We examined the possible physiologic effects of intravenous (IV) amino acids (AAs) and long-chain triacylglycerols (LCTs) on gallbladder (GB) motility and release of cholecystokinin (CCK) on humans. GB contraction was studied in normal volunteers after administration of a fatty meal and IV infusion of AA and LCT. The GB contraction volume was calculated with ultrasound. Cholecystokinin-8 (CCK-8) and cholecystokinin-33/39 (CCK-33/39) were measured by radio-immunoassay. Administration of a fatty meal resulted in GB contraction by 60% of its basal volume and was accompanied by an increase in the serum levels of both CCK-8 and CCK-33/39. Administration of IV AA and LCT resulted in GB contraction by 17 and 37%, respectively, of its basal volume. The latter contractions were accompanied by increased levels of CCK-8 only. We conclude that IV administration of AA and LCT can result in human GB contraction and induce the release of only CCK-8. Continuous IV administration of AA and LCT for greater than 2h causes exhaustion of CCK-8 release, so that the GB returns to its initial volume.