Glucocorticoid repression of the reproductive axis: Effects on GnRH and gonadotropin subunit mRNA levels

Gore, Andrea C.; Attardi, Barbara; DeFranco, Donald B.

doi:10.1016/j.mce.2006.06.002

Cited by 83 publications

(60 citation statements)

References 46 publications

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“…E 2 , P 4 , and T 4 are the most representative steroids, and their main source is from the follicles of gonads, while adrenal tissue is a minor source by several stressinduced synthesis pathways (Rivier & Rivest 1991, Sapolosky et al 2000, Tilbrook et al 2000, Goldstein 2004, Gore et al 2006, Kirby et al 2009). The gonads could affect the hypothalamic-pituitary-adrenal (HPA) axis at all levels (Viau et al 2001, Viau 2002, Garcia et al 2003, Seale et al 2004, Evuarherhe et al 2009).…”

Section: Discussionmentioning

confidence: 99%

Follicle growth and oocyte development after ovary transplantation into back muscle of immune-intact adult castrated male mice

Li¹,

Tao²,

Zhang³

et al. 2010

Reproduction

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Ovary grafting is not only a method of investigating follicle and oocyte development, but also a useful model to explore the possibility of the re-establishment of the reproductive axis in male-to-female sexual reversal. This study investigated ovary survival and follicle development after mouse ovaries were transplanted into immune-intact castrated male mice. Ten-day-old mouse ovaries were transplanted into the back muscle of adult outbred castrated male mice treated with immunosuppressants. Twenty-two days later, the ovary structure and the number of follicles present was examined by hematoxylin and eosin staining. The oocytes were harvested, and then used for in vitro maturation (IVM) and IVF. The results showed that primordial and antral follicles were mainly found in the grafts, and there were obvious differences compared with 32-day-old fresh ovaries (P!0.05). Embryos were derived from collected oocytes after IVM and IVF with a 72.4% cleavage rate and 7.9% blastocyst rate; 12 live pups were generated by embryo transfer. The hormone assay showed that plasma concentrations of both estrogen and progesterone increased after ovarian transplantation (P!0.01). In conclusion, immune-intact adult castrated male mice can support ovary survival and further development of follicles with endocrine function after ovarian transplantation.

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Section: Discussionmentioning

confidence: 99%

Follicle growth and oocyte development after ovary transplantation into back muscle of immune-intact adult castrated male mice

Li¹,

Tao²,

Zhang³

et al. 2010

Reproduction

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“…Cushing's Syndrome), or when women or animals experience chronic stimulation of the hypothalamic-pituitary-adrenal axis [1]. Glucocorticoidrelated reproductive suppression may involve disruption of central [1][2][3][4][5] and peripheral [6][7][8][9][10] functions of the reproductive axis as demonstrated by work in multiple species including rats [11][12][13], mice [14], sheep [15][16][17], humans [18,19] and other primates [7,20].The suppressive effect of glucocorticoids, however, is not universal. Synthetic corticoids variably stimulate the release of pituitary hormones, follicle stimulating hormone (FSH), luteinizing hormone (LH) and prolactin (PRL) [21], enhance FSH action in the follicular phase of the cycle [10], and may accelerate the timing of ovulation and increase the number of oocytes released [22][23][24][25].…”

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confidence: 99%

Dexamethasone Enhances Fertility and Preovulatory Serum Prolactin Levels in eCG/hCG Primed Immature Rats

Rockwell

Koos

2009

Journal of Reproduction and Development

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Abstract. Glucocorticoids have heterogeneous effects on reproductive function. We used a gonadotropin-primed, immature rat model to study the influence of dexamethasone (1 mg/kg), given during the latter stages of follicular development, on litter size, the number of oocytes released, and pituitary hormone levels. Dexamethasone-treated females released a larger number of oocytes at ovulation and gave birth to larger litters indicating the oocytes were viable. Survival to weaning age was not affected but average weight at weaning was lower for pups born to DEXtreated females. Serum FSH and LH were assayed at 12, 24 and 48 h following eCG and did not differ between dexamethasone-treated and control animals, but prolactin showed a prolonged pattern of elevation in DEX-treated females. Prolactin, which normally exhibits an elevation on proestrous, may modulate follicular development. Dexamethasone enhances fertility and fecundity possible through an effect of prolactin on follicle development, or by other direct effects on the ovary. These results may improve our understanding of the usefulness of DEX in assisted reproductive therapies for women. Key words: Fecundity, Glucocorticoids, Ovary (J. Reprod. Dev. 55: [247][248][249][250][251] 2009) eproductive function is often suppressed by the elevation of endogenous, or administration of exogenous, glucocorticoids. Anovulation and menstrual or estrous cycle disruptions can occur in conditions marked by adrenal hyperactivity (e.g. Cushing's Syndrome), or when women or animals experience chronic stimulation of the hypothalamic-pituitary-adrenal axis [1]. Glucocorticoidrelated reproductive suppression may involve disruption of central [1][2][3][4][5] and peripheral [6][7][8][9][10] functions of the reproductive axis as demonstrated by work in multiple species including rats [11][12][13], mice [14], sheep [15][16][17], humans [18,19] and other primates [7,20].The suppressive effect of glucocorticoids, however, is not universal. Synthetic corticoids variably stimulate the release of pituitary hormones, follicle stimulating hormone (FSH), luteinizing hormone (LH) and prolactin (PRL) [21], enhance FSH action in the follicular phase of the cycle [10], and may accelerate the timing of ovulation and increase the number of oocytes released [22][23][24][25]. In addition, acute exposure to stressful stimuli (e.g. restraint), presumably activating the endogenous hypothalamic-pituitary-adrenal axis, can enhance ovulation and increase fertility [26]. These stimulatory effects have been reported in rodent models, especially the rat, usually following treatment with dexamethasone (DEX) but triamcinolone acetonide, corticosterone and cortisol have also been used and some of these compounds give similar results [23,27]. Prior studies did not assess whether DEX-enhanced reproductive function also impacted fertility or offspring quality. The immature, gonadotropin-primed rat model is commonly used to assess follicular development, ovarian steroidogenesis, and ovulation. Because these ani...

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“…In GSD1 patients with suboptimal metabolic control, hypogonadism may be secondary to chronic recurrent elevations of cortisol in response to hypoglycemia, with resulting suppression of GnRH, LH, and FSH release (Gore et al 2006;Breen and Karsch 2006).…”

Section: Discussionmentioning

confidence: 99%

Hypogonadotropic Hypogonadism in Males with Glycogen Storage Disease Type 1

et al. 2017

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Background: Glycogen storage disease type 1 is an autosomal recessive disorder with an incidence of 1 in 100,000. Long-term complications include chronic blood glucose lability, lactic academia, short stature, osteoporosis, delayed puberty, gout, progressive renal insufficiency, systemic or pulmonary hypertension, hepatic adenomas at risk for malignant transformation, anemia, vitamin D deficiency, hyperuricemic nephrocalcinosis, inflammatory bowel syndrome (type 1b), hypertriglyceridemia, and irregular menstrual cycles. We describe hypogonadotropic hypogonadism as a novel complication in glycogen storage disease (GSD) type 1.Case Studies and Methods: Four unrelated patients with GSD 1a (N ¼ 1) and 1b (N ¼ 3) were found to have hypogonadotropic hypogonadism diagnosed at different ages. Institutional Research Ethics Board approval was obtained as appropriate. Participant consent was obtained. A retrospective chart review was performed and clinical symptoms and results of investigations summarized as a case series. Results: All patients were confirmed biochemically to have low luteinizing hormone (LH) and follicular stimulating hormone (FSH), and correspondingly low total testosterone. Clinical symptoms of hypogonadism varied widely. Investigations for other causes of hypogonadotropic hypogonadism were unremarkable. In addition, all patients were found to have disproportionately low bone mineral density at the lumbar spine compared to the hip. Common to all patients was erratic metabolic control, including recurrent hypoglycemia and elevated lactate levels. Discussion: Recurrent elevations in cortisol in response to hypoglycemia may be the underlying pathology leading to suppression of gonadotropin-releasing hormone (GnRH) release. Incorporating clinical and/or biochemical screening of the hypothalamic-pituitary-gonadal axis may be important in the management of this disease. Testosterone therapy however needs to be carefully considered because of the risk of hepatic adenomas.

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Glucocorticoid repression of the reproductive axis: Effects on GnRH and gonadotropin subunit mRNA levels

Cited by 83 publications

References 46 publications

Follicle growth and oocyte development after ovary transplantation into back muscle of immune-intact adult castrated male mice

Follicle growth and oocyte development after ovary transplantation into back muscle of immune-intact adult castrated male mice

Dexamethasone Enhances Fertility and Preovulatory Serum Prolactin Levels in eCG/hCG Primed Immature Rats

Hypogonadotropic Hypogonadism in Males with Glycogen Storage Disease Type 1

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