Effect of intravenous lipid on gastric acid secretion stimulated by intravenous amino acids.

Intraduodenal fat is a potent inhibitor of all forms of gastric acid secretion in humans. Studies were performed in random order on 3 separate days in 5 normal subjects to determine if intravenous fat (Intralipid) altered gastric acid secretion stimulated by intravenous amino acids in humans. Mean (+/- SE) gastric acid output during a 4-hr intravenous amino acid infusion (21 g L-amino acids; Freamine II) plus glucose (50 g. to maintain isocaloric and isoosmolar solutions) was 43.2 +/- 3.2 meq/4 hr. Intraduodenal fat fusion (20 g of Intralipid) significantly (P < 0.02) suppressed amino acid-stimulated acid output. Interestingly, intravenous fat (20 g of Intralipid) also significantly (P < 0.02) inhibited acid secretion (14.8 +/- 6.3 meq/4 hr); similar to the effect observed with intraduodenal fat (12.7 +/- 4.9 meq/4 hr). Serum levels of CCK, gastrin, and GIP were measured at 30-min intervals throughout each study. Cholecystokinin and GIP increased significantly from basal during intraduodenal fat infusion. There were no other changes in serum CCK, gastrin, or GIP during any of the other tests. It is concluded that in normal subjects intravenous fat is a potent inhibitor of intraveous amino acid-stimulated gastric acid secretion, similar in effect to intraduodenal fat. The inhibitory effect of intravenous fat on amino acid-stimulated gastric acid secretion is probably not mediated by release of either CCK of GIP. Circulating fat may play a role in the control of some forms of gastric acid secretion.

RCT Entities:   Population Interventions Outcomes