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A-FABP-PTEN/AKT Regulates Insulin Resistance in Preadipocyte Cell 3T3-L1 Cells
OBJECTIVE: The purpose of this study was to explore the regulation of A-FABP-PTEN/AKT on insulin resistance in preadipocyte 3T3-L1 cell. METHODS: siRNA interference method was used to knock-down the A-FABP expression in 3T3-L1 cells. The cell proliferation was detected by oil-O staining and MTT. The...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8123973/ https://www.ncbi.nlm.nih.gov/pubmed/34007196 http://dx.doi.org/10.2147/DMSO.S305872 |
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author | Wu, Rensiqin Wang, Hui Huangfu, Jian Xiao, Rui |
author_facet | Wu, Rensiqin Wang, Hui Huangfu, Jian Xiao, Rui |
author_sort | Wu, Rensiqin |
collection | PubMed |
description | OBJECTIVE: The purpose of this study was to explore the regulation of A-FABP-PTEN/AKT on insulin resistance in preadipocyte 3T3-L1 cell. METHODS: siRNA interference method was used to knock-down the A-FABP expression in 3T3-L1 cells. The cell proliferation was detected by oil-O staining and MTT. The protein and mRNA expression levels of A-FABP, PTEN and AKT were detected by Western blot and qPCR. RESULTS: Inhibition of A-FABP expression increased cell proliferation activity of the 3T3-L1 cells. Moreover, siRNA3 significantly reduced A-FABP mRNA expression compared with siRNA1 and siRNA2 (P<0.05). The A-FABP mRNA level was significantly increased in the induced 3T3-L1 cells, while the PTEN mRNA expression was significantly decreased (P<0.05). Inhibition of A-FABP can significantly increase the PTEN mRNA expression in the process of induced 3T3-L1 cells (P<0.05). Overexpression of A-FABP can also increase the PTEN mRNA expression in the process of 3T3-L1 cell proliferation (P<0.05). Furthermore, the protein expression levels of PTEN and p-AKT expression were not changed in the process of 3T3-L1 cell proliferation with or without A-FABP interference (P>0.05). However, inhibition of A-FABP significantly increased the PTEN protein expression and reduced the p-AKT protein expression in the induced 3T3-L1 cells. CONCLUSION: Our finding suggested that A-FABP can directly inhibit the phosphorylation of AKT and increase the PTEN expression in the process of normal adipocyte differentiation, which speculated that A-FABP played a crucial role by adjusting the AKT activity in the process of adipocyte differentiation. |
format | Online Article Text |
id | pubmed-8123973 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Dove |
record_format | MEDLINE/PubMed |
spelling | pubmed-81239732021-05-17 A-FABP-PTEN/AKT Regulates Insulin Resistance in Preadipocyte Cell 3T3-L1 Cells Wu, Rensiqin Wang, Hui Huangfu, Jian Xiao, Rui Diabetes Metab Syndr Obes Original Research OBJECTIVE: The purpose of this study was to explore the regulation of A-FABP-PTEN/AKT on insulin resistance in preadipocyte 3T3-L1 cell. METHODS: siRNA interference method was used to knock-down the A-FABP expression in 3T3-L1 cells. The cell proliferation was detected by oil-O staining and MTT. The protein and mRNA expression levels of A-FABP, PTEN and AKT were detected by Western blot and qPCR. RESULTS: Inhibition of A-FABP expression increased cell proliferation activity of the 3T3-L1 cells. Moreover, siRNA3 significantly reduced A-FABP mRNA expression compared with siRNA1 and siRNA2 (P<0.05). The A-FABP mRNA level was significantly increased in the induced 3T3-L1 cells, while the PTEN mRNA expression was significantly decreased (P<0.05). Inhibition of A-FABP can significantly increase the PTEN mRNA expression in the process of induced 3T3-L1 cells (P<0.05). Overexpression of A-FABP can also increase the PTEN mRNA expression in the process of 3T3-L1 cell proliferation (P<0.05). Furthermore, the protein expression levels of PTEN and p-AKT expression were not changed in the process of 3T3-L1 cell proliferation with or without A-FABP interference (P>0.05). However, inhibition of A-FABP significantly increased the PTEN protein expression and reduced the p-AKT protein expression in the induced 3T3-L1 cells. CONCLUSION: Our finding suggested that A-FABP can directly inhibit the phosphorylation of AKT and increase the PTEN expression in the process of normal adipocyte differentiation, which speculated that A-FABP played a crucial role by adjusting the AKT activity in the process of adipocyte differentiation. Dove 2021-05-11 /pmc/articles/PMC8123973/ /pubmed/34007196 http://dx.doi.org/10.2147/DMSO.S305872 Text en © 2021 Wu et al. https://creativecommons.org/licenses/by-nc/3.0/This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/ (https://creativecommons.org/licenses/by-nc/3.0/) ). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php). |
spellingShingle | Original Research Wu, Rensiqin Wang, Hui Huangfu, Jian Xiao, Rui A-FABP-PTEN/AKT Regulates Insulin Resistance in Preadipocyte Cell 3T3-L1 Cells |
title | A-FABP-PTEN/AKT Regulates Insulin Resistance in Preadipocyte Cell 3T3-L1 Cells |
title_full | A-FABP-PTEN/AKT Regulates Insulin Resistance in Preadipocyte Cell 3T3-L1 Cells |
title_fullStr | A-FABP-PTEN/AKT Regulates Insulin Resistance in Preadipocyte Cell 3T3-L1 Cells |
title_full_unstemmed | A-FABP-PTEN/AKT Regulates Insulin Resistance in Preadipocyte Cell 3T3-L1 Cells |
title_short | A-FABP-PTEN/AKT Regulates Insulin Resistance in Preadipocyte Cell 3T3-L1 Cells |
title_sort | a-fabp-pten/akt regulates insulin resistance in preadipocyte cell 3t3-l1 cells |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8123973/ https://www.ncbi.nlm.nih.gov/pubmed/34007196 http://dx.doi.org/10.2147/DMSO.S305872 |
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