Summary of Study ST002474

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR001597. The data can be accessed directly via it's Project DOI: 10.21228/M88H9Z This work is supported by NIH grant, U2C- DK119886.

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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 IDST002474
Study TitleRetinol Dehydrogenase 10 Reduction Mediated Retinol Metabolism Disorder Promotes Diabetic Cardiomyopathy in Male Mice.
Study SummaryIn this study, we identify disordered cardiac retinol metabolism in type 2 diabetic male mice and patients characterized by retinol overload, all-trans retinoic acid deficiency. By supplementing type 2 diabetic male mice with retinol or all-trans retinoic acid, we demonstrate that both cardiac retinol overload and all-trans retinoic acid deficiency promote diabetic cardiomyopathy. Mechanistically, by constructing cardiomyocyte-specific conditional retinol dehydrogenase 10-knockout male mice and overexpressing retinol dehydrogenase 10 in male type 2 diabetic mice via adeno-associated virus, we verify that the reduction in cardiac retinol dehydrogenase 10 is the initiating factor for cardiac retinol metabolism disorder and results in diabetic cardiomyopathy. Therefore, we suggest that the reduction of cardiac retinol dehydrogenase 10 and its mediated disorder of cardiac retinol metabolism is a new mechanism underlying diabetic cardiomyopathy.
Institute
Zhongshan School of Medicine, Sun Yat-sen University
DepartmentDept. of Biochemistry
Last NameYandi
First NameWu
Address74, Zhongshan second street
Emailwuyd3@mail2.sysu.edu.cn
Phone15622158754
Submit Date2023-02-08
PublicationsRetinol Dehydrogenase 10 Reduction Mediated Retinol Metabolism Disorder Promotes Diabetic Cardiomyopathy in Male Mice.
Raw Data AvailableYes
Raw Data File Type(s)mzML
Analysis Type DetailLC-MS
Release Date2023-02-13
Release Version1
Wu Yandi Wu Yandi
https://dx.doi.org/10.21228/M88H9Z
ftp://www.metabolomicsworkbench.org/Studies/ application/zip

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Treatment:

Treatment ID:TR002576
Treatment Summary:RDH10-cKO mice: RDH10-cKO mice, which contain both RDH10fl/fl and MYH6-iCre, were bred by RDH10fl/fl mice and MYH6-iCre mice and were injected tamoxifen intraperitoneally (50 mg/kg, T2859, Sigma -Aldrich, St. Louis, MO) for 5 consecutive days from 5 weeks of age. Age-matched male RDH10fl/fl mice that also received TMX injections served as normal controls for RDH10-cKO mice. Animal treatments: Mice in the Rol treatment group received Rol gavage (800 IU/each, 17772, Sigma-Aldrich, St. Louis, MO) every two days from 8 weeks of age. Mice in the atRA treatment group received atRA intraperitoneal injection (5 mg/kg body weight, R2625, Sigma-Aldrich, St. Louis, MO) daily from 8 weeks of age. Gene therapy: A recombinant AAV9 vector carrying the mouse RDH10 sequence (AAV9-RDH10, DZ-AAV-Rdh10-OE, Dongze, Hanbio Inc, Shanghai, China) was used to overexpress RDH10. 0.8*10^11 vg/per animal of AA9-RDH10 was transferred into T2DM mice, respectively, by tail vein injection at the age of 16 weeks.
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