Cargando…
A Serum Factor Induces Insulin-Independent Translocation of GLUT4 to the Cell Surface which Is Maintained in Insulin Resistance
In response to insulin, glucose transporter GLUT4 translocates from intracellular compartments towards the plasma membrane where it enhances cellular glucose uptake. Here, we show that sera from various species contain a factor that dose-dependently induces GLUT4 translocation and glucose uptake in...
Autores principales: | , , , , |
---|---|
Formato: | Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2010
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3004919/ https://www.ncbi.nlm.nih.gov/pubmed/21187969 http://dx.doi.org/10.1371/journal.pone.0015560 |
_version_ | 1782194055052001280 |
---|---|
author | Berenguer, Marion Martinez, Laurène Giorgetti-Peraldi, Sophie Le Marchand-Brustel, Yannick Govers, Roland |
author_facet | Berenguer, Marion Martinez, Laurène Giorgetti-Peraldi, Sophie Le Marchand-Brustel, Yannick Govers, Roland |
author_sort | Berenguer, Marion |
collection | PubMed |
description | In response to insulin, glucose transporter GLUT4 translocates from intracellular compartments towards the plasma membrane where it enhances cellular glucose uptake. Here, we show that sera from various species contain a factor that dose-dependently induces GLUT4 translocation and glucose uptake in 3T3-L1 adipocytes, human adipocytes, myoblasts and myotubes. Notably, the effect of this factor on GLUT4 is fully maintained in insulin-resistant cells. Our studies demonstrate that the serum-induced increase in cell surface GLUT4 levels is not due to inhibition of its internalization and is not mediated by insulin, PDGF, IGF-1, or HGF. Similarly to insulin, serum also augments cell surface levels of GLUT1 and TfR. Remarkably, the acute effect of serum on GLUT4 is largely additive to that of insulin, while it also sensitizes the cells to insulin. In accordance with these findings, serum does not appear to activate the same repertoire of downstream signaling molecules that are implicated in insulin-induced GLUT4 translocation. We conclude that in addition to insulin, at least one other biological proteinaceous factor exists that contributes to GLUT4 regulation and still functions in insulin resistance. The challenge now is to identify this factor. |
format | Text |
id | pubmed-3004919 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2010 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-30049192010-12-27 A Serum Factor Induces Insulin-Independent Translocation of GLUT4 to the Cell Surface which Is Maintained in Insulin Resistance Berenguer, Marion Martinez, Laurène Giorgetti-Peraldi, Sophie Le Marchand-Brustel, Yannick Govers, Roland PLoS One Research Article In response to insulin, glucose transporter GLUT4 translocates from intracellular compartments towards the plasma membrane where it enhances cellular glucose uptake. Here, we show that sera from various species contain a factor that dose-dependently induces GLUT4 translocation and glucose uptake in 3T3-L1 adipocytes, human adipocytes, myoblasts and myotubes. Notably, the effect of this factor on GLUT4 is fully maintained in insulin-resistant cells. Our studies demonstrate that the serum-induced increase in cell surface GLUT4 levels is not due to inhibition of its internalization and is not mediated by insulin, PDGF, IGF-1, or HGF. Similarly to insulin, serum also augments cell surface levels of GLUT1 and TfR. Remarkably, the acute effect of serum on GLUT4 is largely additive to that of insulin, while it also sensitizes the cells to insulin. In accordance with these findings, serum does not appear to activate the same repertoire of downstream signaling molecules that are implicated in insulin-induced GLUT4 translocation. We conclude that in addition to insulin, at least one other biological proteinaceous factor exists that contributes to GLUT4 regulation and still functions in insulin resistance. The challenge now is to identify this factor. Public Library of Science 2010-12-20 /pmc/articles/PMC3004919/ /pubmed/21187969 http://dx.doi.org/10.1371/journal.pone.0015560 Text en Berenguer et al. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited. |
spellingShingle | Research Article Berenguer, Marion Martinez, Laurène Giorgetti-Peraldi, Sophie Le Marchand-Brustel, Yannick Govers, Roland A Serum Factor Induces Insulin-Independent Translocation of GLUT4 to the Cell Surface which Is Maintained in Insulin Resistance |
title | A Serum Factor Induces Insulin-Independent Translocation of GLUT4 to the Cell Surface which Is Maintained in Insulin Resistance |
title_full | A Serum Factor Induces Insulin-Independent Translocation of GLUT4 to the Cell Surface which Is Maintained in Insulin Resistance |
title_fullStr | A Serum Factor Induces Insulin-Independent Translocation of GLUT4 to the Cell Surface which Is Maintained in Insulin Resistance |
title_full_unstemmed | A Serum Factor Induces Insulin-Independent Translocation of GLUT4 to the Cell Surface which Is Maintained in Insulin Resistance |
title_short | A Serum Factor Induces Insulin-Independent Translocation of GLUT4 to the Cell Surface which Is Maintained in Insulin Resistance |
title_sort | serum factor induces insulin-independent translocation of glut4 to the cell surface which is maintained in insulin resistance |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3004919/ https://www.ncbi.nlm.nih.gov/pubmed/21187969 http://dx.doi.org/10.1371/journal.pone.0015560 |
work_keys_str_mv | AT berenguermarion aserumfactorinducesinsulinindependenttranslocationofglut4tothecellsurfacewhichismaintainedininsulinresistance AT martinezlaurene aserumfactorinducesinsulinindependenttranslocationofglut4tothecellsurfacewhichismaintainedininsulinresistance AT giorgettiperaldisophie aserumfactorinducesinsulinindependenttranslocationofglut4tothecellsurfacewhichismaintainedininsulinresistance AT lemarchandbrustelyannick aserumfactorinducesinsulinindependenttranslocationofglut4tothecellsurfacewhichismaintainedininsulinresistance AT goversroland aserumfactorinducesinsulinindependenttranslocationofglut4tothecellsurfacewhichismaintainedininsulinresistance AT berenguermarion serumfactorinducesinsulinindependenttranslocationofglut4tothecellsurfacewhichismaintainedininsulinresistance AT martinezlaurene serumfactorinducesinsulinindependenttranslocationofglut4tothecellsurfacewhichismaintainedininsulinresistance AT giorgettiperaldisophie serumfactorinducesinsulinindependenttranslocationofglut4tothecellsurfacewhichismaintainedininsulinresistance AT lemarchandbrustelyannick serumfactorinducesinsulinindependenttranslocationofglut4tothecellsurfacewhichismaintainedininsulinresistance AT goversroland serumfactorinducesinsulinindependenttranslocationofglut4tothecellsurfacewhichismaintainedininsulinresistance |