New insights regarding glucocorticoids, stress and gonadotropin suppression

Breen, Kellie M.; Karsch, Fred J.

doi:10.1016/j.yfrne.2006.03.335

Cited by 113 publications

(76 citation statements)

References 89 publications

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“…Stress can act at multiple levels to disrupt breeding, including at the brain, the pituitary, and directly at the level of the gonads (Consten et al 2002, Michael et al 2003, Breen and Karsch 2006, Oakley et al 2009, Schoech et al 2009). In House Sparrows, we found evidence of seasonal regulation of CORT receptors in whole brain, but not in hippocampus or gonads.…”

Section: Discussionmentioning

confidence: 99%

“…Although there is significant GR and MR binding in House Sparrow testes and ovary (Lattin et al 2012b), and CORT can suppress steroidogenesis and other reproductive processes by acting directly on the gonads (Hsueh and Erickson 1978, Sapolsky 1985, Consten et al 2002, 11β hydroxysteroid dehydrogenase type 2, which converts CORT into an inactive metabolite, may also be present in these tissues, as it is in the gonads of other animals (Michael et al 1993, Monder et al 1994, Denari and Ceballos 2005. This may prevent CORT from binding to gonadal GR and MR in situations of short-term stress and could be the reason that the short-term down-regulation of reproduction by stress seems to happen primarily via regulation at the brain and pituitary (Rivier andRivest 1991, Breen andKarsch 2006). Suppressing reproduction at the level of the gonads may have longer-term effects that would persist beyond the duration of a transitory stressor.…”

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confidence: 99%

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Seasonal variation in corticosterone receptor binding in brain, hippocampus, and gonads in House Sparrows (Passer domesticus)

Lattin

Romero

2013

The Auk

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Seasonal variation in corticosterone receptor binding in brain, hippocampus, and gonads in House Sparrows (Passer domesticus)

Lattin

Romero

2013

The Auk

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“…Stress-like levels of cortisol could either reduce pituitary responsiveness to GnRH or inhibit hypothalamic synthesis and secretion of GnRH itself. Breen and Karsch (2006) found that stress-like levels of cortisol directly reduced reproductive neuroendocrine function in ovariectomised ewes by reducing pituitary responsiveness to both endogenous and exogenous GnRH pulses, instead of inhibiting GnRH itself. Furthermore, the suppressive action of cortisol on pituitary responsiveness to GnRH is supported during the presence of oestradiol (Oakley et al 2009).…”

Section: Hpa-hpg Axes Interplay On Gnrhmentioning

confidence: 96%

“…In female animals, gonadotrophin action is dependent upon the target structure on the ovary during the reproductive cycle, being either the corpus luteum or the dominant follicle (Nestor 2012). During the follicular phase of the female reproductive cycle, FSH is responsible for initiating follicular growth and maturation and producing oestrogen from the ovary (Breen & Karsch 2006). During the luteal phase of the female reproductive cycle, LH triggers ovulation and the development of the corpus luteum and stimulates progesterone production from the corpus luteum (Nestor 2012).…”

Section: Functional Interactions Between the Hpa And Hpg Axesmentioning

confidence: 99%

Influences of the stress endocrine system on the reproductive endocrine axis in sheep (Ovis aries)

Narayan

Parisella

2017

Italian Journal of Animal Science

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The hypothalamic-pituitary-adrenal (HPA) axis and the hypothalamic-pituitary-gonadal (HPG) axis systems are inversely related in humans and animals. Although livestock animals, such as sheep (Ovis aries), tend to be well adapted to their environment, it is known that the livestock production processes subject animals to a multitude of physical and psychological stressful stimuli that have the potential to elevate the HPA axis activity. Chronic stress is one of the major challenges in sheep production, as it is difficult to detect and can result in prolonged dysfunction of the HPA axis, causing downstream negative physiological effects such as immunosuppression, increased susceptibility to disease and reproductive dysfunction. The elevation of HPA axis activity during chronic stress has been suggested as the primary neuroendocrine mechanism underlying the aetiology of reproductive dysfunction in sheep. Research in sheep has demonstrated that glucocorticoids act on the HPG axis at the level of the hypothalamus and hypophyseal portal system to decrease gonadotrophin secretion and at the level of the pituitary gland to reduce responsiveness and sensitivity of gonadotroph cells and their receptors to GnRH. Sheep farming enterprises rely on the breeding efficacy of ewes to optimise lambing percentage and reproductive success in order to ensure a profitable business. This review discusses the influences of the HPA axis on the HPG axis and defines any significant reproductive function consequences caused by stress in ewes and places them into perspective for sheep management and productivity.ARTICLE HISTORY

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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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New insights regarding glucocorticoids, stress and gonadotropin suppression

Cited by 113 publications

References 89 publications

Seasonal variation in corticosterone receptor binding in brain, hippocampus, and gonads in House Sparrows (Passer domesticus)

Seasonal variation in corticosterone receptor binding in brain, hippocampus, and gonads in House Sparrows (Passer domesticus)

Influences of the stress endocrine system on the reproductive endocrine axis in sheep (Ovis aries)

Hypogonadotropic Hypogonadism in Males with Glycogen Storage Disease Type 1

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