Giavini E
Dipartimento di Biologia, Università degli Studi, Milan, Italy.
Ann Ist Super Sanita. 1993;29(1):27-34.
Substantial literature indicates that diabetes in pregnant rats and mice induces embryo lethality, growth retardation, and a variable incidence of birth defects. All these embryopathic effects appear to be mediated by several factors, e.g. genetic disposition and the composition of the diets eaten by the animals. Studies carried out on rodent embryos cultured in vitro showed that numerous components of the diabetic state (ketone bodies, somatomedin inhibitors, low concentrations of insulin) display a dysmorphogenic potential. Besides, diabetes-induced malformations have been often related, both in vivo and in vitro studies, to morphological and physiological alterations of the yolk sac, the principal organ for the passage of nutrients from the mother to the rodent embryo. On the whole, in vivo and in vitro experiments indicate that hyperglycemia itself is not a major factor in producing diabetic embryopathies that are more likely ascribable to severe alterations of the embryonic energetic balance.
大量文献表明,妊娠大鼠和小鼠患糖尿病会导致胚胎致死、生长迟缓以及不同发生率的出生缺陷。所有这些胚胎病变效应似乎是由多种因素介导的,例如遗传倾向和动物所食用的饮食成分。对体外培养的啮齿动物胚胎进行的研究表明,糖尿病状态的许多成分(酮体、生长调节素抑制剂、低浓度胰岛素)具有致畸潜力。此外,在体内和体外研究中,糖尿病诱导的畸形通常与卵黄囊的形态和生理改变有关,卵黄囊是营养物质从母体传递到啮齿动物胚胎的主要器官。总体而言,体内和体外实验表明,高血糖本身并不是导致糖尿病胚胎病变的主要因素,这些病变更可能归因于胚胎能量平衡的严重改变。