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Does the CRH binding protein shield the anterior pituitary from placental CRH?
1Department of Biological Sciences, University of Western Sydney Nepean, Kingswood, NSW, Australia. m.thomson@uws.edu.au
Insights
Pregnancy involves increased corticotropin releasing factor (CRH) from the placenta. A CRH binding protein may limit its effect on the pituitary, but evidence suggests it doesn't fully block placental CRH stimulation.
Area of Science:
- Endocrinology
- Reproductive Biology
- Neuroendocrinology
Background:
- The hypothalamic-pituitary-adrenal (HPA) axis regulates stress response.
- Corticotropin releasing factor (CRH) from the hypothalamus stimulates adrenocorticotropin (ACTH) release from the pituitary.
- ACTH stimulates cortisol release from the adrenal glands.
Purpose of the Study:
- To investigate the role of placental corticotropin releasing factor (CRH) during pregnancy.
- To examine the potential function of a CRH binding protein in modulating placental CRH effects.
- To understand the regulation of adrenocorticotropin (ACTH) levels in pregnant women.
Main Methods:
- The abstract does not specify methods.
- Further research would be needed to determine the specific experimental approaches.
Main Results:
- The placenta produces CRH, leading to elevated plasma CRH in the third trimester.
- A CRH binding protein is hypothesized to mitigate excessive pituitary stimulation by placental CRH.
- Pregnant women exhibit only mildly elevated ACTH levels, suggesting some regulation is in place.
- Evidence indicates the CRH binding protein may not completely prevent placental CRH from affecting pituitary corticotropes.
Conclusions:
- Placental CRH significantly contributes to maternal CRH levels in late pregnancy.
- A CRH binding protein likely plays a role in regulating the HPA axis during gestation.
- The interplay between placental CRH, CRH binding protein, and pituitary ACTH requires further elucidation.
Abstract:
Corticotropin releasing factor (CRH) is released from the hypothalamus and travels to the anterior pituitary where it stimulates the release of adrenocorticotropin (ACTH). In turn, ACTH travels through the blood and stimulates the release of cortisol from the adrenal. The placenta is also a source of CRH and is responsible for the dramatic rises in CRH plasma levels in the third trimester of pregnancy. A CRH binding protein may stop placental CRH from overstimulating the pituitary and may contribute to the reason that pregnant women show only mildly elevated levels of ACTH in the blood. There is evidence to suggest, however, that the CRH binding protein does not completely shield the corticotrope from placental CRH.