Lymphatic diamine oxidase secretion stimulated by fat absorption is linked with histamine release.

Diamine oxidase (DAO) is abundantly expressed in mammalian small intestine catalyzing the oxidative breakdown of polyamines and histamine. The aim of this study was to determine the relationship between stimulation of intestinal diamine oxidase secretion with intestinal fat absorption and histamine release. Conscious intestinal lymph fistula rats were used.

Moderate folate deficiency influences polyamine synthesis in rats.

Spermidine, spermine and putrescine are polyamines, essential growth factors in mammalian cells. Decarboxylated S-adenosylmethionine (SAM) is an essential precursor in the formation of both spermidine and spermine. SAM is formed from methionine through the addition of adenosine.

Nutrients regulate diamine oxidase release from intestinal mucosa.

Diamine oxidase is continuously released from the intestinal mucosa and carried to the circulation by the lymphatics. The effect of nutrients on this release was examined. Rats were prepared with duodenal and intestinal lymph cannulas.

Role of mast cell histamine in brown adipose tissue thermogenic response to VMH stimulation.

Electrical stimulation of the ventromedial hypothalamic area in rats caused a significant but transient increase in interscapular brown adipose tissue temperature. This response was markedly reduced by cimetidine, a histamine H2-receptor antagonist, but not by pyrilamine, an H1-receptor antagonist. Histamine is present in substantial amounts within mast cells in brown adipose tissue as injections of compound 48/80, which cause degranulation of connective tissue mast cells, reduced the tissue histamine content by > 85%.

Mucosal histamine elimination and its effect on acid secretion in rabbit gastric mucosa.

Background: Rapid elimination of histamine near the oxyntic cells is important in the termination of the secretory response when the signal for histamine release is discontinued. The mechanism of this local process is still unclear.

Method: Gastric mucosal histamine elimination was, therefore, examined in fundic mucosa mounted in flux chambers and in dispersed mucosal cells.

Uptake and methylation of histamine by dispersed gastric mucosal cells and its possible influence on acid secretion.

Inactivation of histamine by gastric mucosal tissue was examined in dispersed rabbit gastric mucosal cells. Mucosal cells were incubated with [14C]histamine. The formed radioactive metabolites were separated and identified by thin layer co-chromatography and quantitated, in both the cellular and extracellular mediums.

Histamine methyltransferase in dispersed cells from rabbit fundic mucosa.

The cellular distribution of histamine N-methyltransferase was studied in rabbit gastric mucosa. The fundic mucosa was dispersed by collagenase treatment in Hanks' or calcium-free medium. In calcium-free medium, the number of dispersed cells/g wet tissue, as well as their viability was increased; histamine N-methyltransferase recovery was up to three-fold larger than in cells prepared in Hanks' medium.

Histamine uptake and its methylation by isolated oxyntic cells.

The role of the oxyntic cells in the inactivation and elimination of histamine was studied in dispersed and isolated mucosal cells. Gastric mucosal cells from rabbits were incubated with 14C-labelled histamine (1 and 3.2 X 10(-6) M) at 37 degrees C.

Regulation of gastric acid secretion at the cellular level.

Gastric acid secretion is controlled by neurocrine, endocrine, and paracrine pathways. At the organ level, the neurocrine and endocrine systems provide long-range regulation; and near the target cell the paracrine system appears to predominate. The integration of the regulatory commands from these various pathways is complex and, as a result, some pathways have not yet been clearly defined.

Quantitative determination of histamine metabolites by capillary gas chromatography.

A method using capillary gas chromatography is described for the determination of histamine and eight of its basic and acid metabolites in a single biological sample of serum, urine, or gastric juice. Ion-exchange chromatography and extraction with organic solvents are used for isolation and purification, and gas chromatography for identification and quantitation. The heptafluorobutyryl derivatives of histamine and some basic metabolites are compatible with nitrogen-phosphorus and electron capture detection modes and offer an excellent sensitivity (detection limit 0.

Quantitation of histamine and some of its basic methylated metabolites in biological materials by gas-liquid chromatography.

A method which measures histamine, its basic metabolites, and some analogs in biological materials is described. The procedure consists of ion-exchange chromatography and chromatography on silicic acid for isolation and purification, and gas chromatography for identification and quantitation. The isolated compounds are prepared for gas chromatography by double derivatization with heptafluorobutyric anhydride and acetic anhydride.

Acute necrosis of the intestinal mucosa with high serum levels of diamine oxidase.

A patient with acute necrosis of the intestinal mucosa and high serum diamine oxidase activity is described. The 71-year-old woman, with a history of hypertension and cardiovascular and peripheral arteriosclerotic disease, presented with acute epigastric pain, vomiting, and a deteriorating hemodynamic condition. Serum level of the intestinal enzyme diamine oxidase (DAO) obtained on admission, approximately 24 hr after the onset of symptoms, was 7.

Carbonic anhydrase activity and aminopyrine uptake in isolated gastric mucosal cells.

The role of carbonic anhydrase in the regulation and production of gastric acid was examined. Studies were done on isolated rabbit fundic mucosal cells, in which carbonic anhydrase activity and [14C]aminopyrine uptake were measured. The oxyntic cell-enriched cell fractions had the largest carbonic anhydrase content (4.

Release of intestinal diamine oxidase by histamine in rats.

Diamine oxidase activity was measured in the intestinal mucosa, lymph, and in the serum of rats, to determine whether histamine, a substrate of diamine oxidase, liberates this enzyme from its mucosal storage site(s). Histamine induced a sharp rise in intestinal lymph flow, lymph protein, and lymph diamine oxidase, lasting less than 1 h after the histamine injection. The rise in lymph diamine oxidase activity was dose dependent over a narrow concentration range (0.

Effect of intestinal ischemia on diamine oxidase activity in rat intestinal tissue and blood.

This study examines the effect of increasing duration of intestinal ischemia on the mucosal integrity and the release of the enzyme diamine oxidase from the small intestine. Acute ischemia was produced by the occlusion of the superior mesenteric artery, and the subsequent changes in DNA and 125I-albumin content in the lumen were taken as indices of intestinal lesions. Diamine oxidase activity was measured in the intestinal lumen, mucosa, lymph, and serum.

Actions of histamine, secretin, and PGE2 on cyclic AMP production by isolated canine fundic mucosal cells.

Cyclic AMP production was studied in isolated canine fundic gastric mucosal cells. Histamine, prostaglandin E2 (PGE2), and secretin increased cyclic AMP production by unenriched mucosal cells. In separated cell fractions, histamine stimulation of cyclic AMP production correlated with the parietal cell content of the fractions.

Histamine and cyclic AMP in isolated canine parietal cells.

The relationship between cyclic AMP production and the response of isolated canine parietal cells to histamine has been examined. Histamine increased cyclic AMP generation, and this effect correlated with histamine stimulation of oxygen consumption and aminopyrine accumulation. Metiamide inhibited histamine-stimulated cyclic AMP generation and oxygen consumption in a parallel fashion.

Effect of histamine on canine gastric mucosal adenylate cyclase.

The effects of histamine, Nalpha-dimethylhistamine, 4,5-methylhistamine, Ntau-methylhistamine, pentagastrin, carbachol, and NaF on the adenylate cyclase activity from canine gastric mucosa were investigated in cell-free preparations. In gastric fundic mucosa, histamine (10(-4) M), Nalpha-dimethylhistamine (10(-4) M), 4,5-methylhistamine (10(-4 M), and NaF (10)-2) M) significantly (P less than 0.001) increased adenylate cyclase activity (means+/-SE) by 44.

Blocking of olive oil induced plasma protein escape from the intestinal circulation by histamine antagonists and by a diamine oxidase releasing agent.

Earlier studies have shown that feeding of olive oil to rats substantially increased the plasma protein in the intestinal lymph. The possibility of histamine mediating this response was examined. The plasma protein escape from intestinal circulation after olive oil feeding was measured in rats in terms of the amount of Evans Blue labelled plasma protein found in the intestinal lymph.

Interaction of prostaglandins and histamine with enzymes of cyclic AMP metabolism from guinea pig gastric mucosa.

Prostaglandins (PGE1, PGE2, PGA1) and histamine have opposing effects on gastric HCl secretion, but we found that both stimulate adenylate cyclase activity in cell-free membrane preparations of guinea pig gastric fundic mucosa. The stimulatory effect of prostaglandins was found in this study to be specific and dose-dependent over a concentration range from 10(-7) to 10(-4) M. In similar preparations from antral regions of guinea pig gastric mucosa, the adenylate cyclase was stimulated only by PGE1, PGE2, and PGA1 and not by histamine.