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Histidine decarboxylase expression and histamine metabolism in gastric oxyntic mucosa during hypergastrinemia and carcinoid tumor formation.

Artikel i vetenskaplig tidskrift
Författare Lars Kölby
Bo Wängberg
Håkan Ahlman
I M Modlin
G Granérus
E Theodorsson
Ola Nilsson
Publicerad i Endocrinology
Volym 137
Nummer/häfte 10
Sidor 4435-42
ISSN 0013-7227
Publiceringsår 1996
Publicerad vid Institutionen för de kirurgiska disciplinerna, Avdelningen för kirurgi
Sidor 4435-42
Språk en
Länkar www.ncbi.nlm.nih.gov/entrez/query.f...
Ämnesord Animals, Carcinoid Tumor, etiology, metabolism, Female, Gastric Mucosa, metabolism, Gastrins, blood, pharmacology, Histamine H2 Antagonists, administration & dosage, pharmacology, Histamine Release, Histidine Decarboxylase, genetics, metabolism, Male, Muridae, Parietal Cells, Gastric, metabolism, RNA, Messenger, metabolism, Stomach, metabolism, Stomach Neoplasms, etiology, metabolism, Time Factors, Tissue Distribution, Triazoles, administration & dosage, pharmacology
Ämneskategorier Cancer och onkologi, Kirurgi, Gastroenterologi

Sammanfattning

Histamine is an important stimulator of gastric acid secretion. In experimental animals, inhibition of acid secretion by long term histamine2 receptor blockade causes hypergastrinemia, proliferation of enterochromaffin-like (ECL) cells, and formation of histamine-producing gastric carcinoids. The aim of this study was to examine the role of gastrin in histamine synthesis and metabolism of the oxyntic mucosa of normal, hyperplastic, and carcinoid-bearing Mastomys natalensis. Administration of exogenous gastrin to normal animals increased histidine decarboxylase (HDC) messenger RNA (mRNA) expression in the oxyntic mucosa within 30 min, indicating that gastrin stimulates histamine synthesis by regulating HDC mRNA abundance. Endogenous hypergastrinemia, induced by short term histamine2 receptor blockade (loxtidine) for 3-29 days, did not induce tumors, but enhanced the expression of HDC mRNA (2- to 4-fold elevated) and histamine contents (2-fold elevated) in the oxyntic mucosa. Long term histamine2 receptor blockade (7-21 months) resulted in sustained hypergastrinemia and ECL tumor formation. Tumor-bearing animals had a 4-fold increase in HDC mRNA expression and histamine contents of the oxyntic mucosa. Urinary excretion of the histamine metabolite methyl-imidazole-acetic acid was 2-fold elevated. Tumor-bearing animals recovering from histamine2 receptor blockade were normogastrinemic and had normal levels of HDC mRNA and histamine in the oxyntic mucosa as well as normal excretion of methyl-imidazole-acetic acid. The results indicate that ECL cell carcinoids developing during hypergastrinemia are well differentiated tumors that respond to high gastrin levels with increased histamine synthesis and secretion.

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