Reece E A, Pinter E, Leranth C, Hobbins J C, Mahoney M J, Naftolin F
Department of Obstetrics and Gynecology, Yale University School of Medicine, New Haven, Connecticut.
Obstet Gynecol. 1989 Nov;74(5):755-62.
We described previously the morphologic alterations of the visceral endodermal yolk sac cells of rat conceptuses cultured under hyperglycemic conditions which occurred concomitantly with major embryonic malformations. To determine whether the transport function of the yolk sac was impaired simultaneously as a result of these hyperglycemic conditions, horseradish peroxidase was used as a tracer protein to assess the transport function of the visceral endodermal yolk sac cells of conceptuses cultured in both control and hyperglycemic media. Cellular uptake of peroxidase, which was added to the culture medium for 3 or 24 hours, was observed in controls. This differed from the marked diminution in peroxidase uptake seen in conceptuses cultured in hyperglycemic medium. These results demonstrate that during hyperglycemia-induced embryopathy, there is concomitant yolk sac failure evidenced by morphologic alterations and impaired endocytosis. These findings therefore strengthen our hypothesis that diabetes-related malformations, as demonstrated experimentally in rat conceptuses, are associated with impairment in the structure and functions of the visceral yolk sac cells during a critical period of organogenesis.
我们之前描述过，在高血糖条件下培养的大鼠胚胎的脏内胚层卵黄囊细胞的形态学改变，这些改变与主要的胚胎畸形同时出现。为了确定由于这些高血糖条件，卵黄囊的转运功能是否同时受损，辣根过氧化物酶被用作示踪蛋白，以评估在对照培养基和高血糖培养基中培养的胚胎的脏内胚层卵黄囊细胞的转运功能。在对照中观察到添加到培养基中3或24小时的过氧化物酶的细胞摄取。这与在高血糖培养基中培养的胚胎中过氧化物酶摄取的显著减少不同。这些结果表明，在高血糖诱导的胚胎病期间，存在伴随的卵黄囊功能衰竭，表现为形态学改变和内吞作用受损。因此，这些发现强化了我们的假设，即如在大鼠胚胎中实验所示，糖尿病相关的畸形与器官发生关键期内脏卵黄囊细胞的结构和功能受损有关。
