Abstract
When streptozotocin-induced diabetes is produced early in gestation in rats, fetal growth is markedly compromised Cross-linking of proteins is increased in the diabetic, due to formation of advanced non-enzymatic glycosylation products (AGP) Aminoguanidine (A), a nucleophilic hydrazine compound, prevents formation of AGP and cross-linking of arterial proteins in vivo in diabetic rats. We administered aminoguanidine (25 rag/Kg IP) daily to control and diabetic rats from day 5 of gestation to sacrifice on day 21. Aminoguanidine produces increased fetal growth in diabetic pregnancies, while slightly retarding fetal growth in controls. Increased placental size in diabetic pregnancies is unaffected by aminoguanidine. These data suggest that reduced fetal growth in diabetic pregnancies may result from non-enzymatic glycosylation.
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