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Fatty acid uptake in diabetic rat adipocytes
Authors:Fraser  Heather  Coles  Scott M  Woodford  Judith K  Frolov  Audrey A  Murphy  Eric J  Schroeder  Friedhelm  Bernlohr  David A  Grund  Vernon
Institution:(1) Department of Pharmacology, University of Alberta, Edmonton, Alberta, T6G 2H7, Canada;(2) The Cleveland Clinic Foundation, 9500 Euclid Avenue, NC10, Cleveland, OH 44195, USA;(3) The Andrew Jergens Co., 2535 Spring Grove Avenue, Cincinnati, OH 45214-1773, USA;(4) Department of Physiology and Pharmacology, Texas A and M University, TVMC, College Station, Texas 77843-4466, USA;(5) Department of Biochemistry, University of Minnesota, Saint Paul, Minnesota 55108, USA;(6) Department of Pharmaceutical Sciences, School of Pharmacy and Allied Health Sciences, University of Montana, Missoula, Montana 59812-1075, USA
Abstract:The effect of diabetic status and insulin on adipocyte plasma membrane properties and fatty acid uptake was examined. Studies with inhibitors and isolated adipocyte ghost plasma membranes indicated 9Z, 11E, 13E, 15Z-octatetraenoic acid (cis-parinaric acid) uptake was protein mediated. Cis-parinaric acid uptake was inhibited by trypsin treatment or incubation with phloretin, and competed with stearic acid. The initial rate, but not maximal uptake, of cis-parinaric acid uptake was enhanced two-fold in adipocytes from diabetic rats. Concomitantly, the structure and lipid composition of adipocyte ghost membranes was dramatically altered. However, the increased initial rate of cis-parinaric acid uptake in the diabetic adipocytes was not explained by membrane alterations or by a two-fold decrease in cytosolic adipocyte fatty acid binding protein (ALBP), unless ALBP stimulated fatty acid efflux. Thus, diabetic status dramatically altered adipocyte fatty acid uptake, plasma membrane structu re, lipid composition, and cytosolic fatty acid binding protein. (Mol Cell Biochem 167: 51-60, 1997)
Keywords:fatty acid  cis-parinaric acid  adipocyte  transport  diabetes  insulin
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