Summary of project PR001624

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 PR001624. The data can be accessed directly via it's Project DOI: 10.21228/M8S99J This work is supported by NIH grant, U2C- DK119886.

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

Project ID: PR001624
Project DOI:doi: 10.21228/M8S99J
Project Title:LBP resists hepatic oxidative stress by regulating LD homeostasis
Project Summary:Stress elevates the formation of ROS and lipid peroxidation, which induce lipid droplets (LDs) accumulation and adverse metabolic disturbance. Here, we explored the novel role of Lipopolysaccharide-binding protein (LBP) as an anti-oxidant, which can capture unsaturated triglyceride (TG) into LDs to avoid lipid peroxidation. Oxidative stress upregulates LBP level and promotes LDs growth via the LBP/TG phase transition. Upon N-Acetyl-L-cysteine (NAC) elimination of ROS, LBP is exported from LD along with PRDX4, resulting in an increase in phospholipid synthesis. Chronic stress causes LBP upregulation and leads to obesity, which can be rescued by NAC treatment in vivo. These results support that LBP maintains homeostasis by coupling lipid metabolism and redox signal, which provides insights into redox medicine that mitigate stress-induced metabolic dysfunction.
Institute:Department of Endocrinology and Laboratory for Diabetes, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China
Last Name:Zhang
First Name:Qilun
Address:Lujiang road no.17
Email:zql66666@mail.ustc.edu.cn
Phone:+8618356507293

Summary of all studies in project PR001624

Study IDStudy TitleSpeciesInstituteAnalysis
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ST002522 Lipidomics study on the effect of LBP protein on hepatic lipid composition in mice Mus musculus University of Science and Technology of China MS 2024-03-21 1 18 Uploaded data (2.8G)*
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