Abstract
BackgroundThere is substantial evidence both in humans and in animals that a prolonged reduction in plasma thyroid hormone concentration leads to reproductive problems, including disturbed folliculogenesis, impaired ovulation and fertilization rates, miscarriage and pregnancy complications. The objective of the present study is to examine the consequences of chronic hypothyroidism, induced in adulthood, for the size of the ovarian follicle pool. In order to investigate this, adult female rats were provided either a control or an iodide deficient diet in combination with perchlorate supplementation to inhibit iodide uptake by the thyroid. Sixteen weeks later animals were sacrificed. Blood was collected for hormone analyses and ovaries were evaluated histologically.ResultsAt the time of sacrifice, plasma thyroid-stimulating hormone concentrations were 20- to 40-fold increased, thyroxine concentrations were negligible while tri-iothyronin concentrations were decreased by 40% in the hypothyroid group, confirming that the animals were hypothyroid. Primordial, primary and preantral follicle numbers were significantly lower in the hypothyroid ovaries compared to the euthyroid controls, while a downward trend in antral follicle and corpora lutea numbers was observed. Surprisingly the percentage of atretic follicles was not significantly different between the two groups, suggesting that the reduced preantral and antral follicle numbers were presumably not the consequence of increased degeneration of these follicle types in the hypothyroid group. Plasma anti-Müllerian hormone (AMH) levels showed a significant correlation with the growing follicle population represented by the total ovarian number of primary, preantral and antral follicles, suggesting that also under hypothyroid conditions AMH can serve as a surrogate marker to assess the growing ovarian follicle population.ConclusionsThe induction of a chronic hypothyroid condition in adult female rats negatively affects the ovarian follicular reserve and the size of the growing follicle population, which may impact fertility.
Highlights
There is substantial evidence both in humans and in animals that a prolonged reduction in plasma thyroid hormone concentration leads to reproductive problems, including disturbed folliculogenesis, impaired ovulation and fertilization rates, miscarriage and pregnancy complications
There is substantial evidence that a prolonged reduction in thyroid hormone (TH) concentration leads to a broad spectrum of reproductive problems, including disturbed folliculogenesis, impaired ovulation and fertilization rate, and in severe cases to complete ovarian failure [3,4,5,6]
We have developed an animal model of diet-induced hypothyroidism by depleting the endogenous iodine stores of rats to study the effects of chronic hypothyroidism on ovarian follicular development [17]
Summary
There is substantial evidence both in humans and in animals that a prolonged reduction in plasma thyroid hormone concentration leads to reproductive problems, including disturbed folliculogenesis, impaired ovulation and fertilization rates, miscarriage and pregnancy complications. There is substantial evidence that a prolonged reduction in TH concentration leads to a broad spectrum of reproductive problems, including disturbed folliculogenesis, impaired ovulation and fertilization rate, and in severe cases to complete ovarian failure [3,4,5,6]. In the UK for instance, two thirds of pregnant women are iodine deficient and at risk to develop hypothyroidism. This implies that hypothyroidism is a less rare condition in women at reproductive age than anticipated
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