Teixeira Caio Jordão, Santos-Silva Junia Carolina, de Souza Dailson Nogueira, Rafacho Alex, Anhe Gabriel Forato, Bordin Silvana
Department of Pharmacology, Faculty of Medical Sciences, State University of Campinas, Campinas, Brazil.
Department of Physiological Sciences, Center of Biological Sciences, Federal University of Santa Catarina, Florianópolis, Brazil.
Endocr Connect. 2019 Feb 1;8(2):120-131. doi: 10.1530/EC-18-0505.
Pancreatic islets from pregnant rats develop a transitory increase in the pancreatic β-cell proliferation rate and mass. Increased apoptosis during early lactation contributes to the rapid reversal of those morphological changes. Exposure to synthetic glucocorticoids during pregnancy has been previously reported to impair insulin secretion, but its impacts on pancreatic islet morphological changes during pregnancy and lactation have not been described. To address this issue, we assessed the morphological and molecular characteristics of pancreatic islets from rats that underwent undisturbed pregnancy (CTL) or were treated with dexamethasone between the 14th and 19th days of pregnancy (DEX). Pancreatic islets were analyzed on the 20th day of pregnancy (P20) and on the 3rd, 8th, 14th and 21st days of lactation (L3, L8, L14 and L21, respectively). Pancreatic islets from CTL rats exhibited transitory increases in cellular proliferation and pancreatic β-cell mass at P20, which were reversed at L3, when a transitory increase in apoptosis was observed. This was followed by the appearance of morphological features of pancreatic islet neogenesis at L8. Islets from DEX rats did not demonstrate an increase in apoptosis at L3, which coincided with an increase in the expression of M2 macrophage markers relative to M1 macrophage and T lymphocyte markers. Islets from DEX rats also did not exhibit the morphological characteristics of pancreatic islet neogenesis at L8. Our data demonstrate that maternal pancreatic islets undergo a renewal process during lactation that is impaired by exposure to DEX during pregnancy.
妊娠大鼠的胰岛会出现胰腺β细胞增殖率和质量的短暂增加。哺乳早期凋亡增加导致这些形态学变化迅速逆转。先前有报道称，孕期接触合成糖皮质激素会损害胰岛素分泌，但其对孕期和哺乳期胰岛形态学变化的影响尚未见描述。为解决这一问题，我们评估了正常妊娠大鼠（CTL）或在妊娠第14至19天接受地塞米松治疗的大鼠（DEX）胰岛的形态学和分子特征。在妊娠第20天（P20）以及哺乳第3、8、14和21天（分别为L3、L8、L14和L21）对胰岛进行分析。CTL大鼠的胰岛在P20时细胞增殖和胰腺β细胞质量出现短暂增加，在L3时逆转，此时观察到凋亡短暂增加。随后在L8出现胰岛新生的形态学特征。DEX大鼠的胰岛在L3时未显示凋亡增加，这与M2巨噬细胞标志物相对于M1巨噬细胞和T淋巴细胞标志物的表达增加一致。DEX大鼠的胰岛在L8时也未表现出胰岛新生的形态学特征。我们的数据表明，母体胰岛在哺乳期经历一个更新过程，而孕期接触DEX会损害这一过程。
