14C and tripalmitin-14C. Role of intramucosal factors in the uptake of luminal lipids" />
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Research Article Free access | 10.1172/JCI106105
Gastrointestinal Research Laboratory, McGill University Clinic, Royal Victoria Hospital, Montreal, Canada
Allan Bronfman Family Laboratory, Jewish General Hospital, Montreal, Canada
Find articles by Kessler, J. in: JCI | PubMed | Google Scholar
Gastrointestinal Research Laboratory, McGill University Clinic, Royal Victoria Hospital, Montreal, Canada
Allan Bronfman Family Laboratory, Jewish General Hospital, Montreal, Canada
Find articles by Mishkin, S. in: JCI | PubMed | Google Scholar
Gastrointestinal Research Laboratory, McGill University Clinic, Royal Victoria Hospital, Montreal, Canada
Allan Bronfman Family Laboratory, Jewish General Hospital, Montreal, Canada
Find articles by Stein, J. in: JCI | PubMed | Google Scholar
Published August 1, 1969 - More info
The effect of DL-ethionine on the uptake and transport of lipid by the rat small intestine was investigated. A cottonseed oil emulsion containing 14C-labeled tripalmitin or palmitic acid was administered intragastrically to rats pretreated with DL-ethionine, DL-ethionine plus methionine, or saline, and the rats were sacrificed 2, 4, and 6 hr later. Lipids from the plasma, the stomach, the colon, the luminal contents of the small intestine, and the wall of the small intestine were extracted, fractionated, and their radioactivity assayed.
Ethionine markedly inhibited the uptake of lipids by the small intestine. This inhibition was not related to impairment of intraluminal lipolysis since analagous inhibitions were observed when palmitic acid or predigested triglyceride (TG), obtained through a jejunal fistula from normal animals, was administered instead of tripalmitin. Ethionine also inhibited the transport of lipid from the wall of the small intestine. A significant fraction of the administered lipid remained in the wall of the small intestine, and only a small fraction was transported to the blood stream. Although most of the wall radioactivity was in the form of TG, significant proportions were also found in the free fatty acid (FFA) and partial glyceride fractions, indicating a marked inhibition of mucosal reesterification to TG.
The degree of inhibition of mucosal reesterification and the degree of inhibition of transport of wall lipids were directly related to the degree of inhibition of uptake of luminal radioactivity. This relationship suggests that the rate of reesterification, the level of mucosal FFA, and the rate of transport of intramucosal TG may be of importance in determining the extent of uptake of intraluminal lipid by the mucosal cells.
Since a significant fraction of the wall radioactivity was in the form of TG, the decreased transport of wall lipids was attributed to an impairment of chylomicron completion due to inhibition of either the synthesis of chylomicron apoprotein or the association of preformed TG with the protein moiety of chylomicrons. Experiments with labeled amino acids support the first possibility.