热应激诱导氧化应激和妊娠期糖尿病的易感性

Saada M. Mbepera, S. Mshamu, R. Max, J. Malago
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摘要

妊娠期糖尿病(GDM)是一种由妊娠期碳水化合物不耐受引起的高血糖症。这可能是由于妊娠期间胰岛素抵抗或胰岛素分泌受损所致。已经确定了几种导致GDM的原因,其中包括氧化应激(OS),但是妊娠期间热应激与GDM发展的关联有限。因此,本研究旨在探讨热应激与大鼠GDM之间的关系。妊娠和非妊娠Wistar大鼠在41 ~ 42℃下维持21天。于实验第1、8、15、21天人道处死动物。从心脏采集血液样本进行葡萄糖、胰岛素、丙二醛(MDA)和谷胱甘肽过氧化物酶(GPx)分析。胰腺组织固定在中性缓冲福尔马林中,并进行组织病理学研究。研究结果表明,与未怀孕的大鼠相比,怀孕大鼠的热应激诱导葡萄糖显著增加,胰岛素水平下降(P < 0.05)。此外,热处理还伴随着MDA的增加和GPx水平的下降。妊娠大鼠胰脏组织学检查显示,第15天β细胞受损,第21天β细胞数量减少。这些结果表明,与未怀孕的大鼠相比,热应激提高了怀孕大鼠的OS水平,并增加了GDM的机会,因为它与胰腺β细胞缺陷有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Heat Stress Induces Oxidative Stress and Predisposes Rats to Gestational Diabetes Mellitus
Gestational diabetes mellitus (GDM) is a form of hyperglycemia due to carbohydrate intolerance that begins during pregnancy. This may be due to insulin resistance or impairment of insulin secretion during the pregnancy. Several causes of GDM have been identified which include oxidative stress (OS), however the association of heat stress and GDM development during pregnancy is limited. Therefore, this study aimed at examining the association between heat stress and GDM in rats. Pregnant and non-pregnant Wistar rats were maintained at 41 - 42°C for 21 days. On day 1, 8, 15 and 21 of the experiment, animals were humanely sacrificed. Blood samples for glucose, insulin, malondialdehyde (MDA) and glutathione peroxidase (GPx) analyses were collected from the heart. Pancreatic tissues were fixed in neutral buffered formalin, and processed for histopathological studies. The findings demonstrated that, in pregnant rats, heat stress induced a significant increase in glucose linked with a drop in insulin levels than non-pregnant rats (P <0 .05). Also heat treatment was accompanied by an increase in MDA and a drop in GPx levels. Histological examinations of the pancreas revealed damaged β-cells on day 15 and reduction in the number of β-cells by day 21 of the experiment in the pregnant rats. These results suggest that heat stress raises the levels of OS in pregnant rats than non-pregnant rats and increases the chance of GDM as it is associated with β-cell defects in the pancreas.
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