Abstract
Microsomal lauric acid hydroxylation and fatty acid peroxisomal β-oxidation were studied in hepatic subcellulant preparations from streptozotocin-induced diabetic and diabetic insulin-treated rats. 1. 2. The liver microsomes of the streptozotocin diabetic rats displayed a similar activity to hydroxylate lauric acid as the control microsomes. 2. 3. Diabetic insulin-treated rats showed lower (ω1) and ω-lauric acid hydroxylase activities than diabetic and control rats. 3. 4. Streptozotocin-induced diabetes and diabetic insulin-treated rats exhibited no significant changes on peroxisomal palmitoyl CoA β-oxidation compared to the control rats. 4. 5. Both microsomal and peroxisomal fatty acid oxidation responded in a similar way in this model of experimental diabetes.
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