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  • 1
    ISSN: 1435-5922
    Keywords: somatostatin ; substance P ; β-endorphin ; thyrotropin-releasing hormone ; inflammatory bowel disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Regulatory neuropeptides are widely distributed in the gastrointestinal tract, where they play an important role in motility, secretion, and immune and inflammatory responses. In this study, the rectal mucosal content of somatostatin (SOM), substance P (SP), β-endorphin (BE), and thyrotropin-releasing hormone (TRH) was measured by radioimmunoassay in 56 patients with ulcerative colitis (UC), 15 patients with Crohn's disease (CD), 15 patients with acute infectious colitis (AIC), and 11 controls, who showed no inflammation of the rectal mucosa, nor abnormal bowel movements. The content of immunoreactive (ir)-SOM was decreased in UC patients, especially in those with persistent disease activity, while the levels of ir-SP, BE, and TRH were increased in such patients. Some changes of ir-peptide levels were also observed in CD and AIC patients. The changes in neuropeptide levels were analyzed in relation to histological grades of inflammation in UC patients, grades 4–5 showing the most significant changes. The levels of ir-SOM, SP, BE, and TRH showed no significant change in chronic persistent UC when measured 6–12 months after the initial examination. In contrast, in patients with remitting intermittent UC, the levels of SP and BE decreased during remission. Abnormal intestinal neuropeptide content may be implicated in the continued mucosal immune and inflammatory responses that are manifested in patients with inflammatory bowel disease.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1435-5922
    Keywords: cold-restraint stress ; thyrotropin-releasing hormone ; somatostatin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of cold-restraint stress on immunoreactive thyrotropin-releasing hormone (ir-TRH) and immunoreactive somatostatin (ir-SOM) concentrations in the rat stomach were investigated. Rats immobilized with a spring-loaded metallic plate were placed in a room maintained at 4°C for 1–3 h and then decapitated serially for investigation. Gastric ir-TRH and ir-SOM concentrations were measured by individual radioimmunoassays. Cold-restraint stress induced gastric mucosal lesions as well as a decrease of the ir-TRH concentration in the glandular stomach, an increase of the ir-TRH concentration in the gastric juice, and a decrease in gastric pH. In contrast, this stress caused an increase of ir-SOM in the glandular stomach and a decrease of ir-SOM in the gastric juice. However, cold or restraint stress alone did not induce gastric mucosal lesions or changes in gastric ir-TRH and ir-SOM concentrations or the gastric pH. To clarify the endocrine influence of peripheral TRH, pretreatment with thyroid hormone was performed to inhibit elevation of the serum TRH level during cold-restraint stress. Despite this pretreatment, cold-restraint stress still induced ulcer formation, along with changes in gastric ir-TRH and ir-SOM concentrations and gastric pH. These findings suggest that changes in gastric ir-TRH and ir-SOM concentrations may be closely related to ulcer formation due to cold-restraint, and that TRH may act in a paracrine manner in the stomach.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1435-5922
    Keywords: Key words: beta-endorphin ; thyrotropin-releasing hormone ; somatostatin ; stomach
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract: The neuropeptides beta-endorphin (BE), thyrotropin-releasing hormone (TRH), and somatostatin (SOM) in the gastric mucosa have the capacity to regulate gastric function. To clarify the possible role of BE in the interactions of neuropeptides and gastric acid secretion we investigated the effect of the intragastric administration of BE on TRH and SOM release into the gastric lumen. BE (100 ng/kg) induced an immediate decrease in TRH release and a reciprocal increase in SOM release into the gastric lumen, followed by the suppression of gastric acid secretion. When various doses of BE (0–500 ng/kg) were administered, changes in TRH and SOM occurred in a dose-dependent manner. Pretreatment with naloxone dihydrochloride (5 mg/kg, intraperitoneally) completely inhibited the BE-induced changes in the release of these peptides. These findings suggest that BE has a paracrine effect on TRH and SOM release into the gastric lumen through opioid receptors, and that these interactions may be involved in the regulation of gastric acid secretion.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1573-2568
    Keywords: somatostatin ; Helicobacter pylori ; human stomach ; ammonia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Immunoreactive-somatostatin (ir-somatostatin) concentrations of the gastric mucosa and gastric juice withHelicobacter pylori infection were measured in the human stomach. One hundred seventy-one patients (106 males, 65 females;, mean age, 52.0; range, 19–84 years) were registered. Gastric juice and mucosa were obtained with the usual endoscopy procedure. Somatostatin concentration was measured by radioimmunoassay. The irsomatostatin concentrations in theH. pylori-negative group were significantly higher than in the positive group gastric mucosa, whereas its levels in gastric juice tended to decrease withH. pylori infection. There was an inverse correlation between luminal ammonia levels and ir-somatostatin concentrations of the gastric mucosa. On the other hand, ir-somatostatin concentrations of the gastric mucosa significantly decreased with chronic and active inflammatory change. This decrease was not correlated with the grade of active inflammation, which was in close relation, toH. pylori infection, but with the grade of chronic inflammation. These results indicate thatH. pylori may reduce ir-somatostatin concentrations of the human stomach and that its effect is partly mediated via luminal ammonia produced byH. pylori.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1573-2568
    Keywords: plaunotol ; omeprazole ; gastrin ; secretin ; somatostatin ; calcitonin gene-related peptide ; vasoactive intestinal polypeptide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Omeprazole markedly inhibits basal and stimulated gastric acid secretion and has the ability to produce hypergastrinemia and hyperplasia of enterochromaffin-like cells in humans. On the other hand, paunotol, an acyclic diterpene alcohol, has been reported to inhibit gastrin release by stimulating endogenous secretin release. We investigated the effect of plaunotol on serum gastrin levels after six to eight weeks of omeprazole (20 mg/day) administration in 22 patients (16 males, 6 females; mean age 52.3, range 36–70 years) with peptic ulcer disease. The patients were randomized to the following two groups: 11 subjects with omerprazole alone (single group) and 11 with omeprazole plus plaunotol (240 mg/day) (combination group) treatment. There were no significant differences between the two groups concerning age, sex, ulcer stage, ulcer history, environmental factors, andHelicobacter pylori (HP) prevalence. After complete drug(s) administration, serum immunoreactive (ir) -gastrin levels increased significantly in the single group (P〈0.001) in contrast to the combination group, and plaunotol significantly inhibited hypergastrinemia induced by omeprazole administration (P〈0.001). Significant increases in serum ir-calcitonin gene-related peptide concentrations were observed in the combination group compared to the single group (P〈0.05). However, there were no significant changes in serum ir-secretin, somatostatin, and vasoactive intestinal polypeptide levels as well as ulcer healing and HP prevalence between the two groups. These findings suggest that plaunotol may suppress hypergastrinemia induced by long-term omeprazole administration, at least partly, via a certain brain-gut hormone affecting gastrin release.
    Type of Medium: Electronic Resource
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