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 structure, lipid composition, and cytosolic fatty acid binding protein.
Subject(s)
Adipocytes/metabolism , Diabetes Mellitus, Experimental/metabolism , Fatty Acids/metabolism , Fatty Acids/pharmacokinetics , Neoplasm Proteins , Nerve Tissue Proteins , Adipocytes/drug effects , Animals , Biological Transport , Carrier Proteins/metabolism , Cell Membrane/chemistry , Cell Membrane/ultrastructure , Cytosol/metabolism , Diabetes Mellitus, Experimental/chemically induced , Diabetes Mellitus, Experimental/drug therapy , Fatty Acid-Binding Protein 7 , Fatty Acid-Binding Proteins , Fatty Acids, Unsaturated/metabolism , Fatty Acids, Unsaturated/pharmacokinetics , Insulin/pharmacology , Male , Myelin P2 Protein/metabolism , Rats , Rats, WistarABSTRACT
A retrospective study was undertaken to determine the frequency of alloimmunization in two multitransfused patient populations. Three hundred eighteen unselected patients whose transfusion records were available were studied. One hundred fifty-seven patients had sickle cell disease (SCD) and 161 had thalassemia. Forty-four antibodies were detected in 23 of the 99 transfused SCD patients. The predominate antibodies were in the Rh group: seventeen were anti-rh"(E), eight were anti-rh'(C), and four were anti-rh'w(Cw). Of the remaining antibodies, five were anti-Kell, three were anti-Jka, two were anti-Jkb, three were anti-Fya, one was anti-Bga, and one was anti-S. In the thalassemic patients, six antibodies were detected in 4 of the 39 transfused patients. Of these, there were two anti-Kell and one anti-Rho (D), anti-rh'(C), anti-rh'w(Cw), and anti-Fya each. Although the SCD patients were more likely to have been transfused at the parent institution than were the thalassemic patients (69% vs. 24%, p less than 0.05), the frequencies of alloimmunized patients, the total number of antibodies, and the number of Rh antibodies did not differ significantly (p greater than 0.05) for transfused patients in the two populations.
