{"title":"利拉鲁肽对胰腺β细胞胰岛素分泌和β细胞存活相关GPCR基因表达的影响。","authors":"Melikenur Türkol, Türker Bilgen","doi":"10.55730/1300-0144.5997","DOIUrl":null,"url":null,"abstract":"<p><strong>Background/aim: </strong>Liraglutide as a long-acting glucagon-like peptide drug has anti-hyperglycemic and antiobesity effects. G protein-coupled receptors (GPCRs) are well-known drug target molecules that conduct critical signaling pathways related with diseases. Research has confirmed the role of many GPCRs genes in the regulation of pancreatic beta cell functions and insulin secretion. Liraglutide dependent expressional changes in GPCR genes may let us determine new drug targets.</p><p><strong>Materials and methods: </strong>Therefore, we investigated the changes in expression of GPR75, GPR56, GLP1R, M3R, and CB1R genes, which are the GPCR family members, in response to liraglutide treatment in the NIT-1 mouse pancreatic beta cells in this study. Changes at the mRNA levels of these GPCR genes were determined by a qPCR and the ddCT method, and using a control gene and untreated control groups.</p><p><strong>Results: </strong>We found statistically significant increases at the mRNA levels of GPR75, GPR56, M3R, and CB1R genes with 10nM of liraglutide at min 60, while there was no time and dose-dependent change in all of the genes investigated. We detected that the GLP1R gene expressions were stable amongst different time points and doses of liraglutide, except for a statistically significant decrease in the GLP1R gene expression in response to 1000nM of liraglutide treatment compared to 10nM and 100nM concentrations.</p><p><strong>Conclusion: </strong>Our results indicate that in vitro liraglutide administration in pancreatic beta cells appears to increase the expressions of GPR75, GPR56, M3R and CB1R genes which have already been related to insulin secretion and beta cell survive. Liraglutide may exert this effect through the GLP1R or other cellular pathways undescribed yet. Combined usage of liraglutide and the specific ligands of GPR75, GPR56, M3R, and CB1R may provide a better response in terms of insulin secretion and beta cell survival, making them good targets for antidiabetic and antiobesity therapy.</p>","PeriodicalId":23361,"journal":{"name":"Turkish Journal of Medical Sciences","volume":"55 2","pages":"525-530"},"PeriodicalIF":1.2000,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12058015/pdf/","citationCount":"0","resultStr":"{\"title\":\"The effects of liraglutide on expressions of insulin secretion and beta cell survive associated GPCR genes in pancreatic beta cells.\",\"authors\":\"Melikenur Türkol, Türker Bilgen\",\"doi\":\"10.55730/1300-0144.5997\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background/aim: </strong>Liraglutide as a long-acting glucagon-like peptide drug has anti-hyperglycemic and antiobesity effects. G protein-coupled receptors (GPCRs) are well-known drug target molecules that conduct critical signaling pathways related with diseases. Research has confirmed the role of many GPCRs genes in the regulation of pancreatic beta cell functions and insulin secretion. Liraglutide dependent expressional changes in GPCR genes may let us determine new drug targets.</p><p><strong>Materials and methods: </strong>Therefore, we investigated the changes in expression of GPR75, GPR56, GLP1R, M3R, and CB1R genes, which are the GPCR family members, in response to liraglutide treatment in the NIT-1 mouse pancreatic beta cells in this study. Changes at the mRNA levels of these GPCR genes were determined by a qPCR and the ddCT method, and using a control gene and untreated control groups.</p><p><strong>Results: </strong>We found statistically significant increases at the mRNA levels of GPR75, GPR56, M3R, and CB1R genes with 10nM of liraglutide at min 60, while there was no time and dose-dependent change in all of the genes investigated. We detected that the GLP1R gene expressions were stable amongst different time points and doses of liraglutide, except for a statistically significant decrease in the GLP1R gene expression in response to 1000nM of liraglutide treatment compared to 10nM and 100nM concentrations.</p><p><strong>Conclusion: </strong>Our results indicate that in vitro liraglutide administration in pancreatic beta cells appears to increase the expressions of GPR75, GPR56, M3R and CB1R genes which have already been related to insulin secretion and beta cell survive. Liraglutide may exert this effect through the GLP1R or other cellular pathways undescribed yet. Combined usage of liraglutide and the specific ligands of GPR75, GPR56, M3R, and CB1R may provide a better response in terms of insulin secretion and beta cell survival, making them good targets for antidiabetic and antiobesity therapy.</p>\",\"PeriodicalId\":23361,\"journal\":{\"name\":\"Turkish Journal of Medical Sciences\",\"volume\":\"55 2\",\"pages\":\"525-530\"},\"PeriodicalIF\":1.2000,\"publicationDate\":\"2025-03-20\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12058015/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Turkish Journal of Medical Sciences\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.55730/1300-0144.5997\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q2\",\"JCRName\":\"MEDICINE, GENERAL & INTERNAL\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Turkish Journal of Medical Sciences","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.55730/1300-0144.5997","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/1 0:00:00","PubModel":"eCollection","JCR":"Q2","JCRName":"MEDICINE, GENERAL & INTERNAL","Score":null,"Total":0}
The effects of liraglutide on expressions of insulin secretion and beta cell survive associated GPCR genes in pancreatic beta cells.
Background/aim: Liraglutide as a long-acting glucagon-like peptide drug has anti-hyperglycemic and antiobesity effects. G protein-coupled receptors (GPCRs) are well-known drug target molecules that conduct critical signaling pathways related with diseases. Research has confirmed the role of many GPCRs genes in the regulation of pancreatic beta cell functions and insulin secretion. Liraglutide dependent expressional changes in GPCR genes may let us determine new drug targets.
Materials and methods: Therefore, we investigated the changes in expression of GPR75, GPR56, GLP1R, M3R, and CB1R genes, which are the GPCR family members, in response to liraglutide treatment in the NIT-1 mouse pancreatic beta cells in this study. Changes at the mRNA levels of these GPCR genes were determined by a qPCR and the ddCT method, and using a control gene and untreated control groups.
Results: We found statistically significant increases at the mRNA levels of GPR75, GPR56, M3R, and CB1R genes with 10nM of liraglutide at min 60, while there was no time and dose-dependent change in all of the genes investigated. We detected that the GLP1R gene expressions were stable amongst different time points and doses of liraglutide, except for a statistically significant decrease in the GLP1R gene expression in response to 1000nM of liraglutide treatment compared to 10nM and 100nM concentrations.
Conclusion: Our results indicate that in vitro liraglutide administration in pancreatic beta cells appears to increase the expressions of GPR75, GPR56, M3R and CB1R genes which have already been related to insulin secretion and beta cell survive. Liraglutide may exert this effect through the GLP1R or other cellular pathways undescribed yet. Combined usage of liraglutide and the specific ligands of GPR75, GPR56, M3R, and CB1R may provide a better response in terms of insulin secretion and beta cell survival, making them good targets for antidiabetic and antiobesity therapy.
期刊介绍：
Turkish Journal of Medical sciences is a peer-reviewed comprehensive resource that provides critical up-to-date information on the broad spectrum of general medical sciences. The Journal intended to publish original medical scientific papers regarding the priority based on the prominence, significance, and timeliness of the findings. However since the audience of the Journal is not limited to any subspeciality in a wide variety of medical disciplines, the papers focusing on the technical details of a given medical subspeciality may not be evaluated for publication.
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