Growth retardation during early organogenesis in embryos of experimentally diabetic rats.
Embryos from rats rendered diabetic with streptozotocin for 1 wk or more before conception were examined on day 11.5 of gestation (i.e., at the 26-29-somite stage of normal rat embryonic development). The studies were designed to assess whether poorly regulated maternal diabetes is associated with demonstrable abnormalities even during this early phase of embryogenesis. We found that manifest retardations in growth and development were invariably present as judged by significant reductions in crown-rump length and somite number, respectively. Total protein and DNA content of the embryos were also reduced, although not symmetrically, so that protein/DNA ratios were increased. Gross dysmorphogenic lesions in neural tissue disproportional to the overall growth retardation at 11.5 days could not be demonstrated. The findings suggest that maternal diabetes can compromise intra-uterine growth and development during the period preceding and coinciding with the establishment of circulation in the allantoic placenta. The possible multifactorial determinants remain to be elucidated. It also remains to be established whether the early embryotoxicity provides a setting conducive to the increased dysmorphogenesis that is traditionally recognized during the later stages of pregnancy complicated by diabetes.
D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D001835:Body Weight; D004247:DNA / Q000032:analysis; D003921:Diabetes Mellitus, Experimental / Q000150:complications / Q000196:embryology*; D004622:Embryo, Mammalian / Q000032:analysis; D005260:Female; D005317:Fetal Growth Retardation / Q000209:etiology*; D005328:Fetal Viability; D005865:Gestational Age; D009024:Morphogenesis; D011247:Pregnancy; D011254:Pregnancy in Diabetics / Q000150:complications; D051381:Rats
D001786:Blood Glucose; D004247:DNA