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镉暴露的雄性C57BL/6小鼠胰岛素分泌减少但血糖稳态未改变

Decreased Insulin Secretion but Unchanged Glucose Homeostasis in Cadmium-Exposed Male C57BL/6 Mice.

作者信息

Li Xiaoyin, Li Mengyang, Xu Jiming, Zhang Xiang, Xiao Wei, Zhang Zengli

机构信息

School of Public Health, Soochow University, 199 Ren'ai Road, Suzhou 215123, China.

出版信息

J Toxicol. 2019 Jun 20;2019:8121834. doi: 10.1155/2019/8121834. eCollection 2019.

DOI:10.1155/2019/8121834
PMID:31320898
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6610724/
Abstract

Cadmium (Cd) is a well-known toxic metal element that is largely distributed in the environment. Cd causes toxicity to most organs. Accumulating evidence suggests that Cd exposure is associated with islet dysfunction and development of diabetes, but the association remains controversial. The aim of this study is to evaluate the possible effects of chronic Cd exposure on glucose metabolism in male C57BL/6 mice. Mice were intraperitoneally injected with CdCl solution (1 mg.kg) twice a week for 24 weeks. Fasting blood glucose (FBG) levels and body weights were measured weekly. After 24 weeks, the intraperitoneal glucose tolerance test (IPGTT), intraperitoneal insulin tolerance test (IPITT), and fasting serum insulin (FSI) level test were performed. The insulin resistance index (HOMA-IR) and pancreatic cell function index (HOMA-) were calculated and analyzed. The expression of insulin receptor (IR) in mouse liver was detected by real-time PCR. Pancreatic tissue was collected for histological examination. The results demonstrated that FBG, IPGTT, HOMA-IR, and HOMA- were identical between Cd exposure and control mice. In contract, mean fasting serum insulin level, area under the curve (AUC) of IPITT, and IR expression in livers of Cd-exposed mice decreased significantly compared with control mice. Cd administration induced islet atrophy and decreased islet area. The results suggested that Cd exposure decreased insulin secretion and maintained glucose homeostasis in male C57BL/6 mice and that pancreatic functions should be monitored in populations chronically exposed to Cd.

摘要

镉(Cd)是一种广为人知的有毒金属元素,在环境中广泛分布。镉会对大多数器官产生毒性。越来越多的证据表明,镉暴露与胰岛功能障碍和糖尿病的发生有关,但这种关联仍存在争议。本研究的目的是评估慢性镉暴露对雄性C57BL/6小鼠葡萄糖代谢的可能影响。小鼠每周两次腹腔注射氯化镉溶液(1毫克/千克),持续24周。每周测量空腹血糖(FBG)水平和体重。24周后,进行腹腔葡萄糖耐量试验(IPGTT)、腹腔胰岛素耐量试验(IPITT)和空腹血清胰岛素(FSI)水平测试。计算并分析胰岛素抵抗指数(HOMA-IR)和胰岛β细胞功能指数(HOMA-β)。通过实时PCR检测小鼠肝脏中胰岛素受体(IR)的表达。收集胰腺组织进行组织学检查。结果表明,镉暴露小鼠和对照小鼠之间的FBG、IPGTT、HOMA-IR和HOMA-β没有差异。相反,与对照小鼠相比,镉暴露小鼠的平均空腹血清胰岛素水平、IPITT曲线下面积(AUC)和肝脏中IR的表达显著降低。镉给药导致胰岛萎缩并减小胰岛面积。结果表明,镉暴露降低了雄性C57BL/6小鼠的胰岛素分泌并维持了葡萄糖稳态,并且应该对长期接触镉的人群的胰腺功能进行监测。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c95/6610724/021ef4cff34a/JT2019-8121834.006.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c95/6610724/3661fb44a277/JT2019-8121834.002.jpg
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