Komatsu S, Yamamoto M, Arishima K, Eguchi Y
Department of Anatomy II, School of Veterinary Medicine, Azabu University, Sagamihara, Japan.
J Anat. 1998 Nov;193 ( Pt 4)(Pt 4):551-7. doi: 10.1046/j.1469-7580.1998.19340551.x.
To investigate the effect of maternal adrenocortical hormones on the development of fetal pancreatic islet cells, pregnant rats were adrenalectomised on d 6 of gestation. On d 12-16 the growth patterns of fetal insulin-producing B cells, glucagon-producing A cells, and somatostatin-producing D cells were observed histometrically. Maternal adrenalectomy resulted in growth retardation of fetal B cells on d 12-15. Maternal corticosterone therapy prevented this retardation. Maternal adrenalectomy, however, did not affect the developmental patterns of A and D cells. By Western blotting and immunohistochemistry, glucocorticoid receptors were demonstrated to be present in the islet cells from d 12 to d 15. These results suggest that maternal adrenocortical hormones, glucocorticoids in particular, maintain the early development of fetal pancreatic B cells through their specific intracellular glucocorticoid receptor.
为研究母体肾上腺皮质激素对胎儿胰岛细胞发育的影响,在妊娠第6天对孕鼠进行肾上腺切除术。在妊娠第12 - 16天,通过组织测量法观察胎儿产生胰岛素的B细胞、产生胰高血糖素的A细胞和产生生长抑素的D细胞的生长模式。母体肾上腺切除术导致胎儿B细胞在第12 - 15天生长迟缓。母体皮质酮治疗可预防这种生长迟缓。然而,母体肾上腺切除术并不影响A细胞和D细胞的发育模式。通过蛋白质印迹法和免疫组织化学方法,证明在第12天至第15天胰岛细胞中存在糖皮质激素受体。这些结果表明,母体肾上腺皮质激素,尤其是糖皮质激素,通过其特定的细胞内糖皮质激素受体维持胎儿胰腺B细胞的早期发育。