Relationship between melatonin levels in plasma and gastrointestinal tissues and the incidence and severity of gastric ulcers in pigs

Bubenik, George A.; Ayles, H. L.; Friendship, Robert; Brown, Gregory M.; Ball, Ronald O.

doi:10.1111/j.1600-079x.1998.tb00367.x

Cited by 50 publications

(49 citation statements)

References 27 publications

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“…Although binding site parameters exhibited diurnal variation in some species, this was not confirmed in others [52,54,69]. In addition, large variations of melatonin concentrations in the individual segments of the GIT were found among many species of birds and mammals [9,35,38,44,57,64,66,[68][69][70]. Often, these tremendous variations of melatonin concentrations in GIT tissues appears to be related to food intake rather than to photoperiodicity as is the case of pineal-produced melatonin [41,70,71].…”

Section: Ontogeny and Phylogenymentioning

confidence: 99%

“…As an injection or an alimentary administration of exogenous melatonin and its precursor tryptophan resulted in a significant accumulation of melatonin in the GIT [39,49,[55][56][57], it was initially questioned whether the presence of melatonin in the digestive system is due to its accumulation from the circulation (particularly during the night) or due to an independent synthesis in situ [49]. A significant diurnal variation of melatonin concentrations in some GI tissues (with plasma concentration much higher during the night) was reported by several authors in intact animals, mostly birds [52,[58][59][60].…”

Section: Ontogeny and Phylogenymentioning

confidence: 99%

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Localization, Physiological Significance and Possible Clinical Implication of Gastrointestinal Melatonin

2001

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The gastrointestinal tract (GIT) is a major source of extrapineal melatonin. In some animals, tissue concentrations of melatonin in the GIT surpass blood levels by 10–100 times and the digestive tract contributes significantly to melatonin concentrations in the peripheral blood, particularly during the day. Some melatonin found in the GIT may originate from the pineal gland, as the organs of the digestive system contain binding sites, which in some species exhibit circadian variation. Unlike the production of pineal melatonin, which is under the photoperiodic control, release of GI melatonin seems to be related to periodicity of food intake. Melatonin and melatonin binding sites were localized in all GI tissues of mammalian and avian embryos. Postnatally, melatonin was localized in the GIT of newborn mice and rats. Phylogenetically, melatonin and melatonin binding sites were detected in GIT of numerous mammals, birds and lower vertebrates. Melatonin is probably produced in the serotonin-rich enterochromaffin cells (EC) of the GI mucosa and can be released into the portal vein postprandially. In addition, melatonin can act as an autocrine or a paracrine hormone affecting the function of GI epithelium, lymphatic tissues of the immune system and the smooth muscles of the digestive tube. Finally, melatonin may act as a luminal hormone, synchronizing the sequential digestive processes. Higher peripheral and tissue levels of melatonin were observed not only after food intake but also after a long-term food deprivation. Such melatonin release may have a direct effect on the various GI tissues but may also act indirectly via the CNS; such action might be mediated by sympathetic or parasympathetic nerves. Melatonin can protect GI mucosa from ulceration by its antioxidant action, stimulation of the immune system and by fostering microcirculation and epithelial regeneration. Melatonin may reduce the secretion of pepsin and the hydrochloric acid and influence the activity of the myoelectric complexes of the gut via its action in the CNS. Tissue or blood levels of melatonin may serve as a marker of GI lesions or tumors. Clinically, melatonin has a potential for a prevention or treatment of colorectal cancer, ulcerative colitis, irritable bowel syndrome, children colic and diarrhea.

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Section: Ontogeny and Phylogenymentioning

confidence: 99%

Section: Ontogeny and Phylogenymentioning

confidence: 99%

Localization, Physiological Significance and Possible Clinical Implication of Gastrointestinal Melatonin

2001

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“…The ulcers in this case may have been due to a local deficiency of the melatonin synthesis [7] . Recently, melatonin (combined with other natural supplements) was successfully used to heal a patient with a giant ulcer of 6 cm (about 3.2 inches).…”

Section: Clinical Usementioning

confidence: 78%

“…Bubenik et al [7] demonstrated that a 4-wk administration of melatonin in the diet significantly reduced the incidence of spontaneous gastric ulcers in young pigs. The ulcers in this case may have been due to a local deficiency of the melatonin synthesis [7] .…”

Section: Clinical Usementioning

confidence: 99%

Which is the best choice for gastroesophageal disorders: Melatonin or proton pump inhibitors?

Torres

Pereira²

2010

WJGPT

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Author contributions: Oliveira-Torres JDF is credited with valuable discussions related to patient biopsy samples, drawing of the structures, acquisition, analysis and interpretation of data (database search work in pubmed and web of science), organization of references and valuable discussions about the questions of referees; Pereira RS is credited with the main idea of chemical structure comparison between omeprazole and melatonin and the possible mechanism of action, writing of the manuscript and answers for the referees. AbstractMelatonin is used in many countries to improve sleep disorders. Melatonin is a hormone produced by the pineal gland and enterochromaffin cells which control sleep and gastrointestinal motility. Low levels of melatonin lead to gastroesophageal reflux disease (GERD). Most of patients with GERD have a sleep disorder. So, low melatonin levels is the main cause of insomnia. Beyond this, it has an inhibitory action on gastric acid secretion and seems to control the lower esophageal sphincter. Proton pump inhibitors (PPIs) are a group of drugs whose main action is a pronounced and long-lasting reduction of gastric acid production. They are the most potent inhibitors of acid secretion available today. Omeprazole (one of the PPIs) and melatonin have similarities in their chemical structures. Therefore, we could consider omeprazole as a rough copy of melatonin. In this paper, we compare the advantages and disadvantages of the clinical use of melatonin and PPIs.

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“…The physiological role of the melatonin produced in the gut remains unclear. In the gastrointestinal system, melatonin relaxes the smooth muscles of the gut and blood vessels and increases mucosal blood flow, thus preventing the development or initiating the healing of gastric and intestinal ulcers [6,23,49,51,52]. It is also an effective agent against experimental colitis [48].…”

Section: Discussionmentioning

confidence: 99%

Pinealectomy aggravates acute pancreatitis in the rat

Jaworek

Żwirska-Korczala

Szklarczyk

et al. 2010

Pharmacological Reports

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Abstract:Melatonin, a pineal indoleamine, protects the pancreas against acute damage; however, the involvement of the pineal gland in the pancreatoprotective action of melatonin is unknown. The primary aim of this study was to determine the effects of pinealectomy on the course of acute caerulein-induced pancreatitis (AP) in rats. AP was induced by a subcutaneous infusion of caerulein (25 µg/kg) into pinealectomized or sham-operated animals. Melatonin (5 or 25 mg/kg) was given via intraperitoneal (ip) injection 30 min prior to the induction of AP. The pancreatic content of the lipid peroxidation products malondialdehyde and 4-hydroxynonenal (MDA + 4HNE) and the activity of an antioxidative enzyme, glutathione peroxidase (GSH-Px), were measured in each group of rats. Melatonin blood levels were measured by radioimmunoassay (RIA). In the sham-operated rats, AP was confirmed with histological examination and manifested as pancreatic edema and an increase in the blood lipase level (by 1,500%). In addition, the pancreatic content of MDA + 4HNE was increased by 200%, and pancreatic glutathione peroxydase (GSH-Px) activity was reduced by 40%. Pinealectomy significantly aggravated the histological manifestations of AP, reduced the GSH-Px activity and markedly augmented the levels of MDA + 4HNE in the pancreas of rats with or without AP as compared to sham-operated animals. Melatonin was undetectable in the blood of the pinealectomized rats with or without AP. Treatment with melatonin (25 mg/kg, ip) prevented the development of AP in the sham-operated rats and significantly reduced pancreatic inflammation in the animals previously subjected to pinealectomy. In conclusion, pineal melatonin contributes to the pancreatic protection through the activation of the antioxidative defense mechanism in pancreatic tissue as well as its direct antioxidant effects.

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Relationship between melatonin levels in plasma and gastrointestinal tissues and the incidence and severity of gastric ulcers in pigs

Cited by 50 publications

References 27 publications

Localization, Physiological Significance and Possible Clinical Implication of Gastrointestinal Melatonin

Localization, Physiological Significance and Possible Clinical Implication of Gastrointestinal Melatonin

Which is the best choice for gastroesophageal disorders: Melatonin or proton pump inhibitors?

Pinealectomy aggravates acute pancreatitis in the rat

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