Melatonin's role as a co-adjuvant treatment in colonic diseases: A review
Melatonin is produced in the pineal gland as well as many other organs, including the enterochromaffin cells of the digestive mucosa. Melatonin is a powerful antioxidant that resists oxidative stress due to its capacity to directly scavenge reactive species, to modulate the antioxidant defense syste...
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Published in: | Life sciences (1973) Vol. 170; pp. 72 - 81 |
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Abstract | Melatonin is produced in the pineal gland as well as many other organs, including the enterochromaffin cells of the digestive mucosa. Melatonin is a powerful antioxidant that resists oxidative stress due to its capacity to directly scavenge reactive species, to modulate the antioxidant defense system by increasing the activities of antioxidant enzymes, and to stimulate the innate immune response through its direct and indirect actions. In addition, the dysregulation of the circadian system is observed to be related with alterations in colonic motility and cell disruptions due to the modifications of clock genes expression. In the gastrointestinal tract, the activities of melatonin are mediated by melatonin receptors (MT2), serotonin (5-HT), and cholecystokinin B (CCK2) receptors and via receptor-independent processes. The levels of melatonin in the gastrointestinal tract exceed by 10–100 times the blood concentrations. Also, there is an estimated 400 times more melatonin in the gut than in the pineal gland. Gut melatonin secretion is suggested to be influenced by the food intake. Low dose melatonin treatment accelerates intestinal transit time whereas high doses may decrease gut motility. Melatonin has been studied as a co-adjuvant treatment in several gastrointestinal diseases including irritable bowel syndrome (IBS), constipation-predominant IBS (IBS-C), diarrhea-predominant IBS (IBS-D), Crohn's disease, ulcerative colitis, and necrotizing enterocolitis. The purpose of this review is to provide information regarding the potential benefits of melatonin as a co-adjuvant treatment in gastrointestinal diseases, especially IBS, Crohn's disease, ulcerative colitis, and necrotizing enterocolitis.
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AbstractList | Melatonin is produced in the pineal gland as well as many other organs, including the enterochromaffin cells of the digestive mucosa. Melatonin is a powerful antioxidant that resists oxidative stress due to its capacity to directly scavenge reactive species, to modulate the antioxidant defense system by increasing the activities of antioxidant enzymes, and to stimulate the innate immune response through its direct and indirect actions. In addition, the dysregulation of the circadian system is observed to be related with alterations in colonic motility and cell disruptions due to the modifications of clock genes expression. In the gastrointestinal tract, the activities of melatonin are mediated by melatonin receptors (MT2), serotonin (5-HT), and cholecystokinin B (CCK2) receptors and via receptor-independent processes. The levels of melatonin in the gastrointestinal tract exceed by 10-100 times the blood concentrations. Also, there is an estimated 400 times more melatonin in the gut than in the pineal gland. Gut melatonin secretion is suggested to be influenced by the food intake. Low dose melatonin treatment accelerates intestinal transit time whereas high doses may decrease gut motility. Melatonin has been studied as a co-adjuvant treatment in several gastrointestinal diseases including irritable bowel syndrome (IBS), constipation-predominant IBS (IBS-C), diarrhea-predominant IBS (IBS-D), Crohn's disease, ulcerative colitis, and necrotizing enterocolitis. The purpose of this review is to provide information regarding the potential benefits of melatonin as a co-adjuvant treatment in gastrointestinal diseases, especially IBS, Crohn's disease, ulcerative colitis, and necrotizing enterocolitis. Melatonin is produced in the pineal gland as well as many other organs, including the enterochromaffin cells of the digestive mucosa. Melatonin is a powerful antioxidant that resists oxidative stress due to its capacity to directly scavenge reactive species, to modulate the antioxidant defense system by increasing the activities of antioxidant enzymes, and to stimulate the innate immune response through its direct and indirect actions. In addition, the dysregulation of the circadian system is observed to be related with alterations in colonic motility and cell disruptions due to the modifications of clock genes expression. In the gastrointestinal tract, the activities of melatonin are mediated by melatonin receptors (MT2), serotonin (5-HT), and cholecystokinin B (CCK2) receptors and via receptor-independent processes. The levels of melatonin in the gastrointestinal tract exceed by 10–100 times the blood concentrations. Also, there is an estimated 400 times more melatonin in the gut than in the pineal gland. Gut melatonin secretion is suggested to be influenced by the food intake. Low dose melatonin treatment accelerates intestinal transit time whereas high doses may decrease gut motility. Melatonin has been studied as a co-adjuvant treatment in several gastrointestinal diseases including irritable bowel syndrome (IBS), constipation-predominant IBS (IBS-C), diarrhea-predominant IBS (IBS-D), Crohn's disease, ulcerative colitis, and necrotizing enterocolitis. The purpose of this review is to provide information regarding the potential benefits of melatonin as a co-adjuvant treatment in gastrointestinal diseases, especially IBS, Crohn's disease, ulcerative colitis, and necrotizing enterocolitis. [Display omitted] |
Author | López-Pingarrón, Laura Esteban-Zubero, Eduardo Ochoa-Moneo, Purificación Rivas-Jiménez, Miguel Castán-Ruiz, Silvia Tan, Dun-Xian García, José Joaquín Reiter, Russel J. Buisac-Ramón, Celia Alatorre-Jiménez, Moisés Alejandro Antoñanzas-Lombarte, Ángel |
Author_xml | – sequence: 1 givenname: Eduardo orcidid: 0000-0003-3957-3749 surname: Esteban-Zubero fullname: Esteban-Zubero, Eduardo email: eezubero@gmail.com organization: Department of Pharmacology and Physiology, University of Zaragoza. Calle Domingo Miral s/n, 50009 Zaragoza, Spain – sequence: 2 givenname: Laura surname: López-Pingarrón fullname: López-Pingarrón, Laura organization: Department of Medicine, Psychiatry and Dermatology, University of Zaragoza. Calle Domingo Miral s/n, 50009 Zaragoza, Spain – sequence: 3 givenname: Moisés Alejandro surname: Alatorre-Jiménez fullname: Alatorre-Jiménez, Moisés Alejandro organization: Department of Cellular and Structural Biology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229, USA – sequence: 4 givenname: Purificación surname: Ochoa-Moneo fullname: Ochoa-Moneo, Purificación organization: Department of Medicine, Psychiatry and Dermatology, University of Zaragoza. Calle Domingo Miral s/n, 50009 Zaragoza, Spain – sequence: 5 givenname: Celia surname: Buisac-Ramón fullname: Buisac-Ramón, Celia organization: Primary Care Unit, Sector Zaragoza III, Avenida San Juan Bosco 5, 50009 Zaragoza, Spain – sequence: 6 givenname: Miguel surname: Rivas-Jiménez fullname: Rivas-Jiménez, Miguel organization: Department of Medicine, Psychiatry and Dermatology, University of Zaragoza. Calle Domingo Miral s/n, 50009 Zaragoza, Spain – sequence: 7 givenname: Silvia surname: Castán-Ruiz fullname: Castán-Ruiz, Silvia organization: Primary Care Unit, Sector Zaragoza III, Avenida San Juan Bosco 5, 50009 Zaragoza, Spain – sequence: 8 givenname: Ángel surname: Antoñanzas-Lombarte fullname: Antoñanzas-Lombarte, Ángel organization: Department of Medicine, Psychiatry and Dermatology, University of Zaragoza. Calle Domingo Miral s/n, 50009 Zaragoza, Spain – sequence: 9 givenname: Dun-Xian surname: Tan fullname: Tan, Dun-Xian organization: Department of Cellular and Structural Biology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229, USA – sequence: 10 givenname: José Joaquín surname: García fullname: García, José Joaquín organization: Department of Pharmacology and Physiology, University of Zaragoza. Calle Domingo Miral s/n, 50009 Zaragoza, Spain – sequence: 11 givenname: Russel J. surname: Reiter fullname: Reiter, Russel J. email: reiter@uthscsa.edu organization: Department of Cellular and Structural Biology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229, USA |
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SubjectTerms | Adjuvant therapy Animals Antioxidants Cell Proliferation Cholecystokinin Circadian rhythms Colitis - metabolism Colitis, Ulcerative - metabolism Colonic Diseases - metabolism Constipation Crohn's Disease Crohns disease Diarrhea Digestive system Diseases Enterocolitis Enterocolitis, Necrotizing - metabolism Enzymes Food intake Gastric motility Gastrointestinal diseases Gastrointestinal Diseases - metabolism Gastrointestinal Diseases - therapy Gastrointestinal tract Gastrointestinal Tract - metabolism Gene expression Humans Immune response Immune system Inflammatory bowel disease Innate immunity Intestinal transit time Intestine Intestines - metabolism Irritable bowel syndrome Irritable Bowel Syndrome - metabolism Melatonin Melatonin - physiology Melatonin - secretion Melatonin receptors Mucosa Necrotizing enterocolitis Organs Oxidative stress Pineal gland Pineal Gland - metabolism Receptors Receptors, Melatonin - metabolism Resists Risk Factors Serotonin Serotonin - metabolism Sleep Th17 Cells - cytology Th2 Cells - cytology Transit time Ulcerative colitis |
Title | Melatonin's role as a co-adjuvant treatment in colonic diseases: A review |
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