Glucagon‐like peptide‐1 receptor is expressed in human and rodent testis

间质细胞 生物 内分泌学 内科学 免疫组织化学 支持细胞 受体 肠促胰岛素 啮齿动物 激素 精子发生 促黄体激素 免疫学 医学 糖尿病 2型糖尿病 生态学
作者
Rosario Caltabiano,D. F. Condorelli,Salvatore Panza,Carla Boitani,Nicolò Musso,Davor Ježek,Lorenzo Memeo,Lorenzo Colarossi,Vittoria Rago,Valentina Mularoni,Saveria Spadola,Roberto Castiglione,Marta Santoro,Saveria Aquila,Rosario D’Agata
出处
期刊:International Journal of Andrology [Wiley]
卷期号:8 (6): 1935-1945 被引量:30
标识
DOI:10.1111/andr.12871
摘要

Abstract Background The incretin hormone glucagon‐like peptide‐l (GLP‐1) is an important regulator of post‐prandial insulin secretion, acting through a G protein‐coupled cell surface receptor (GLP‐1R). In addition to its expression in pancreatic β‐cells, several studies suggested that GLP‐1R is located in extra‐pancreatic tissues. Objectives In this study, we examined for the first time the testicular distribution of the GLP‐1R, both in normal human and neoplastic testicular tissues as well as in rodent testis and rodent testicular cell lines. Methods and Methods The GLP‐1R distribution in testicular section has been evaluated by immunohistochemistry, the specificity of IHC was validated by demonstrating a positive staining for GLP‐1RmRNA by RISH technology. While GLP‐1R expression in terms of protein was detected by western blot analysis, Moreover, mRNA levels were determined in human testis, in rodent Leydig, and Sertoli cell lines. Results Using immunohistochemistrya specific staining for GLP‐1R was detected in Leydig cells. The specificity of IHC was validated by demonstrating a positive staining for GLP‐1RmRNA only in these cell types. Species differences in the GLP‐1R expression between humans and rodents were observed. Interestingly, a decreased expression of the receptor in rodent tumor Leydig cell line and an absence in human Leydig tumor samples was detected. Discussion It may be hypothesized that GLP‐1R acts like an oncosuppressor in Leydig tumors. A role in regulation of hormone secretion by GLP‐1 has been shown in other endocrine cells, therefore we hypothesized that GLP‐1R is able to modulate somehow the Leydig cell function. Conclusion In our findings, a careful evaluation of human testicular tissues and rodent testis revealed Leydig cells as a potential target for GLP‐1. Collectively, an effect of GLP‐1R in Leydig cell function may be presumed although future studies are needed to ascertain the GLP‐1R’s role both in normal and tumor Leydig cells.
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