DHA (omega-3 fatty acid) increases the action of brain-derived neurotrophic factor (BDNF)

Abstract

Neurons have high energy needs, requiring a continuous supply of glucose from the blood. Tight regulation of glucose metabolism in response to stimuli is essential for brain physiology. Glucose metabolism and cerebral blood flow are closely coordinated during neuronal activity to maintain proper brain function. In a previous article, we have already detailed the mechanisms by which the PI3K/Akt signaling pathway is involved in the efficiency of glucose uptake by stimulating GLUT-1 action and NO-mediated vasodilation. In this article, we now clarify how the activation of BDNF helps to stimulate the IRS-1/PI3K/Akt signaling pathway and upregulates NMDA receptor activity. In short, high-frequency neuronal activity induces the secretion of BDNF, whose presence boosts this important pathway. DHA, via the PPARα-RXRα and PPARɣ-RXRα heterodimers, is involved in the critical regulation of BDNF activation. As a preferential ligand of PPARs and RXRα, DHA plays an important role in the gene expression of CREB and CPE, and it is involved in the regulation and expression of tPA, as well as the inhibition of PAI-1. BDNF boosts the IGF-1/estradiol/PI3K/Akt signaling pathway, and DHA boosts the action of BDNF.