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

• DOI: 10.1111/andr.12871
• Publication Date: 2020-07-24T16:06:17Z
• Authors: Rosario Caltabiano; Daniele 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
• Keywords: Male; 0301 basic medicine; 0303 health sciences; Sertoli cells; Leydig cells; GLP-1R; leydig cells; pancreatic cells; sertoli cells; Glucagon-Like Peptide-1 Receptor; Cell Line; Mice, Inbred C57BL; pancreatic cells; 03 medical and health sciences; Testis; Animals; Exenatide; Humans; GLP-1R

AbstractBackgroundThe 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.ObjectivesIn 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 MethodsThe 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.ResultsUsing 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.DiscussionIt 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.ConclusionIn 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.