Ovarian LH/hCG receptors and plasma level of LH,17-ß estradiol and progesterone in gonadotropin — induced PCO syndrome in rats

Abstract

The aim of this work was to investigate the morphologic changes, LH/hCG receptor content in the ovaries and plasma levels of LH, progesterone and estradiol of hypo--and hyperthyroid rats injected with PMSG and hCG. The hypothyroid state was induced by thyreoidectomy (Tr-X) and the hyperthyroid condition by injections of 40 micrograms L-thyroxine daily during 21 days (T4). Gonadotropins were injected during 14 days in daily doses: PMSG--5 i.u. and hCG--10 i.u. The following 8 groups (n = 10-20) were established: control (euthyroid, no treatment), Tr-X, PMSG + hCG, Tr-X + hCG, Tr-X + PMSG, Tr-X + PMSG + hCG, T4 and T4 + PMSG. At the end of experiments rats were sacrificed, ovaries weighed, macroscopically inspected and concentration of LH/hCG receptors was estimated. In blood plasma the level of LH, progesterone and 17-beta estradiol was also analysed. The experiments showed that injections of PMSG alone, or PMSG + hCG in eu-or hypothyroid rats, appear the most effective in induction of PCO syndrome in rats. Low levels of thyroid hormones sensitized the ovaries to gonadotropin action, but a hyperthyroid status diminished or inhibited this response. Thyroid function is also essential in production of LH/hCG receptors in the ovaries. In hypothyroid animals the amount of these receptors was greatly increased, while in hyperthyroid animals they decreased. The level of plasma LH, progesterone, and estradiol showed insignificantly differences and various inconsiderable deviations from norm. These differences were not dependent on large doses of gonadotropins, altered thyroid function, or on cystic or luteinizing changes in the ovary.

Elevated antithyroid peroxidase antibodies indicating Hashimoto's thyroiditis are associated with the treatment response in infertile women with polycystic ovary syndrome

“…First, both are known to have a genetic background (13,14). Second, HT may contribute to the development of PCOS via overt or even subclinical hypothyroidism (3)(4)(5)(6). Third, the imbalance of normal to high estrogen and low progesterone may propagate the development of autoimmune diseases via the immune stimulatory activity of estrogen (9).…”

Polycystic ovary syndrome and thyroid disorder: a comprehensive narrative review of the literature

“…Few preclinical data showed a strong interaction between hypothalamus-pituitary-gonadal and hypothalamus-pituitary-thyroid axes, suggesting an association between PCOS and thyroid disorders. Hypothyroidism in rats after thyroidectomy increased ovary size and the local concentration of luteinizing hormone (LH)/human chorionic gonadotropin receptors ( 45 ). Therefore, low levels of thyroid hormones appeared to sensitize the ovaries to gonadotropin action and favor the development of PCOS in rats ( 46 ).…”