Gut Peptides and Enteral Feeding in Critically Ill Patients: Implications for Gastric Dysmotility and Appetite
While enteral nutrition is the preferred mode of nutritional delivery in the critically ill, adequate delivery of enteral feeds to critically ill patients is frequently hampered by a variety of factors, the most frequent of which is gastric dysmotility. Impaired gastric motor function in these patients not only involves all regions of the stomach but is also associated with an enhanced enterogastric inhibitory feedback. The etiology of impaired gastric motility during critical illness remains unclear. In addition to mechanical ventilation, medication, hyperglycemia, shock, circulating inflammatory cytokines, and the admission diagnosis, a number of recent findings suggest that disturbances to the gastrointestinal hormones which mediate enterogastric feedback inhibition may be important. The motor abnormalities that have been identified in both proximal and distal regions of the stomach in response to small intestinal nutrient stimulation are consistent with enhanced enterogastric inhibitory effects. Plasma levels of the two major gastrointestinal hormones, cholecystokinin (CCK) and peptide YY (PYY), that mediate this enterogastric feedback are significantly elevated in critically ill patients. More importantly, both fasting and nutrient-stimulated plasma concentrations of CCK and PYY are higher in patients with delayed gastric emptying, and there is an inverse relationship between the rate of gastric emptying and both the plasma levels as well as the integrated changes in the plasma levels of CCK and PYY. These findings strongly support the potential role of plasma CCK and PYY in the pathogenesis of gastric dysmotility in critically ill patients.
KeywordsGastric Emptying Critical Illness Enteral Nutrition Delayed Gastric Emptying Migrate Motor Complex
Intensive care unit
Glucagons-like peptide 1
Isolated pyloric pressure wave
Migrating motor complex
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