Microsomal and peroxisomal fatty acid oxidation in streptozotocin diabetic rat liver.
ABSTRACT Microsomal lauric acid hydroxylation and fatty acid peroxisomal beta-oxidation were studied in hepatic subcellulant preparations from streptozotocin-induced diabetic and diabetic insulin-treated rats. 2. The liver microsomes of the streptozotocin diabetic rats displayed a similar activity to hydroxylate lauric acid as the control microsomes. 3. Diabetic insulin-treated rats showed lower (omega 1) and omega-lauric acid hydroxylase activities than diabetic and control rats. 4. Streptozotocin-induced diabetes and diabetic insulin-treated rats exhibited no significant changes on peroxisomal palmitoyl CoA beta-oxidation compared to the control rats. 5. Both microsomal and peroxisomal fatty acid oxidation responded in a similar way in this model of experimental diabetes.
Drug Metabolism Reviews 02/1987; 18(4):441-515. DOI:10.3109/03602538708994130 · 6.29 Impact Factor
[Show abstract] [Hide abstract]
ABSTRACT: Dicarboxylic acids are excreted in urine when fatty acid oxidation is increased (ketosis) or inhibited (defects in beta-oxidation) and in Reye's syndrome. omega-Hydroxylation and omega-oxidation of C6-C12 fatty acids were measured by mass spectrometry in rat liver microsomes and homogenates, and beta-oxidation of the dicarboxylic acids in liver homogenates and isolated mitochondria and peroxisomes. Medium-chain fatty acids formed large amounts of medium-chain dicarboxylic acids, which were easily beta-oxidized both in vitro and in vivo, in contrast to the long-chain C16-dicarboxylic acid, which was toxic to starved rats. Increment of fatty acid oxidation in rats by starvation or diabetes increased C6:C10 dicarboxylic acid ratio in rats fed medium-chain triacylglycerols, and increased short-chain dicarboxylic acid excretion in urine in rats fed medium-chain dicarboxylic acids. Valproate, which inhibits fatty acid oxidation and may induce Reye like syndromes, caused the pattern of C6-C10-dicarboxylic aciduria seen in beta-oxidation defects, but only in starved rats. It is suggested, that the origin of urinary short-chain dicarboxylic acids is omega-oxidized medium-chain fatty acids, which after peroxisomal beta-oxidation accumulate as C6-C8-dicarboxylic acids. C10-C12-dicarboxylic acids were also metabolized in the mitochondria, but did not accumulate as C6-C8-dicarboxylic acids, indicating that beta-oxidation was completed beyond the level of adipyl CoA.Biochimica et Biophysica Acta 03/1992; 1124(1):71-9. DOI:10.1016/0005-2760(92)90128-I · 4.66 Impact Factor
Pharmacology [?] Therapeutics 02/1990; 45(1):1-38. DOI:10.1016/0163-7258(90)90006-N · 7.75 Impact Factor