TY - JOUR
T1 - A possible hepatic factor in the control of plasma free fatty acid levels
AU - Bernal, Roberto
AU - Hutson, Duane G.
AU - Dombro, Roy S.
AU - Livingstone, Alan
AU - Levi, Joe U.
AU - Zeppa, Robert
N1 - Funding Information:
From the Veterans Administration Medical Center, Miami, Florida and the Department of Surgery, University of Miami School of Medicine, Miami, Florida. Received for publication February 21. 1980. Supported in part by The Veterans Administration Medical Center, Miami. Florida and the Department of Surgery, University of Miami School of Medicine, Miami, Florida. Address reprint requests to Duane G. Hutson, M.D., Surgical Service (I 121, Veterans Administration Medical Center, 1201 N. W. 16 Street. Miami, Florida 3312.5. 0 I982 by Grune & Stratton. Inc. 0026~495/82/3106-0003$01.00/0
Copyright:
Copyright 2014 Elsevier B.V., All rights reserved.
PY - 1982/6
Y1 - 1982/6
N2 - Insulin acts as a regulator of lipid metabolism by inhibiting the rate of lipolysis. Hyperinsulinemia, produced by the peripheral infusion of glucose, therefore, causes a lowering of plasma free fatty acids (FFA) by decreasing the mobilization of fats from peripheral deposits. Based on previous studies, it was postulated that a lowering of plasma FFA could be produced, in the absence of hyperinsulinemia, by the infusion of glucose directly into the liver. This study was undertaken to investigate the existence of endogenous factors other than insulin, which inhibit lipolysis. It was determined that glucose at a dosage of 0.125 gm/kg/hr could be infused into the portal vein of dogs without increasing plasma insulin levels. This dosage significantly lowered plasma FFA levels when injected into the portal vein but had no effect on plasma FFA when infused peripherally. There were significant decreases in FFA turnover following portal glucose administration, with no changes in fractional turnover. This indicated that the lowered plasma FFA concentrations found following portal infusions of glucose, were due to reduced lipid mobilization from adipose tissue, rather than increased tissue uptake of FFA. These results suggested the exitence of an hepatic factor, stimulated by portal glucose infusion, which lowered FFA mobilization from adipose tissue.
AB - Insulin acts as a regulator of lipid metabolism by inhibiting the rate of lipolysis. Hyperinsulinemia, produced by the peripheral infusion of glucose, therefore, causes a lowering of plasma free fatty acids (FFA) by decreasing the mobilization of fats from peripheral deposits. Based on previous studies, it was postulated that a lowering of plasma FFA could be produced, in the absence of hyperinsulinemia, by the infusion of glucose directly into the liver. This study was undertaken to investigate the existence of endogenous factors other than insulin, which inhibit lipolysis. It was determined that glucose at a dosage of 0.125 gm/kg/hr could be infused into the portal vein of dogs without increasing plasma insulin levels. This dosage significantly lowered plasma FFA levels when injected into the portal vein but had no effect on plasma FFA when infused peripherally. There were significant decreases in FFA turnover following portal glucose administration, with no changes in fractional turnover. This indicated that the lowered plasma FFA concentrations found following portal infusions of glucose, were due to reduced lipid mobilization from adipose tissue, rather than increased tissue uptake of FFA. These results suggested the exitence of an hepatic factor, stimulated by portal glucose infusion, which lowered FFA mobilization from adipose tissue.
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U2 - 10.1016/0026-0495(82)90090-7
DO - 10.1016/0026-0495(82)90090-7
M3 - Article
C2 - 7043182
AN - SCOPUS:0020051151
VL - 31
SP - 533
EP - 537
JO - Metabolism: Clinical and Experimental
JF - Metabolism: Clinical and Experimental
SN - 0026-0495
IS - 6
ER -