Mechanism of decreased arachidonic acid in the renal cortex of rats with diabetes mellitus |
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Authors: | Leslie S Ramsammy Brenda Haynes Christine Josepovitz George J Kaloyanides |
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Affiliation: | (1) Division of Nephrology and Hypertension, Department of Medicine, School of Medicine, Health Sciences Center, State University of New York at Stony Brook, 11794-8152 Stony Brook, New York;(2) Research Service, VA Medical Center Northport, 11768 New York |
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Abstract: | The purpose of this study was to investigate the roles of decreased synthesis and increased consumption in the depression
of arachidonic acid levels in renal cortex and glomeruli of rats with streptozotocin-induced diabetes mellitus. In diabetic
rats, arachidonic acid was depressed 33.2% in renal cortex, 47.4% in liver and 66.1% in heart compared to values of control
rats. Δ6 Desaturase activity was depressed in renal cortex, liver and heart of diabetic rats to 53.3, 55.5 and 63.7%, respectively,
of control values. Δ5 Desaturase activity was also depressed 43.7, 55.5 and 47.6% in renal cortex, liver and heart of diabetic
rats, respectively. In other rats the activities of five enzymes involved in the synthesis and esterification of arachidonic
acid were measured in renal cortex and in isolated glomeruli. Both tissues from diabetic rats showed depressed activities
of Δ5 and Δ6 desaturases, increased activities of long-chain acyl-CoA synthetase and 1-acyl-sn-glycero-3-phosphocholine acyltransferase and no change in the activity of elongase as compared to those in control tissues.
Malondialdehyde, an end product of lipid peroxidation, was lower in the renal cortex of diabetic rats than in control rats,
whereas β-oxidation of linoleic acid and arachidonic acid were similar in diabetic and in control rats. Basal and stimulated
prostaglandin E2 synthesis were significantly higher in isolated glomeruli from diabetic rats compared to those in control rats. In isolated
tubules, prostaglandin E2 synthesis was similarly low in both groups. From these data we conclude that the reduced level of arachidonic acid esterified
in lipids of the kidney cortex is caused principally by depressed synthesis of arachidonic acid secondary to decreased activity
of Δ5 and Δ6 desaturases. Increased consumption of arachidonic acid to support prostaglandin synthesis may have contributed
to the depression of arachidonic acid in glomeruli but not in tubules. |
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