Endocrine Abstracts

Background: The menstrual pattern is influenced by thyroid hormones directly through impact on the ovaries and indirectly through impact on SHBG, PRL, and GnRH secretion and coagulation factors. Treating thyroid dysfunction can reverse menstrual abnormalities and thus improve fertility.

Aim: Elucidating the molecular mechanisms underlying the link between thyroid and ovarian function is important for determining the relationship between thyroid status, fertility and menstrual disorders. Our previous work has demonstrated how granulosa cells population can be considered a thyroid hormone target, being its survival induced by T3 under specific circumstances via cell cycle and metabolism regulation.

Materials and methods: To characterize thyroid hormone action in the ovary, the direct effect of triiodothyronine T3 was analyzed in vitro using a culture system of rat follicles and granulosa cells obtained directly from female rats, and their growth and function in response to T3 treatment (10–7M) have been evaluated.

Results: Our results showed that both cell growth and follicle dimensions were significantly incremented (up to 40%) by 2–7 days of hormone treatment, as shown by cell growth analyses and follicle dimensions measures. The same cells and follicles were moreover capable of a 50% incremented production of 17 B estradiol, in response to testosterone supply, when treated with 48 h T3 10–7 M. Even the basal production of estradiol was augmented by the hormone presence, as measured by chemiluminescence.

To investigate the mechanisms underlying the observed effects, the major steroidogenic genes were analyzed by RT-PCR, namely FSHR, cyp 19a1, cyp 17, p450 scc, 3BHSD and StAR. All the genes analyzed, and in particular the aromatase and 17B-HSD, which are directly responsible for estradiol production, were significantly upregulated by the 48 h T3 treatment.

Conclusion: In conclusion our data show unambiguously the T3 ability to promote ovarian function in rats, providing interesting results about the T3 ability of directly target steroidogenesis.

Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.

Funding: This research did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector