Summary of Study ST003300

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 PR002050. The data can be accessed directly via it's Project DOI: 10.21228/M8MZ4N This work is supported by NIH grant, U2C- DK119886.

See: https://www.metabolomicsworkbench.org/about/howtocite.php

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 IDST003300
Study TitleHypothalamic SLC7A14 accounts for aging-reduced lipolysis in white adipose tissue
Study SummaryThe central nervous system has been implicated in the age-induced reduction in adipose tissue lipolysis. SLC7A14 is a lysosomal membrane protein highly expressed in the brain. Herein, we investigated the possible role of hypothalamic SLC7A14 in the age-induced lipolysis reduction. In this study, we demonstrated the expression of SLC7A14 was reduced in proopiomelanocortin (POMC) neurons of aged mice. Overexpression of SLC7A14 in POMC neurons alleviated the age-induced reduction in white adipose tissue (WAT) lipolysis, whereas SLC7A14 deletion mimicked the age-induced lipolysis impairment. Moreover, POMC SLC7A14 regulated WAT lipolysis independently of sympathetic nerves in WAT. Metabolomics analysis revealed that POMC SLC7A14 increased the primary bile acid taurochenodeoxycholic acid (TCDCA) content, which mediated the SLC7A14 knockout- or age-induced WAT lipolysis impairment. Furthermore, SLC7A14-increased TCDCA content is dependent on intestinal apical sodium-dependent bile acid transporter (ASBT), which is regulated by intestinal sympathetic afferent nerves. Finally, SLC7A14 regulated the intestinal sympathetic afferent nerves by inhibiting mTORC1 signaling through inhibiting TSC1 phosphorylation. Collectively, our study suggests the function for central SLC7A14 and an upstream mechanism for the mTORC1 signaling pathway. Moreover, our data provides insights into the brain–gut–adipose tissue crosstalk in age-induced lipolysis impairment.
Institute
Shanghai Institutes for Biological Sciences (SIBS) Chinese Academy of Sciences (CAS)
Last NameLiu
First NameKan
AddressNo. 320, Yueyang Road, Shanghai
Emailliukan2019@sibs.ac.cn
Phone021-17718134725
Submit Date2024-05-13
Raw Data AvailableYes
Raw Data File Type(s)mzML
Analysis Type DetailLC-MS
Release Date2024-07-15
Release Version1
Kan Liu Kan Liu
https://dx.doi.org/10.21228/M8MZ4N
ftp://www.metabolomicsworkbench.org/Studies/ application/zip

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Factors:

Subject type: Mammal; Subject species: Mus musculus (Factor headings shown in green)

mb_sample_id local_sample_id Sample source Genotype Treatment
SA358120QC2Blood serum QC control
SA358121QC1Blood serum QC control
SA358122QC3Blood serum QC control
SA358123oe1Blood serum SLC7A14_OE control
SA358124oe2Blood serum SLC7A15_OE control
SA358125oe3Blood serum SLC7A16_OE control
SA358126oe4Blood serum SLC7A17_OE control
SA358127control3Blood serum WT control
SA358128control1Blood serum WT control
SA358129control2Blood serum WT control
SA358130control4Blood serum WT control
SA358131control5Blood serum WT control
Showing results 1 to 12 of 12
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