Abstract
Adipokines influence energy metabolism and have effects on male reproduction, including spermatogenesis and/or Sertoli cell maturation; however, the relationship between these active proteins and androgens in testicular cells is limited. Here, we studied the impact of short-term exposure to flutamide (an anti-androgen that blocks androgen receptors) on the expression of chemerin, apelin, vaspin and their receptors (CCRL2, CMKLR1, GPR1, APLNR, GRP78, respectively) in adult rat testes. Moreover, the levels of expression of lipid metabolism-modulating proteins (PLIN1, perilipin1; TSPO, translocator protein) and intercellular adherens junction proteins (nectin-2 and afadin) were determined in testicular cells. Plasma levels of adipokines, testosterone and cholesterol were also evaluated. Gene expression techniques used included the quantitative real-time polymerase chain reaction (qRT-PCR), Western blot (WB) and immunohistochemistry (IHC). The androgen-mediated effects observed post-flutamide treatment were found at the gonadal level as chemerin, apelin, and vaspin gene expression alterations at mRNA and protein levels were detected, whereas the cellular targets for these adipokines were recognised by localisation of respective receptors in testicular cells. Plasma concentrations of all adipokines were unchanged, whereas plasma cholesterol content and testosterone level increased after flutamide exposure. Differential distribution of adipokine receptors indicates potential para- or autocrine action of the adipokines within the rat testes. Additionally, changes in the expression of PLIN1 and TSPO, involved in the initial step of testosterone synthesis in Leydig cells, suggest that testicular cells represent a target of flutamide action. Increase in the gene expression of PLIN1 and TSPO and higher total plasma cholesterol content indicates enhanced availability of cholesterol in Leydig cells as a result of androgen-mediated effects of flutamide. Alterations in adherens junction protein expression in the testis confirm the flutamide efficacy in disruption of androgen signalling and presumably lead to impaired para- and autocrine communication, important for proper functioning of adipokines.
Highlights
Adipose-derived hormones, including adiponectin, leptin, visfatin, resistin, chemerin, apelin, vaspin and many others, are called adipokines
In a very recent study it was demonstrated that long treatment of human cultured Sertoli cells with chemerin, visfatin or resistin at high concentrations suppresses FSH receptor expression and up-regulates that of the cytochrome P450 CYP26A1, which in turn induces a phenotype characteristic of the pre-pubertal state [15]
We focus our attention on the influence of androgen signalling disrupted by flutamide on the expression of chemerin, apelin and vaspin, as well as on the expression of lipid metabolism-modulating proteins (PLIN1 and translocator protein (TSPO)) at the gonadal level
Summary
Adipose-derived hormones, including adiponectin, leptin, visfatin, resistin, chemerin, apelin, vaspin and many others, are called adipokines. These bioactive proteins act via binding to specific receptors that are frequently located on cells that do not produce adipokines, suggesting a regulatory mechanism that functions through endo- and/or paracrine interactions [1]. It was demonstrated that adiponectin, along with other adipokines (e.g., leptin, resistin), plays a role in the interaction between metabolism and reproductive functions at the hypothalamic, pituitary and gonadal levels (for review, see [8,9]) in humans, rodents, and agronomic species. The presence of chemerin and visfatin has been detected in the human testis, data concerning the pathogenic role of other adipokines in male reproductive disorders remain to be investigated
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
