Peripheral Mononuclear Cell Resistin mRNA Expression Is Increased in Type 2 Diabetic Women
Resistin has been shown to cause insulin resistance and to impair glucose tolerance in rodents, but in humans its physiological role still remains elusive. The aim of this study was to examine whether resistin mRNA expression in human peripheral mononuclear cells (PBMCs) and its corresponding plasma...
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Wiley
2008-01-01
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Series: | Mediators of Inflammation |
Online Access: | http://dx.doi.org/10.1155/2008/892864 |
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author | Panayoula C. Tsiotra Constantine Tsigos Eleni Anastasiou Eleni Yfanti Eleni Boutati Emmanouil Souvatzoglou Ioannis Kyrou Sotirios A. Raptis |
author_facet | Panayoula C. Tsiotra Constantine Tsigos Eleni Anastasiou Eleni Yfanti Eleni Boutati Emmanouil Souvatzoglou Ioannis Kyrou Sotirios A. Raptis |
author_sort | Panayoula C. Tsiotra |
collection | DOAJ |
description | Resistin has been shown to cause insulin resistance and to impair glucose tolerance in rodents, but in humans its physiological role still remains elusive. The aim of this study was to examine whether resistin mRNA expression in human peripheral mononuclear cells (PBMCs) and its corresponding plasma levels are altered in type 2 diabetes. Resistin mRNA levels were easily detectable in human PBMC, and found to be higher in DM2 compared to healthy women (P=.05). Similarly, mononuclear mRNA levels of the proinflammatory cytokines IL-1β, TNF-α, and IL-6 were all significantly higher in DM2 compared to control women (P<.001). The corresponding plasma resistin levels were slightly, but not significantly, increased in DM2 women (P=.051), and overall, they correlated significantly with BMI (r=0.406, P=.010) and waist circumference (r=0.516, P=.003), but not with fasting insulin levels or HOMA-IR. Resistin mRNA expression is increased in PBMC from DM2 women, together with increased expression of the inflammatory cytokines IL-1β, TNF-α, and IL-6, independent of obesity. These results suggest that resistin and cytokines might contribute to the low-grade inflammation and the increased atherogenic risk observed in these patients. |
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institution | Kabale University |
issn | 0962-9351 1466-1861 |
language | English |
publishDate | 2008-01-01 |
publisher | Wiley |
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series | Mediators of Inflammation |
spelling | doaj-art-3b0d43b6c1c34da08e4ce27d382f6b9a2025-02-03T06:00:15ZengWileyMediators of Inflammation0962-93511466-18612008-01-01200810.1155/2008/892864892864Peripheral Mononuclear Cell Resistin mRNA Expression Is Increased in Type 2 Diabetic WomenPanayoula C. Tsiotra0Constantine Tsigos1Eleni Anastasiou2Eleni Yfanti3Eleni Boutati4Emmanouil Souvatzoglou5Ioannis Kyrou6Sotirios A. Raptis7Division of Basic Sciences, Hellenic National Center for the Research, Prevention and Treatment of Diabetes Mellitus and Its Complications (HNDC), 10675 Athens, GreeceDivision of Basic Sciences, Hellenic National Center for the Research, Prevention and Treatment of Diabetes Mellitus and Its Complications (HNDC), 10675 Athens, GreeceDepartment of Internal Medicine, First Endocrine Section and Diabetes Centre, “Alexandra” Hospital, 11528 Athens, GreeceDivision of Basic Sciences, Hellenic National Center for the Research, Prevention and Treatment of Diabetes Mellitus and Its Complications (HNDC), 10675 Athens, GreeceSecond Department of Internal Medicine, Research Institute and Diabetes Center, Athens University Medical School, “Attikon” University General Hospital, Haidari, 11527 Athens, GreeceDepartment of Internal Medicine, First Endocrine Section and Diabetes Centre, “Alexandra” Hospital, 11528 Athens, GreeceDivision of Basic Sciences, Hellenic National Center for the Research, Prevention and Treatment of Diabetes Mellitus and Its Complications (HNDC), 10675 Athens, GreeceDivision of Basic Sciences, Hellenic National Center for the Research, Prevention and Treatment of Diabetes Mellitus and Its Complications (HNDC), 10675 Athens, GreeceResistin has been shown to cause insulin resistance and to impair glucose tolerance in rodents, but in humans its physiological role still remains elusive. The aim of this study was to examine whether resistin mRNA expression in human peripheral mononuclear cells (PBMCs) and its corresponding plasma levels are altered in type 2 diabetes. Resistin mRNA levels were easily detectable in human PBMC, and found to be higher in DM2 compared to healthy women (P=.05). Similarly, mononuclear mRNA levels of the proinflammatory cytokines IL-1β, TNF-α, and IL-6 were all significantly higher in DM2 compared to control women (P<.001). The corresponding plasma resistin levels were slightly, but not significantly, increased in DM2 women (P=.051), and overall, they correlated significantly with BMI (r=0.406, P=.010) and waist circumference (r=0.516, P=.003), but not with fasting insulin levels or HOMA-IR. Resistin mRNA expression is increased in PBMC from DM2 women, together with increased expression of the inflammatory cytokines IL-1β, TNF-α, and IL-6, independent of obesity. These results suggest that resistin and cytokines might contribute to the low-grade inflammation and the increased atherogenic risk observed in these patients.http://dx.doi.org/10.1155/2008/892864 |
spellingShingle | Panayoula C. Tsiotra Constantine Tsigos Eleni Anastasiou Eleni Yfanti Eleni Boutati Emmanouil Souvatzoglou Ioannis Kyrou Sotirios A. Raptis Peripheral Mononuclear Cell Resistin mRNA Expression Is Increased in Type 2 Diabetic Women Mediators of Inflammation |
title | Peripheral Mononuclear Cell Resistin mRNA Expression Is Increased in Type 2 Diabetic Women |
title_full | Peripheral Mononuclear Cell Resistin mRNA Expression Is Increased in Type 2 Diabetic Women |
title_fullStr | Peripheral Mononuclear Cell Resistin mRNA Expression Is Increased in Type 2 Diabetic Women |
title_full_unstemmed | Peripheral Mononuclear Cell Resistin mRNA Expression Is Increased in Type 2 Diabetic Women |
title_short | Peripheral Mononuclear Cell Resistin mRNA Expression Is Increased in Type 2 Diabetic Women |
title_sort | peripheral mononuclear cell resistin mrna expression is increased in type 2 diabetic women |
url | http://dx.doi.org/10.1155/2008/892864 |
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