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The osmotic laxative magnesium sulphate activates the ileal brake
Author(s) -
Vu Vu,
Nouwens,
Biemond,
Lamers,
Masclee
Publication year - 2000
Publication title -
alimentary pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.308
H-Index - 177
eISSN - 1365-2036
pISSN - 0269-2813
DOI - 10.1046/j.1365-2036.2000.00746.x
Subject(s) - postprandial , medicine , endocrinology , peptide yy , lactulose , laxative , placebo , meal , ingestion , gastroenterology , neuropeptide , constipation , neuropeptide y receptor , receptor , alternative medicine , pathology , insulin
Background: Alterations in gastrointestinal motility and hormone secretion, especially activation of the ileal brake, have been documented in malabsorption. Aim: To investigate whether artificially‐induced accelerated small intestinal transit activates the ileal brake mechanism. Methods: Eight healthy volunteers (four female, four male; age 21 ± 3 years) participated in four experiments: (a) meal with either oral magnesium sulphate (MgSO 4 ) or placebo; and (b) fasting with either oral MgSO 4 or placebo. Antroduodenal motility was recorded by perfusion manometry. Duodenocaecal transit time was determined by the lactulose H 2 breath test. Gall‐bladder volume was measured by ultrasound at regular intervals, and blood samples were drawn for determination of cholecystokinin and peptide YY (RIA). Twenty‐four hour faecal weight and fat excretion were determined. Results: MgS0 4 significantly accelerated duodenocaecal transit time and increased faecal fat and weight in all subjects. MgSO 4 significantly delayed the reoccurrence of phase III and affected antroduodenal motility during fasting but not after meal ingestion. Postprandial gall‐bladder relaxation and postprandial peptide YY release were significantly increased during the MgSO 4 experiment compared to placebo. Conclusions: The osmotic laxative MgS0 4 accelerates intestinal transit both in the fasting and fed state. MgS0 4 activates the ileal brake mechanism only in the fed state, with peptide YY release and inhibition of gall‐bladder emptying.