Differential effect of visfatin inhibition on the testicular androgen and estrogen receptors expression in early pubertal mice

• Published in: Endocrine 2024-06, Vol.84 (3), p.1216-1228
• Main Authors: Rempuia, Vanlal, Gurusubramanian, Guruswami, Roy, Vikas Kumar
• Format: Article
• Language: English
• Subjects: Acrylamides - pharmacology; Adipose tissue; Animals; Apoptosis; Apoptosis - drug effects; Aromatase; Aromatase - metabolism; Bcl-2 protein; Body weight; Cell Proliferation - drug effects; Diabetes; Endocrinology; Epithelium; Estrogen receptors; Estrogens; Humanities and Social Sciences; Internal Medicine; Male; Medicine; Medicine & Public Health; Mice; multidisciplinary; Nicotinamide Phosphoribosyltransferase - metabolism; Original Article; Ovaries; Piperidines - pharmacology; Puberty; Receptors, Androgen - metabolism; Receptors, Estrogen - metabolism; Science; Seminiferous tubule; Sexual Maturation - drug effects; Sexual Maturation - physiology; Steroidogenesis; Testes; Testis - drug effects; Testis - metabolism; Testosterone - blood; Testosterone - pharmacology
• ISSN: 1559-0100; 1355-008X; 1559-0100
• DOI: 10.1007/s12020-024-03692-9

Background It is now well known that visfatin is expressed in the testis and ovary of various animals. Visfatin is known to regulate gonadal functions such as steroidogenesis, proliferation, and apoptosis in the ovary and testis of mice. Recently, we have shown that visfatin has an inhibitory role in the infantile mice testis. It has also been shown that visfatin stimulates testicular steroidogenesis in adult rats. However, the role of visfatin during puberty has not been investigated in relation to the above-mentioned process. Objective The objective of the present study was to examine the effect of visfatin inhibition by FK866 from PND25 to PND35 (pre-pubertal to early pubertal) in male Swiss albino mice on steroidogenesis, proliferation, and apoptosis. Methods Sixteen mice (25 days old) were divided into two groups, one group was given normal saline and the other group was administered with an inhibitor of visfatin (FK866) at the dose of 1.5 mg/kg by intraperitoneal injection for 10 days. Histopathological and immunohistochemical analysis, western blot analysis and hormonal assay were done. Results Visfatin inhibition resulted in increased estrogen secretion, body weight, seminiferous tubule diameter, germinal epithelium height, and proliferation along with increased expression of BCl2, casapse3, ERs and aromatase expression in the mice testis. Visfatin inhibition down-regulated the testicular visfatin expression and also decreased abundance in the adipose tissues. Conclusion In conclusion, decreased AR expression and increased ERs expression by FK866, suggest that visfatin might have a stimulatory effect on AR signaling than ERs in the early pubertal stage of mice.