Canavan J P, Goldspink D F
Department of Cardiovascular Studies, University of Leeds, England, United Kingdom.
Diabetes. 1988 Dec;37(12):1671-7. doi: 10.2337/diab.37.12.1671.
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.
在正常对照、已确诊糖尿病、妊娠期糖尿病和胰岛素维持治疗的糖尿病母亲中，研究了妊娠第14天至21天大鼠胎儿的发育生长情况。对胎儿体重和蛋白质质量的测量显示，糖尿病妊娠中胎儿生长受到抑制，这可能是由于增生减少所致。肝脏和皮肤的生长似乎与整个胎儿成比例受到抑制，而肺、脑，尤其是心脏相对较好地免受生长迟缓的影响。通过测量体内胎儿蛋白质周转速率，解释了发育过程中的胎儿生长及其与高血糖状态相关的生长迟缓。在正常发育过程中，蛋白质合成和降解速率均逐渐下降。然而，在糖尿病妊娠中，胎儿蛋白质合成始终低于对照速率，而在妊娠末期蛋白质降解急剧增加。在血糖不正常的情况下，蛋白质合成和分解的这些变化可能共同导致胎儿较小。
