Antioxidative component of docosahexaenoic acid in the brain in diabetes

Abstract

The mechanisms underlying diabetic encephalopathy are only partially understood. This chapter tries to address the mechanisms of diabetes-induced cell and tissue damage in the brain, and discusses whether docosahexaenoic acid (DHA) could attenuate the degenerative changes observed in the diabetic brain. DHA is involved in brain and retina physiological functions, aging, and neurological and behavioral illnesses. There are a large number of bioactive metabolites of DHA, namely, maresins, protectins, resolvins, electrophilic oxo-derivatives, epoxides, neuroprostanes, neuroketals, and different DHA conjugates. Among them stands out Neuroprotectin D1 (NPD1), the first identified stereoselective bioactive product of DHA, NDP1 exerts neuroprotection in models of experimental diabetes. Overall, NPD1 promotes brain cell survival via the induction of antiapoptotic and neuroprotective gene expression programs that suppress neurotoxicity. Thus NPD1 elicits potent cell-protective, antiinflammatory, prosurvival, and repair signaling. Recent research has put forward the neuroprotective effects of docosanoids and the recently introduced elovanoids (DHA-elongated 32- or 34-carbon fatty acids by the action of elongation of very long chain fatty acids-4—ELOVL4).