Eff ects of menopause and diabetes on the rat thyroid gland: A histopathological and stereological examining

Menopause, represents the end of woman’s reproductive life, is defined as the changeless stoppage of ovarian follicular activity and the menstrual cycle. This physiological process is characterized by alterations related with sex hormones and stepwise decrease of estrogen secretion. Thus, estradiol ranging from 5 to 25 pg/mL, while rising titers of gonadotrophins, so the levels of follicle stimulating hormone change between 40 and 250 mU/mL and luteinizing hormone changes from 30 to 150 mU/Ml [1,2]. Estrogen is an important regulatory hormone for oxidative stress [3]. Estrogen is known to increase producing thyroxine-binding globulin (TBG) that responsible for carrying the thyroid hormones in circulation. In premenopausal period, the changes in E2 levels affect TBG levels, this would also lead to changes in thyroxine and triiodothyronine levels. This changes in premenopausal term generally be short-term fluctuations in free thyroxine and free triiodothyronine levels cause may be. However, these changes do not reach the level of clinical importance. Among postmenopausal women, the age-related increasing of thyroid-stimulating hormone is remarkable. This average is higher than men in the same age profile [2,4,5]. In addition, the physiological effects of estrogen and progesterone on thyroid parafollicular cells enhance secretion of calcitonin [6,7].