Gastrointestinal hormonal dysfunction in gastroparesis and functional dyspepsia

Authors

  • J. Khoo,

    1. Centre of Clinical Research Excellence in Nutritional Physiology, School of Medicine, University of Adelaide, Royal Adelaide Hospital, Adelaide, SA, Australia
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  • C. K. Rayner,

    1. Centre of Clinical Research Excellence in Nutritional Physiology, School of Medicine, University of Adelaide, Royal Adelaide Hospital, Adelaide, SA, Australia
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  • C. Feinle-Bisset,

    1. Centre of Clinical Research Excellence in Nutritional Physiology, School of Medicine, University of Adelaide, Royal Adelaide Hospital, Adelaide, SA, Australia
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  • K. L. Jones,

    1. Centre of Clinical Research Excellence in Nutritional Physiology, School of Medicine, University of Adelaide, Royal Adelaide Hospital, Adelaide, SA, Australia
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  • M. Horowitz

    1. Centre of Clinical Research Excellence in Nutritional Physiology, School of Medicine, University of Adelaide, Royal Adelaide Hospital, Adelaide, SA, Australia
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Address for Correspondence
Professor Michael Horowitz, Discipline of Medicine, Level 6 Eleanor Harrald Building, Royal Adelaide Hospital, The University of Adelaide, SA 5005, Australia.
Tel: +61 (0)8 8222 5501; fax: +61 (0)8 8223 3870;
e-mail: michael.horowitz@adelaide.edu.au

Abstract

Background  Numerous hormones secreted by the gut, during both the fasted state and in response to a meal, influence gastrointestinal motor and/or sensory function, and appear to contribute to the pathogenesis of delayed gastric emptying associated with gastroparesis, functional dyspepsia (FD) and feed intolerance in critical illness. Gut hormones are, accordingly, potential targets for the management of these patients.

Purpose  This article will discuss the hypersensitivity to enteral fat and endogenous (nutrient-stimulated) and exogenous cholecystokinin (CCK) in patients with FD, and the elevation in both fasting and postprandial CCK levels evident in this group. It will review the use of pharmacological agonists of motilin and ghrelin, which accelerate gastric emptying, in the management of gastroparesis and FD. The frequent finding of markedly delayed gastric emptying in the critically ill will be examined; this is associated with elevated plasma CCK and peptide YY in both the fasted and postprandial states, which may account for the increase in small intestinal nutrient inhibitory feedback on gastric motility in this group. The concepts that the rate of gastric emptying is a major determinant of postprandial glycemic excursions in diabetes, and that modulation of gastric emptying may improve glycemic control, will be addressed; in type 1 and insulin-treated type 2 diabetic patients, co-ordination of insulin administration with nutrient delivery and absorption should be optimized, while type 2 patients who are not on insulin are likely to respond to dietary and/or pharmacological interventions which slow gastric emptying.

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