnant dams was given the 24% casein diet in amounts which matched the food intake of the protein deprived dams (PF-PD), and another group received the control ration in the quantity eaten by its PTU-fed counterpart (PF-PTU). Blood glucose was significantly reduced in progeny of PD dams, while liver glycogen levels were significantly depressed in young of both PD and PTU dams. Progeny of dams in the PF-PD and PF-PTU groups showed no significant change in either blood glucose or liver glycogen as compared with controls. Hepatic levels of glucose-6-phosphatase (G6Pase), {alpha}-glucan phosphorylase (P'lase), phosphoglucomutase (PGM), glucose-6-phosphate dehydrogenase (G6PDH) and phosphoenolpyruvate carboxykinase (PEPCK) were, therefore, examined only in 21-day fetal young of ad libitum-fed control, PD and PTU dams. G6Pase, PGM, G6PDH and PEPCK were significantly increased in PD pups. In the PTU young, G6Pase was decreased and G6PDH and PEPCK increased. These observations suggest that the reduction in blood glucose in PD progeny is not due to altered levels of the enzymes examined, but may result from increased utilization of glucose by the liver and possibly other peripheral tissues. Depression in liver glycogen may be the consequence of maternal malnutrition and hypothyroidism resulting in a net deficit of substrate available for fetal glycogen synthesis.


KEY WORDS: • development • fetus • glycogen • protein deficiency

1 Presented in part at the 1979 joint meeting of the American Institute of Nutrition, American Society for Clinical Nutrition and Nutrition Society of Canada, Guelph, Ontario, Canada, 5–7 July 1979.

2 To whom reprint request should be sent.

Manuscript received 13 November 1979.





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