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Research Article Free access | 10.1172/JCI114131
Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas 75235 8887.
Find articles by Woollett, L. in: JCI | PubMed | Google Scholar
Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas 75235 8887.
Find articles by Spady, D. in: JCI | PubMed | Google Scholar
Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas 75235 8887.
Find articles by Dietschy, J. in: JCI | PubMed | Google Scholar
Published July 1, 1989 - More info
These studies were designed to elucidate how shorter (MCT) and longer (HCO) chain-length saturated triacylglycerols and cholesterol interact to alter steady-state plasma LDL-cholesterol levels. When either MCT or HCO was fed in the absence of cholesterol, there was little effect on receptor-dependent LDL transport but a 36-43% increase in LDL-cholesterol production. Cholesterol feeding in the absence of triacylglycerol led to significant suppression of receptor-dependent LDL transport and a 26-31% increase in LDL-cholesterol production. However, when the longer chain-length saturated triacylglycerol was fed together with cholesterol there was a marked increase in the suppression of receptor-dependent LDL transport and an 82% increase in production rate. Together, these two alterations accounted for the observed eightfold increase in plasma LDL-cholesterol concentration. In contrast, feeding the shorter chain-length saturated triacylglycerol with cholesterol actually enhanced receptor-dependent LDL transport while also causing a smaller increase (52%) in the LDL-cholesterol production rate. As a result of these two opposing events, MCT feeding had essentially no net effect on plasma LDL-cholesterol levels beyond that induced by cholesterol feeding alone.