Abstract
Abstract Lipid peroxidation in vitro by isolated rat adipose tissue was measured by the thiobarbituric acid reaction. Incubation of isolated fat cells with adrenocorticotrophic hormone or epinephrine stimulated total lipolysis as measured by glycerol release, but not lipid peroxidation. Epinephrine inhibited lipid peroxidation produced by ascorbate. However, prior treatment with epinephrine caused increased lipid peroxidation by epididymal fat pads. The isolated fat cells of vitamin E-deficient rats contained no detectable tocopherol. These fat cells showed no significant differences in lipid peroxidation, total lipolysis, or basal or insulin-stimulated glucose carbon incorporation into CO2 and total lipids, as compared to fat cells from vitamin Ereplete animals. Enhancement of lipid peroxidation in vitro by incubation of isolated fat cells with ascorbate caused no change in glucose carbon utilization or total lipolysis. We conclude that the thiobarbituric acid test, applied to fat cells, is not an indicator of total lipolysis, nor of vitamin E deficiency. Fat cell glucose utilization and lipolysis are not altered by either vitamin E deficiency or increased lipid peroxidation.
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