Summary of Study ST002298

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench,, where it has been assigned Project ID PR001472. The data can be accessed directly via it's Project DOI: 10.21228/M8FT53 This work is supported by NIH grant, U2C- DK119886.


This study contains a large results data set and is not available in the mwTab file. It is only available for download via FTP as data file(s) here.

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Study IDST002298
Study TitleNAD(P) deficiency plays an important role in the restraint-stress-induced depression in the rat model
Study SummaryThe 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.
Anhui Science and Technology University
Last NameLi
First NameJinquan
AddressNo. 9, Donghua Road, Fengyang, Anhui Province, 233100, China
Phone86 133 2875 1890
Submit Date2022-07-30
Raw Data AvailableYes
Raw Data File Type(s)fid
Analysis Type DetailNMR
Release Date2023-08-15
Release Version1
Jinquan Li Jinquan Li application/zip

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Sample Preparation:

Sampleprep ID:SP002390
Sampleprep Summary:Samples of plasma (255 μl) were mixed with 255 μl of phosphate D2O buffer solution (NaH2PO4 and K2HPO4, 60 mM, pH 7.4). After centrifugation at 10000 × g at 4°C for 10 min to remove the precipitates, the supernatants were transferred to 5 mm NMR tubes and analyzed by NMR. Samples of urine (455 μl) were mixed with 55 μl of D2O buffer solution (NaH2PO4 and K2HPO4, 1.5 M, including 0.1% TSP (sodium 3-(trimethylsilyl) propionate-2,2,3,3-d4), pH 7.4) to minimize any gross variation in the pH of the urine samples. The mixture was left to stand for 10 min and centrifuged at 10000 × g at 4°C for 10 min to remove the precipitates. The supernatants were transferred to 5 mm NMR tubes and analyzed by NMR. The polar metabolites in the rat tissue were extracted according to the protocol established in our previous work. In brief, pre-weighed brain, kidney, liver, lung, or spleen samples (100 mg) were homogenized in 400 μl of CH3OH and 85 μl of H2O at 4°C. The homogenates were transferred into a 2.5-ml tube, combined with 400 μl of CHCl3 and 200 μl of H2O, and then kept in a vortex for 60 s. After 10-min partitioning on ice, the samples were centrifuged for 5 min (10000 × g, 4°C). The upper supernatants were transferred into 1.5-ml tubes and lyophilized to remove CH3OH and H2O. The extracts were reconstituted in 0.5 ml D2O containing 1 mM TSP, then transferred into 5-mm NMR tubes and analyzed by NMR spectroscopy.