PR001472 (Project)

Description:The metabolic dysfunction or irreversible metabolic changes from stress may cause body vulnerability, potentially leading to the onset of psychiatric and non-psychiatric illnesses. Nevertheless, little is known about the biochemical events that cause depression due to stress. Our study employed open field test, plasma adrenocorticotropic hormone (ACTH) and corticosterone determination, serum biochemical analysis, quantitative PCR, immunoblotting, enzyme activity assay, and NMR-based metabolomics to analyze and identify the biochemical variations of body fluids (serum and urine) and tissues (brain, kidney, liver, lung, and spleen) in an acute restraint stress-induced rat model of depression. Our data suggested that the post-stress effects on biochemical alterations involved different biochemical pathways, including regulating the NAD(P) pool, glucose homeostasis, biosynthesis and degradation of heme, and uric acid production and metabolism. The urinary excretion of nicotinate and nicotinamide N-oxide increased significantly. Thus, we conclude that the depletion of NAD(P) precursors may occur in response to restraint stress. Our results show a close association between NAD(P) deficiency and post-stress metabolic dysfunction, which would provide a ground for developing recovery-promoting micronutrients in treating depression.