TY - JOUR
T1 - Effects of interruption of the enterohepatic circulation of bile acids on the transport of very low density-lipoprotein triglycerides
AU - Beil, Ulrich
AU - Crouse, John R.
AU - Einarsson, Kurt
AU - Grundy, Scott M
N1 - Funding Information:
From the Veterans Administration Medical Center and University of California, San Diego, California. Received for publication April 14, 1981. Supported in part by the Veterans Administration and the National Institutes of Health, Grants HL-14197 and AM-16667. The work also was supported by Public Health Service International Research Fellowship (No. 1 FO5TW02467-O1) and by the Upjohn Corporation, Kalamazoo, Michigan. Address reprint requests to Scott M. Grundy, M.D., Center for Human Nutrition (Room G4-100), University of Texas Health Science Center, Dallas, Texas 75236. © 1982 by Grune & Stratton, Inc. 00 26~949 5/8 2/310 3-000 5 501.00/0
PY - 1982/5
Y1 - 1982/5
N2 - 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.
AB - 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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U2 - 10.1016/0026-0495(82)90231-1
DO - 10.1016/0026-0495(82)90231-1
M3 - Article
C2 - 7078426
AN - SCOPUS:0020074674
SN - 0026-0495
VL - 31
SP - 438
EP - 444
JO - Metabolism
JF - Metabolism
IS - 5
ER -