Exogenous visfatin suppresses pituitary gonadotrophins and stimulates testosterone secretion in a male mouse
Vanlal Rempuia1, Guruswami Gurusubramanian1, Vikas Kumar Roy1
1Department of Zoology, Mizoram University, Aizawl, Mizoram, India.
Abstract:
Visfatin expression has been shown in the testis and pituitary. However, the role of visfatin in the pituitary and testis axis is fragmentary. Furthermore, no study has shown the effects of visfatin on the pituitary gonadotrophins and testicular steroid hormonal secretions in a male mouse. The present study has investigated the effects of exogenous visfatin (most likely a state of hypervisfatinemia) on the gonadotrophins, testosterone, estradiol, androstenedione, and progesterone in a male mouse. The exogenous visfatin was given for 35 days, which covers one spermatogenic cycle. The circulating testosterone was elevated after visfatin treatment, along with down-regulation of AR and steroidogenic markers in the testis. However, the expression of CYP17 was up-regulated in visfatin-treated testis. Visfatin treatment also elevated apoptosis in the different germ cells of the testis. The levels of circulating LH and FSH were also suppressed after visfatin treatment. The immunolocalization of AR exhibited decreased abundance in the pituitary of visfatin-treated mice; thus, it can be suggested that pituitary gonadotrophins secretion might be suppressed by direct action of visfatin rather than via elevated testosterone. In conclusion, our results showed that exogenous visfatin suppresses gonadotrophins and stimulates testicular testosterone secretions in a differential manner. Visfatin has inhibitory effects on pituitary gonadotrophins secretion and stimulatory effects on testosterone secretion from the testis. Thus, conditions similar to hypervisfatinemia likely impair the release of hormones from the pituitary and testis.
Insights
Exogenous visfatin (a hormone) suppressed pituitary gonadotropins (LH and FSH) while paradoxically increasing testicular testosterone in male mice. Hypervisfatinemia may impair pituitary and testicular hormone release.
Area of Science:
- Endocrinology
- Reproductive Biology
- Molecular Biology
Background:
- Visfatin is expressed in the testis and pituitary, but its role in the hypothalamic-pituitary-gonadal axis is not fully understood.
- Previous studies have not investigated the specific effects of visfatin on pituitary gonadotropins and testicular steroid hormones in male mice.
Purpose of the Study:
- To investigate the effects of exogenous visfatin administration on gonadotropins (LH, FSH), testosterone, estradiol, androstenedione, and progesterone in male mice.
- To elucidate the impact of visfatin on the pituitary-testis axis and its potential role in reproductive hormonal regulation.
Main Methods:
- Male mice were treated with exogenous visfatin for 35 days, covering a full spermatogenic cycle.
- Hormone levels (testosterone, estradiol, androstenedione, progesterone, LH, FSH) were measured in circulation.
- Testicular expression of androgen receptor (AR) and steroidogenic markers, including CYP17, was analyzed.
- Apoptosis in testicular germ cells was assessed.
- AR abundance in the pituitary was examined using immunolocalization.
Main Results:
- Visfatin treatment led to elevated circulating testosterone levels.
- Testicular AR and steroidogenic markers were down-regulated, while CYP17 expression was up-regulated.
- Increased apoptosis was observed in testicular germ cells of visfatin-treated mice.
- Circulating levels of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were suppressed.
- Decreased AR abundance in the pituitary suggests direct visfatin action on gonadotropin secretion.
Conclusions:
- Exogenous visfatin differentially affects gonadotropin and testosterone secretion, suppressing pituitary gonadotropins while stimulating testicular testosterone production.
- Visfatin exhibits inhibitory effects on pituitary gonadotropin secretion and stimulatory effects on testicular testosterone secretion.
- Conditions mimicking hypervisfatinemia may disrupt hormone release from the pituitary and testis, potentially impairing reproductive function.
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