The developmental growth of the rat fetus was studied between days 14 and 21 of pregnancy in normal control, established-diabetic, gestational-diabetic, and insulin-maintained–diabetic mothers. Measurements of fetal body weights and protein mass revealed a suppression of growth in the diabetic pregnancies, probably arising from reduced hyperplasia. Growth of the liver and skin appeared to be suppressed in proportion to the whole fetus, whereas the lung, brain, and particularly the heart were relatively well protected from growth retardation. Fetal growth during development, and its retardation in association with the hyperglycemic state, was explained by measuring the rates of fetal protein turnover in vivo. Both the protein synthetic and degradative rates gradually declined during normal development. However, in the diabetic pregnancies, fetal protein synthesis was consistently lower than control rates, whereas protein degradation increased sharply toward the end of gestation. These changes in protein synthesis and breakdown probably combine to yield a smaller fetus in the absence of normoglycemia.
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Original Articles| December 01 1988
Maternal Diabetes in Rats: II. Effects on Fetal Growth and Protein Turnover
James P Canavan;
Address correspondence and reprint requests to Dr. David F. Goldspink, Heart Research Unit, Killingbeck Hospital, York Road, Leeds LS14 6UQ, UK.
James P Canavan, David F Goldspink; Maternal Diabetes in Rats: II. Effects on Fetal Growth and Protein Turnover. Diabetes 1 December 1988; 37 (12): 1671–1677. https://doi.org/10.2337/diab.37.12.1671
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