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Association of TNF-α Gene Expression and Release in Response to Anti-Diabetic Drugs from Human Adipocytes in vitro

INTRODUCTION: TNF-α, a proinflammatory cytokine secreted by activated immune cells, and overexpression of it in adipocytes, has an important role in insulin resistance progression and diabetes development. AIM AND OBJECTIVE: Subcutaneous adipocytes derived from mesenchymal stem cells were used for i...

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Autores principales: Saxena, Madhukar, Ali, Daoud, Modi, Dinesh Raj, Almarzoug, Mohammed H A, Hussain, S A, Manohrdas, S
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7399456/
https://www.ncbi.nlm.nih.gov/pubmed/32801814
http://dx.doi.org/10.2147/DMSO.S265362
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author Saxena, Madhukar
Ali, Daoud
Modi, Dinesh Raj
Almarzoug, Mohammed H A
Hussain, S A
Manohrdas, S
author_facet Saxena, Madhukar
Ali, Daoud
Modi, Dinesh Raj
Almarzoug, Mohammed H A
Hussain, S A
Manohrdas, S
author_sort Saxena, Madhukar
collection PubMed
description INTRODUCTION: TNF-α, a proinflammatory cytokine secreted by activated immune cells, and overexpression of it in adipocytes, has an important role in insulin resistance progression and diabetes development. AIM AND OBJECTIVE: Subcutaneous adipocytes derived from mesenchymal stem cells were used for in vitro analysis to find the role of antidiabetic drugs on TNF-α in high glucose-fed adipocytes. METHODS: In vitro adipocytes were used along with variable concentration of anti-diabetic drugs. The level of TNF-α was measured by ELISA and the mRNA level was quantified using SYBR-Green real-time PCR. All data were statistically analyzed. RESULTS: The level of TNF-α and the mRNA expression were observed and analyzed with normal adipocytes. TNF-α level and expression of it showed agonistic behavior, ie no change at low concentration while enhances with the increase of glucose. The level was decreased significantly when the adipocytes were treated with metformin (p=0.015) and pioglitazone (p=0.020). A combination of drugs showed that the expression of TNF-α was almost the same as for metformin alone. However, insulin increases the TNF-α expression as for pioglitazone. DISCUSSION: Such a report on adipocytes may be helpful for clinical benefits to understand the additional mechanism of adipocytes on the release and expression of TNF-α. However, anti-diabetic drugs including insulin up-regulate the TNF-α gene expression in mild or severe glucose load.
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spelling pubmed-73994562020-08-14 Association of TNF-α Gene Expression and Release in Response to Anti-Diabetic Drugs from Human Adipocytes in vitro Saxena, Madhukar Ali, Daoud Modi, Dinesh Raj Almarzoug, Mohammed H A Hussain, S A Manohrdas, S Diabetes Metab Syndr Obes Original Research INTRODUCTION: TNF-α, a proinflammatory cytokine secreted by activated immune cells, and overexpression of it in adipocytes, has an important role in insulin resistance progression and diabetes development. AIM AND OBJECTIVE: Subcutaneous adipocytes derived from mesenchymal stem cells were used for in vitro analysis to find the role of antidiabetic drugs on TNF-α in high glucose-fed adipocytes. METHODS: In vitro adipocytes were used along with variable concentration of anti-diabetic drugs. The level of TNF-α was measured by ELISA and the mRNA level was quantified using SYBR-Green real-time PCR. All data were statistically analyzed. RESULTS: The level of TNF-α and the mRNA expression were observed and analyzed with normal adipocytes. TNF-α level and expression of it showed agonistic behavior, ie no change at low concentration while enhances with the increase of glucose. The level was decreased significantly when the adipocytes were treated with metformin (p=0.015) and pioglitazone (p=0.020). A combination of drugs showed that the expression of TNF-α was almost the same as for metformin alone. However, insulin increases the TNF-α expression as for pioglitazone. DISCUSSION: Such a report on adipocytes may be helpful for clinical benefits to understand the additional mechanism of adipocytes on the release and expression of TNF-α. However, anti-diabetic drugs including insulin up-regulate the TNF-α gene expression in mild or severe glucose load. Dove 2020-07-24 /pmc/articles/PMC7399456/ /pubmed/32801814 http://dx.doi.org/10.2147/DMSO.S265362 Text en © 2020 Saxena et al. http://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/). 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
Saxena, Madhukar
Ali, Daoud
Modi, Dinesh Raj
Almarzoug, Mohammed H A
Hussain, S A
Manohrdas, S
Association of TNF-α Gene Expression and Release in Response to Anti-Diabetic Drugs from Human Adipocytes in vitro
title Association of TNF-α Gene Expression and Release in Response to Anti-Diabetic Drugs from Human Adipocytes in vitro
title_full Association of TNF-α Gene Expression and Release in Response to Anti-Diabetic Drugs from Human Adipocytes in vitro
title_fullStr Association of TNF-α Gene Expression and Release in Response to Anti-Diabetic Drugs from Human Adipocytes in vitro
title_full_unstemmed Association of TNF-α Gene Expression and Release in Response to Anti-Diabetic Drugs from Human Adipocytes in vitro
title_short Association of TNF-α Gene Expression and Release in Response to Anti-Diabetic Drugs from Human Adipocytes in vitro
title_sort association of tnf-α gene expression and release in response to anti-diabetic drugs from human adipocytes in vitro
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7399456/
https://www.ncbi.nlm.nih.gov/pubmed/32801814
http://dx.doi.org/10.2147/DMSO.S265362
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