effect of chloroquine on intestinal lipid metabolism most studies that have quantitated recovery of infused lipid in the intestinal mucosa and mesenteric lymph have only been able to recapture 5075 one possibility is that the missing lipid enters a triacylglycerol tg storage pool in the enterocyte and is hydrolyzed by lysosomal lipase and the free fatty acid released is transported by the portal vein this postulate was tested by comparing glyceryl trioleate toinfused rats pretreated with the lysosomotropic drug chloroquine 63 mgkg1h1 with saline controls chloroquine increased mucosal tg from 94 6 to 128 8 mumol additionally the specific activity of the mucosal tg relative to the infused 3hto was reduced in the treated rats the mucosal tg increase was not due to impaired tg output which remained the same as controls we conclude that the tg in the acid lipasesensitive pool derives most of its glycerideglycerol from endogenous sources furthermore the increment in mucosal tg caused by chloroquine is not enough to explain the majority of the acyl groups unaccounted for in the mucosa and lymph after a tg infusion for these a direct passage of acyl groups through the enterocyte is postulated