University of Lincoln
Browse

Iron Inhibits the Secretion of Apolipoprotein E in Cultured Human Adipocytes

Version 4 2024-03-12, 17:12
Version 3 2023-10-29, 14:06
journal contribution
posted on 2024-03-12, 17:12 authored by L.J. Britton, Kim Bridle, Jon Whitehead, V. Nathan Subramaniam, Darrell H.G. Crawford, Lesley-Anne Jaskowski, Jingjing He, Choaping Ng, Jayde E. Ruelcke, Ahmed Mohamed, Janske Reiling, Nishreen Santrampurwala, Michelle M. Hill
<p>Nonalcoholic steatohepatitis (NASH) is characterized by adipose tissue dysfunction with insulin resistance and the dysregulation of adipokines 1. Recent data indicate repartitioning of iron from the liver to adipocytes in obesity and a role for iron in the development of adipose tissue dysfunction 2,3. However, the molecular mechanisms have not been established. To test the hypothesis that iron modulates adipokine release, we performed a quantitative proteomics analysis of the human Simpson-Golabi-Behmel Syndrome (SGBS) adipocyte secretome after 48 hours of treatment with ferric ammonium citrate (FAC). We used stable isotope-labeled amino acids in cell culture (SILAC) to characterize changes in the adipocyte secretome in response to iron. This technique has enabled direct comparison of quantities of individual proteins in the adipocyte secretome in response to iron using a proteomics approach as a tool for the identification of novel treatment targets in NASH.</p>

History

School affiliated with

  • Department of Life Sciences (Research Outputs)

Publication Title

Cellular and Molecular Gastroenterology and Hepatology

Volume

6

Issue

2

Pages/Article Number

215-217.e8

Publisher

Elsevier

ISSN

2352-345X

Date Submitted

2019-02-13

Date Accepted

2018-04-02

Date of First Publication

2018-01-01

Date of Final Publication

2018-01-01

Date Document First Uploaded

2019-02-13

ePrints ID

34483

Usage metrics

    University of Lincoln (Research Outputs)

    Keywords

    Exports

    RefWorks
    BibTeX
    Ref. manager
    Endnote
    DataCite
    NLM
    DC