A Model of Insulin Resistance in Mice, Born to Diabetic Pregnancy, Is Associated with Alterations of Transcription-Related Genes in Pancreas and Epididymal Adipose Tissue

Objective. This study is conducted on a model of insulin-resistant (IR) mice born to dams which were rendered diabetic by the administration of streptozotocin. Methods. Adult IR and control offspring were selected and we determined the mRNA expression of transcription factors known to modulate pancr...

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Main Authors: Akadiri Yessoufou, Kabirou Moutairou, Naim Akhtar Khan
Format: Article
Language:English
Published: Hindawi Limited 2011-01-01
Series:Journal of Obesity
Online Access:http://dx.doi.org/10.1155/2011/654967
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spelling doaj-4fa2b745332e41edbc9d633fba750edd2020-11-24T22:52:08ZengHindawi LimitedJournal of Obesity2090-07082090-07162011-01-01201110.1155/2011/654967654967A Model of Insulin Resistance in Mice, Born to Diabetic Pregnancy, Is Associated with Alterations of Transcription-Related Genes in Pancreas and Epididymal Adipose TissueAkadiri Yessoufou0Kabirou Moutairou1Naim Akhtar Khan2Faculty of Life Sciences, University of Bourgogne, UPRES EA 4183 Lipides et Signalisation Cellulaire, 6 Boulevard Gabriel, 21000 Dijon, FranceLaboratory of Cell Biology and Physiology, Department of Biochemistry and Cellular Biology, Faculty of Sciences and Techniques, University of Abomey-Calavi and Institute of Biomedical and Applied Sciences (ISBA), 01 BP 918 Cotonou, BeninFaculty of Life Sciences, University of Bourgogne, UPRES EA 4183 Lipides et Signalisation Cellulaire, 6 Boulevard Gabriel, 21000 Dijon, FranceObjective. This study is conducted on a model of insulin-resistant (IR) mice born to dams which were rendered diabetic by the administration of streptozotocin. Methods. Adult IR and control offspring were selected and we determined the mRNA expression of transcription factors known to modulate pancreatic and adipose tissue activities and inflammation. Results. We observed that serum insulin increased, and the mRNA of insulin gene transcription factors, Pdx-1, Nkx6.1 and Maf-A, were upregulated in IR mice pancreas. Besides, their pancreatic functional capacity seemed to be exhausted as evidenced by low expression of pancreatic Glut2 and glucokinase mRNA. Though IR offspring exhibited reduced epididymal adipose tissue, their adipocytes seemed to be differentiated into macrophage-like cells, as they exhibited upregulated CD14 and CD68 antigens, generally expressed by macrophages. However, there was no peripheral macrophages infiltration into epididymal adipose tissue, as the expression of F4/80, a true macrophage marker, was undetectable. Furthermore, the expression of IL-6, TNF-α and TLR-2, key players of insulin resistance, was upregulated in the adipose tissue of IR offspring. Conclusion. Insulin resistant state in mice, born to diabetic pregnancy, alters the expression of function-related genes in pancreas and epididymal adipose tissue and these offspring are prone to develop metabolic syndrome.http://dx.doi.org/10.1155/2011/654967
collection DOAJ
language English
format Article
sources DOAJ
author Akadiri Yessoufou
Kabirou Moutairou
Naim Akhtar Khan
spellingShingle Akadiri Yessoufou
Kabirou Moutairou
Naim Akhtar Khan
A Model of Insulin Resistance in Mice, Born to Diabetic Pregnancy, Is Associated with Alterations of Transcription-Related Genes in Pancreas and Epididymal Adipose Tissue
Journal of Obesity
author_facet Akadiri Yessoufou
Kabirou Moutairou
Naim Akhtar Khan
author_sort Akadiri Yessoufou
title A Model of Insulin Resistance in Mice, Born to Diabetic Pregnancy, Is Associated with Alterations of Transcription-Related Genes in Pancreas and Epididymal Adipose Tissue
title_short A Model of Insulin Resistance in Mice, Born to Diabetic Pregnancy, Is Associated with Alterations of Transcription-Related Genes in Pancreas and Epididymal Adipose Tissue
title_full A Model of Insulin Resistance in Mice, Born to Diabetic Pregnancy, Is Associated with Alterations of Transcription-Related Genes in Pancreas and Epididymal Adipose Tissue
title_fullStr A Model of Insulin Resistance in Mice, Born to Diabetic Pregnancy, Is Associated with Alterations of Transcription-Related Genes in Pancreas and Epididymal Adipose Tissue
title_full_unstemmed A Model of Insulin Resistance in Mice, Born to Diabetic Pregnancy, Is Associated with Alterations of Transcription-Related Genes in Pancreas and Epididymal Adipose Tissue
title_sort model of insulin resistance in mice, born to diabetic pregnancy, is associated with alterations of transcription-related genes in pancreas and epididymal adipose tissue
publisher Hindawi Limited
series Journal of Obesity
issn 2090-0708
2090-0716
publishDate 2011-01-01
description Objective. This study is conducted on a model of insulin-resistant (IR) mice born to dams which were rendered diabetic by the administration of streptozotocin. Methods. Adult IR and control offspring were selected and we determined the mRNA expression of transcription factors known to modulate pancreatic and adipose tissue activities and inflammation. Results. We observed that serum insulin increased, and the mRNA of insulin gene transcription factors, Pdx-1, Nkx6.1 and Maf-A, were upregulated in IR mice pancreas. Besides, their pancreatic functional capacity seemed to be exhausted as evidenced by low expression of pancreatic Glut2 and glucokinase mRNA. Though IR offspring exhibited reduced epididymal adipose tissue, their adipocytes seemed to be differentiated into macrophage-like cells, as they exhibited upregulated CD14 and CD68 antigens, generally expressed by macrophages. However, there was no peripheral macrophages infiltration into epididymal adipose tissue, as the expression of F4/80, a true macrophage marker, was undetectable. Furthermore, the expression of IL-6, TNF-α and TLR-2, key players of insulin resistance, was upregulated in the adipose tissue of IR offspring. Conclusion. Insulin resistant state in mice, born to diabetic pregnancy, alters the expression of function-related genes in pancreas and epididymal adipose tissue and these offspring are prone to develop metabolic syndrome.
url http://dx.doi.org/10.1155/2011/654967
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