Effects of interruption of the enterohepatic circulation of bile acids on the transport of very low density-lipoprotein triglycerides

U Beil, JR Crouse, K Einarsson, SM Grundy - Metabolism, 1982 - Elsevier
U Beil, JR Crouse, K Einarsson, SM Grundy
Metabolism, 1982Elsevier
An increase in plasma very low density lipoprotein-triglycerides (VLDL-TG) is seen
frequently during treatment with bile acid-binding resins. The purpose of this study was to
determine whether this increment in VLDL-TG is due mainly to an increase in synthesis of
VLDL, or to an enhanced catabolism. Three types of patients were studied:(1) 7
normotriglyceridemic subjects.(2) 4 obese patients, and (3) 9 hypertriglyceridemic patients.
Before treatment they underwent a study of VLDL-TG kinetics that employed …
Abstract
An increase in plasma very low density lipoprotein-triglycerides (VLDL-TG) is seen frequently during treatment with bile acid-binding resins. The purpose of this study was to determine whether this increment in VLDL-TG is due mainly to an increase in synthesis of VLDL, or to an enhanced catabolism. Three types of patients were studied: (1) 7 normotriglyceridemic subjects. (2) 4 obese patients, and (3) 9 hypertriglyceridemic patients. Before treatment they underwent a study of VLDL-TG kinetics that employed multicompartmental analysis of specific activity curves following injection of 3H-glycerol. The patients were then treated with a bile acid-binding resin, either cholestyramine or colestipol, for several weeks to several months. At the end of the treatment period, they were readmitted to the hospital for a second study of VLDL-TG kinetics. The patients showed a variable response to resin therapy. Many had an increase in concentrations of VLDL-TG, but others had no change or even a slight decrease. However, analysis of the data showed a high correlation between change in production rates of VLDL-TG and change in concentration. Also, when the data for the 20 patients were combined, there was a statistically significant increase in both synthetic rates and concentrations of VLDL-TG; in contrast, the fractional catabolic rate (FCR) was unchanged by therapy. Therefore, our data show that when treatment with bile acid sequestrants causes an increase in plasma VLDL-TG, the increase is due to an increment in production and not to a decrease in catabolism.
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