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This manifests as a shift toward a lipid storage phenotype, driven by a detrimental circuit involving CD36, fatty acid binding proteins (FABPs) and peroxisome proliferator-activated receptors (PPARs) [77, 78]

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In the stress-sedentary model, researchers conducted pharmacodynamic assessments using endurance running, a nontraditional pharmacologic tool, and observed an ameliorative effect on neurexins- and neuroligin 1 expression and synaptic plasticity [54]

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