Aerts L, Vercruysse L, Van Assche F A
Laboratory of Obstetrics and Gynaecology, U.Z. Gasthuisberg, Leuven, Belgium.
Diabetes Res Clin Pract. 1997 Oct;38(1):9-19. doi: 10.1016/s0168-8227(97)00080-6.
Diabetes of the mother during pregnancy induces structural and functional adaptations in the fetal endocrine pancreas. We have previously shown in our experimental rat model, that the impact of this abnormal intra-uterine milieu leads, in the adult offspring, to a disturbance of the glucose homeostasis and to the development of gestational diabetes. The aim of the present work is to investigate wether these functional differences can be explained by structural differences at the level of the endocrine pancreas. Therefore the size and the structure of the endocrine pancreas, as well as the contribution of the insulin-, glucagon-, somatostatin- and PP-cells, were investigated morphometrically in the adult youngsters of mildly and of severely diabetic mothers, since both display a disturbed glucose tolerance but with divergent characteristics. Also the adaptation of their endocrine pancreas to pregnancy was measured and compared to that of a control pregnancy. In the offspring of mildly diabetic mothers, the size of the endocrine pancreas and the distribution of the islets of Langerhans are normal. Also the doubling of the endocrine mass during pregnancy is similar to controls. The high proportion of A-cells, especially in relation to a normal B-cell mass and the low amount of PP-cells, might play a role in the impairment of the insulin response in these animals and in the development of gestational diabetes. In the offspring of severely diabetic mothers a clear hypertrophy of the endocrine pancreas is noted, which is mainly due to the presence of numerous small islets and which does not increase further during pregnancy. In these animals, the size of the endocrine pancreas and of the B-cell mass have reached 'pregnant' values without pregnancy, which coincides with an exaggerated insulin output and peripheral insulin resistance, as during normal pregnancy. No further increase in islet mass is seen during pregnancy, which is associated with gestational diabetes.
母亲孕期患糖尿病会使胎儿内分泌胰腺发生结构和功能上的适应性变化。我们之前在实验大鼠模型中表明,这种异常的子宫内环境会导致成年后代出现葡萄糖稳态紊乱以及妊娠期糖尿病的发生。本研究的目的是探讨这些功能差异是否可以通过内分泌胰腺水平的结构差异来解释。因此,我们对轻度和重度糖尿病母亲的成年子代的内分泌胰腺的大小和结构,以及胰岛素、胰高血糖素、生长抑素和PP细胞的贡献进行了形态计量学研究,因为这两组子代均表现出糖耐量受损,但特征有所不同。我们还测量了它们的内分泌胰腺对妊娠的适应性,并与正常妊娠进行比较。在轻度糖尿病母亲的子代中,内分泌胰腺的大小和胰岛的分布是正常的。妊娠期间内分泌组织质量增加一倍的情况也与对照组相似。A细胞比例较高,尤其是相对于正常的B细胞数量而言,以及PP细胞数量较少,可能在这些动物胰岛素反应受损和妊娠期糖尿病的发生中起作用。在重度糖尿病母亲的子代中,观察到内分泌胰腺明显肥大,这主要是由于存在大量小胰岛,且在妊娠期间不会进一步增大。在这些动物中,内分泌胰腺和B细胞质量在未妊娠时就已达到“妊娠”状态下的值,这与正常妊娠期间胰岛素分泌过多和外周胰岛素抵抗相一致。妊娠期间未观察到胰岛质量进一步增加,这与妊娠期糖尿病有关。