宫内慢性缺氧导致成年子代大鼠胰岛发育不良，通过 INS 和 PDX-1 的上调得到代偿。

Islet hypoplasia of adult offspring rats caused by intrauterine chronic hypoxia is compensated by up-regulation of INS and PDX-1.

机构信息

Department of Ultrasonography, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, China.

Department of Radiology, Quanzhou Women's and Children's Hospital, Quanzhou, China.

出版信息

Islets. 2023 Dec 31;15(1):2231610. doi: 10.1080/19382014.2023.2231610.

DOI:10.1080/19382014.2023.2231610

PMID:37409484

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10327515/

Abstract

BACKGROUND

Intrauterine chronic hypoxia (ICH) can lead to pancreatic dysmetabolism in offspring. This study aimed to determine the changes in islet function of offspring through a rat ICH model and detect the factors affecting islet function.

METHODS

Twenty couples of healthy Sprague - Dawley adult rats were randomly mated, and the pregnant rats were randomly allocated to ICH and normal control (NC) groups. Pregnant rats in the ICH group were placed in a hypoxic chamber with 13% oxygen concentration for hypoxia treatment twice a day for 4 h until delivery at 21 days. NC group is inlet with normal air from beginning to end. After delivery, blood was taken from the heart of pregnant rats for blood gas analysis. The weight of the offspring rats was measured at 12 h after birth and 16 weeks after birth. At 16 weeks, the immunohistochemical results of β-cell total, islet area, insulin (INS), and glucose transporter 2 (GLUT2) proteins were obtained from the islets. The mRNA data of INS and pancreatic and duodenal homeobox 1 (PDX-1) genes were obtained from pancreas.

RESULTS

We found the β-cell total, islet area, and the positive cell area of INS and GLUT2 of offspring rats in ICH group were lower than those of NC group, while the levels of INS and PDX-1 genes were higher in ICH group than in NC group.

CONCLUSIONS

ICH can lead to islet hypoplasia in adult male offspring rats. However, this is within the compensatory range.

摘要

背景

宫内慢性缺氧（ICH）可导致后代胰腺代谢异常。本研究旨在通过大鼠 ICH 模型确定后代胰岛功能的变化，并检测影响胰岛功能的因素。

方法

将 20 对健康的 Sprague-Dawley 成年大鼠随机交配，将孕鼠随机分为 ICH 组和正常对照组（NC）。ICH 组的孕鼠每天两次置于 13%氧浓度的缺氧室中缺氧处理 4 小时，直至 21 天分娩。NC 组从始至终都在输入正常空气。分娩后，从孕鼠心脏取血进行血气分析。在出生后 12 小时和 16 周时测量子代大鼠的体重。在 16 周时，从胰岛获得β细胞总数、胰岛面积、胰岛素（INS）和葡萄糖转运蛋白 2（GLUT2）蛋白的免疫组化结果。从胰腺获得 INS 和胰腺十二指肠同源盒 1（PDX-1）基因的 mRNA 数据。