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Updated: Jul 3, 2026
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Isolation of Leukocytes from the Human Maternal-fetal Interface
Published on: May 21, 2015
Beta-endrophin immunoreactivity during human pregnancy.
1Maternal Health Research Centre, Endocrine Unit, John Hunter Hospital, New Lambton Heights, New South Wales, Australia.
The Journal of Clinical Endocrinology and Metabolism
|December 1, 1992
Summary
The placenta acetylates beta-endorphin (beta E), inactivating its opiate activity. Elevated beta E in pregnancy plasma originates from the pituitary, not the placenta, despite placental corticotropin-releasing factor.
Area of Science:
- Reproductive Endocrinology
- Neuroendocrinology
- Peptide Hormone Research
Background:
- The human placenta is a known source of peptide hormones during pregnancy.
- Previous research detected beta-endorphin (beta E) immunoreactivity in placental extracts, but its secretion and bioactivity in maternal circulation remained unclear.
Purpose of the Study:
- To determine if placental beta-endorphin (beta E) is secreted into maternal circulation.
- To assess if placental beta E is opiate receptor active during pregnancy.
- To elucidate the nature of beta E immunoreactivity (IR) in the placenta.
Main Methods:
- Simultaneous measurement of beta E IR and N-alpha-acetylated beta E (Ac beta E) IR in human pituitary, placental, and plasma extracts using homologous RIAs.
- Gel filtration chromatography to analyze the size and acetylation status of beta E in different tissues and plasma.
- Comparison of beta E31:beta-lipotropin ratios in pituitary, placental, and plasma extracts.
Main Results:
- Placental extracts showed extensive N-alpha-acetylation (up to 60%) of beta E31, rendering it opiate inactive, unlike pituitary extracts (<1% acetylation).
- Plasma beta E IR during pregnancy was primarily non-acetylated and similar in size to beta-lipotropin, resembling pituitary beta E.
- Elevated plasma beta E IR in late pregnancy is consistent with a pituitary origin, potentially influenced by placental corticotropin-releasing factor.
Conclusions:
- The placenta extensively acetylates beta-endorphin, destroying its opiate bioactivity.
- Maternal plasma beta-endorphin during pregnancy originates mainly from the pituitary gland.
- Elevated pituitary-derived beta E in pregnancy may be linked to placental corticotropin-releasing factor.
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