The endocrine pancreas in virgin and pregnant offspring of diabetic pregnant rats
The endocrine pancreas in virgin and pregnant offspring of diabetic pregnant rats
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DOI：
10.1016/s0168-8227(97)00080-6
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发表时间：
1997-10-01
影响因子：
5.1
通讯作者：
VanAssche, FA
中科院分区：
文献类型：
--
作者：
Aerts, L;Vercruysse, L;VanAssche, FA
母亲在怀孕期间患有糖尿病会引起胎儿内分泌胰腺的结构和功能适应。我们之前在实验大鼠模型中表明，这种异常的子宫内环境的影响会导致成年后代的葡萄糖稳态紊乱并导致妊娠期糖尿病的发生。目前工作的目的是研究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青少年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测量研究，因为两者都表现出葡萄糖耐量紊乱，但具有不同的特征。还测量了他们的内分泌胰腺对怀孕的适应情况，并与对照怀孕的情况进行比较。在轻度糖尿病母亲的后代中，内分泌胰腺的大小和胰岛的分布是正常的。怀孕期间内分泌质量的倍增也与对照组相似。高比例的 A 细胞，特别是相对于正常的 B 细胞群和低含量的 PP 细胞，可能在这些动物的胰岛素反应受损和妊娠糖尿病的发展中发挥作用。严重糖尿病母亲的后代中，内分泌胰腺明显肥大，这主要是由于存在大量小胰岛，并且在怀孕期间不会进一步增加。在这些动物中，内分泌胰腺和 B 细胞群的大小在没有怀孕的情况下就达到了“怀孕”值，这与正常怀孕期间的胰岛素输出过量和外周胰岛素抵抗相一致。怀孕期间没有看到胰岛质量进一步增加，这与妊娠糖尿病有关。 (C) 1997 爱思唯尔科学爱尔兰有限公司
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. (C) 1997 Elsevier Science Ireland Ltd.