Fogarty Program HEEDs the call to action.

Introduction Delayed gastric emptying and feed intolerance occur frequently in the critically ill. In these patients, gastric motor responses to nutrients are disturbed. Peptide YY (PYY) slows gastric emptying. The aim of this study was to determine fasting and nutrient-stimulated plasma PYY concentrations and their relationship to cholecystokinin (CCK) in critically ill patients. Methods Studies were performed in 19 unselected mechanically ventilated critically ill patients (12 males; 48 ± 7 years old) in a randomised, single-blind fashion. Subjects received a 60-minute duodenal infusion of Ensure® at either 1 or 2 kcal/minute. Blood samples were collected at baseline and at 20, 40, 60, and 180 minutes following commencement of the nutrient infusion for the measurement of plasma PYY and CCK concentrations (using radioimmunoassay). Patient data were compared to 24 healthy subjects (17 males; 43 ± 2 years old). Results Fasting PYY concentration was higher in patients (P < 0.05), particularly in those with feed intolerance (P < 0.05). Plasma PYY concentrations were higher in patients during nutrient infusion (area under the curve [AUC] at 1 kcal/minute: 2,265 ± 718 versus 1,125 ± 138 pmol/l.min, P < 0.05; at 2 kcal/minute: 2,276 ± 303 versus 1,378 ± 210 pmol/l.min, P = 0.01) compared to healthy subjects. The magnitude of PYY elevation was greater in patients during the 1 kcal/minute infusion (AUC: 441 ± 153 versus 186 ± 58 pmol/l.min, P < 0.05), but not the 2 kcal/minute infusion. Fasting and nutrientstimulated plasma CCK concentrations were higher in patients (P < 0.05). There was a relationship between plasma PYY and CCK concentrations during fasting (r = 0.52, P < 0.05) and nutrient infusion (r = 0.98, P < 0.0001). Conclusion In critical illness, both fasting and nutrientstimulated plasma PYY concentrations are elevated, particularly in patients with feed intolerance, in conjunction with increased CCK concentrations. Introduction A number of hormones released from the small intestine in response to nutrients modulate gastric emptying and energy intake [1-3]. Peptide YY (PYY) is an important humoral mediator of the entero-gastric feedback mechanism, which leads to a slowing of gastric emptying and small intestinal transit [4-6] and possibly to a suppression of energy intake [1,7,8]. PYY release from the distal small intestine is stimulated both directly by luminal nutrients, particularly the digestion products of fat which activate PYY-secreting cells [7], and indirectly by neuro-endocrine mechanisms, including the release of cholecystokinin (CCK) and insulin-like growth factor-1 [8]. The initial release of PYY after food intake [2,9] is likely to be mediated by CCK [9] and its subsequent release is likely to be mediated through stimulation of PYY-secreting cells by luminal nutrients [9]. Exogenous administration of PYY slows gastric emptying [3,10], which is associated with an inhibition of antral motility [10]. This may contribute to a reduction in energy intake and