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Serum estradiol but not gonadotropin levels decrease acutely after insulin-induced hypoglycemia in cycling women.
1Department of Medicine, Maine Medical Center, Portland 04102.
The Journal of Clinical Endocrinology and Metabolism
|October 1, 1992
Summary
Stress and hypoglycemia acutely lower estradiol in women, but do not suppress gonadotropin-releasing hormone (GnRH) over two hours. Corticotropin-releasing hormone (CRH) may not be the primary driver of acute GnRH suppression in humans.
Area of Science:
- Endocrinology
- Neuroendocrinology
- Reproductive Biology
Background:
- Corticotropin-releasing hormone (CRH) is known to suppress gonadotropin-releasing hormone (GnRH) in animal models.
- The acute effects of CRH on the human hypothalamic-pituitary-gonadal (HPG) axis are not well-defined.
Purpose of the Study:
- To evaluate the acute impact of adrenal axis activation on the HPG axis in humans.
- To investigate the role of endogenous CRH in modulating GnRH secretion during acute stress.
Main Methods:
- Insulin-induced hypoglycemia was used to stimulate endogenous CRH secretion in eight cycling women.
- Serum samples were collected over 120 minutes post-injection of insulin or saline.
- Cortisol levels in hypoglycemic women were compared to those in acutely ill patients with hypogonadotropism.
Main Results:
- Insulin-induced hypoglycemia significantly increased cortisol levels, mimicking stress responses.
- Serum estradiol levels were significantly reduced during hypoglycemia compared to control.
- Serum levels of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) showed no significant change.
Conclusions:
- Acute stress and hypoglycemia can rapidly decrease circulating estradiol levels in women.
- Endogenous CRH does not appear to play a significant role in the acute (2-hour) suppression of GnRH in humans.
- Longer-term effects of CRH on GnRH require further investigation, particularly in conditions like hypothalamic amenorrhea.