Suppr超能文献

胃饥饿素对大鼠胰岛和CRI-D2细胞系中Kiss-1和KissR基因转录及胰岛素分泌的影响。

The effect of ghrelin on Kiss-1 and KissR gene transcription and insulin secretion in rat islets of Langerhans and CRI-D2 cell line.

作者信息

Sagheb Mandana Mahmoodzaeh, Azarpira Negar, Mokhtary Mokhtar

机构信息

Department of Biology, Kazeroon Branch, Islamic Azad University, Kazeroon, Iran.

Transplant Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.

出版信息

Iran J Basic Med Sci. 2017 Jan;20(1):36-40. doi: 10.22038/ijbms.2017.8090.

Abstract

OBJECTIVES

Ghrelin is a peptide hormone that has been shown to have numerous central and peripheral effects. The central effects including GH secretion, food intake, and energy homeostasis are partly mediated by Kiss1- KissR signaling pathway. Ghrelin and its receptor are also expressed in the pancreatic islets. Ghrelin is one of the key metabolic factors controlling insulin secretion from the islets of Langerhans. We hypothesize that the inhibitory effect of ghrelin on KiSS-1 and KissR in the islet cells may be similar to the same inhibitory effect of ghrelin in the hypothalamus.

MATERIALS AND METHODS

To investigate the effect of ghrelin, we isolated the islets from adult male rats by collagenase and cultured CRI-D2 cell lines. Then, we incubated them with different concentrations of ghrelin for 24 hr. After RNA extraction and cDNA synthesis from both islets and CRI-D2 cells, the relative expression of KiSS-1 and KissR was evaluated by means of real-time PCR. Furthermore, we measured the amount of insulin secreted by the islets after incubation in different concentrations of ghrelin and glucose after 1 hr. Besides, we checked the viability of the cells after 24 hr cultivation.

RESULTS

Ghrelin significantly decreased the KiSS-1 and KissR mRNA transcription in rat islets and CRI-D2 cells. Besides, Ghrelin suppressed insulin secretion from pancreatic beta cells and CRI-D2 cells.

CONCLUSION

These findings indicate the possibility that KiSS-1 and KissR mRNA expression is mediator of ghrelin function in the islets of Langerhans.

摘要

目的

胃饥饿素是一种肽类激素,已被证明具有多种中枢和外周作用。其包括生长激素分泌、食物摄入和能量稳态在内的中枢作用部分由Kiss1-KissR信号通路介导。胃饥饿素及其受体也在胰岛中表达。胃饥饿素是控制胰岛细胞胰岛素分泌的关键代谢因子之一。我们假设胃饥饿素对胰岛细胞中KiSS-1和KissR的抑制作用可能与它在下丘脑中的抑制作用相似。

材料与方法

为了研究胃饥饿素的作用,我们用胶原酶从成年雄性大鼠中分离出胰岛,并培养CRI-D2细胞系。然后,我们将它们与不同浓度的胃饥饿素孵育24小时。从胰岛和CRI-D2细胞中提取RNA并合成cDNA后,通过实时PCR评估KiSS-1和KissR的相对表达。此外,我们在不同浓度的胃饥饿素和葡萄糖中孵育1小时后,测量胰岛分泌的胰岛素量。此外,我们在培养24小时后检查细胞的活力。

结果

胃饥饿素显著降低大鼠胰岛和CRI-D2细胞中KiSS-1和KissR mRNA的转录。此外,胃饥饿素抑制胰腺β细胞和CRI-D2细胞的胰岛素分泌。

结论

这些发现表明KiSS-1和KissR mRNA表达可能是胃饥饿素在胰岛中发挥功能的介质。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27ee/5243972/e6d3eb5e65ee/IJBMS-20-36-g001.jpg

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验