The osmotic laxative magnesium sulphate activates the ileal brake

Background: Alterations in gastrointestinal motility and hormone secretion, especially activation of the ileal brake, have been documented in malabsor ption. Aim: To investigate whether artificially-induced accelerated small intestin al transit activates the ileal brake mechanism. Methods: Eight healthy volunteers (four female, four male; age 21 +/- 3 yea rs) participated in four experiments: (a) meal with either oral magnesium s ulphate (MgSO4) or placebo; and (b) fasting with either oral MgSO4 or place bo. Antroduodenal motility was recorded by perfusion manometry. Duodenocaec al transit time was determined by the lactulose H-2 breath test. Gall-bladd er volume was measured by ultrasound at regular intervals, and blood sample s were drawn for determination of cholecystokinin and peptide YY (RIA). Twe nty-four hour faecal weight and fat excretion were determined. Results: MgSO4 significantly accelerated duodenocaecal transit time and inc reased faecal fat and weight in all subjects. MgSO4 significantly delayed t he reoccurrence of phase III and affected antroduodenal motility during fas ting but not after meal ingestion. Postprandial gall-bladder relaxation and postprandial peptide YY release were significantly increased during the Mg SO4 experiment compared to placebo. Conclusions: The osmotic laxative MgSO4 accelerates intestinal transit both in the fasting and fed state. MgSO4 activates the ileal brake mechanism on ly in the fed state, with peptide YY release and inhibition of gall-bladder emptying.