Summary of project PR002050

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

Project ID: PR002050
Project DOI:doi: 10.21228/M8MZ4N
Project Title:Hypothalamic SLC7A14 accounts for aging-reduced lipolysis in white adipose tissue
Project Type:Mass spectrometry
Project Summary:The 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 Name:Liu
First Name:Kan
Address:No. 320, Yueyang Road, Shanghai, Shanghai, Shanghai/Shanghai/xuhui, 200000, China
Email:liukan2019@sibs.ac.cn
Phone:021-17718134725

Summary of all studies in project PR002050

Study IDStudy TitleSpeciesInstituteAnalysis
(* : Contains Untargted data)
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(* : Contains raw data)
ST003300 Hypothalamic SLC7A14 accounts for aging-reduced lipolysis in white adipose tissue Mus musculus Shanghai Institutes for Biological Sciences (SIBS) Chinese Academy of Sciences (CAS) MS* 2024-07-15 1 12 Uploaded data (6.1G)*
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