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Fluctuation of fetal rat hepatic histidine decarboxylase activity through the glucocorticoid-ACTH system.

Abstract
Our studies suggest that the fluctuation of HDC activity in fetal liver in late gestation is regulated by the plasma glucocorticoid level through the pituitary-adrenal system. Taken together, these results support the conclusion that glucocorticoid promotes a rapid increase in HDC synthesis in fetal liver histamine-forming cells, as well as in mouse mastocytoma P-815 cells and rat glandular stomachs.
AuthorsE Ohmori, N Imanishi, M Ohgoh, T Fukui, A Ichikawa
JournalBiochemical pharmacology (Biochem Pharmacol) Vol. 41 Issue 5 Pg. 844-7 (Mar 01 1991) ISSN: 0006-2952 [Print] England
PMID1847820 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Histamine
  • Adrenocorticotropic Hormone
  • Histidine Decarboxylase
  • Corticosterone
Topics
  • Adrenocorticotropic Hormone (blood, metabolism)
  • Animals
  • Corticosterone (blood, metabolism)
  • Fetus (enzymology)
  • Histamine (metabolism)
  • Histidine Decarboxylase (biosynthesis, blood)
  • Liver (embryology, enzymology)
  • Pituitary-Adrenal System (physiology)
  • Rats
  • Rats, Inbred Strains

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