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Adipocytokine Levels in Genetically High Risk for Type 2 Diabetes in the Indian Population: A Cross-Sectional Study
Introduction. In view of the noteworthy role of adipocytokines in the onset of insulin resistance and diabetes in gene-knockout-rat-model-cell-line studies we aimed to study the influence of genetic predisposition for diabetes on adipocytokine levels and their role in building insulin-resistance-lik...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi Publishing Corporation
2012
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3505654/ https://www.ncbi.nlm.nih.gov/pubmed/23213322 http://dx.doi.org/10.1155/2012/386524 |
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author | Bose, K. Subhash Chandra Gupta, Shachin K. Vyas, Prerna |
author_facet | Bose, K. Subhash Chandra Gupta, Shachin K. Vyas, Prerna |
author_sort | Bose, K. Subhash Chandra |
collection | PubMed |
description | Introduction. In view of the noteworthy role of adipocytokines in the onset of insulin resistance and diabetes in gene-knockout-rat-model-cell-line studies we aimed to study the influence of genetic predisposition for diabetes on adipocytokine levels and their role in building insulin-resistance-like environment well before the onset of diabetes; thus a hypothesis can be drawn on their role in developing diabetes in high risk population. Methods. Ages between 18 and 22 years were selected and divided into three groups. Group I (n = 81): control group with no family history of diabetes. Group II (n = 157): with one of their parents with history of type 2 diabetes. Group III (n = 47): with both parents having history of type 2 diabetes. In all the groups we estimated fasting plasma glucose, insulin and adipocytokines like adiponectin, leptin, TNF-α, and IL-6. Results. Of all adipocytokines we observed significantly lower levels of adiponectin (8.7 ± 1 μg/mL in group III and 9.5 ± 1.3 μg/mL group II) when compared to control (11.0 ± 1.2 μg/mL; P < 0.01) and it has strong correlation with family history of diabetes with Pearson's coefficient of −0.502. Linear regression analysis showed significant negative association with HOMA-IR (P < 0.01) and logistic regression analysis showed highest association with parental diabetes (P < 0.01; OR .260, 95% CI .260–.468). Conclusion. Genetic predisposition for diabetes may influence adiponectin gene expression leading to decrease in its plasma concentration, which might play a key role in developing diabetes in near future. |
format | Online Article Text |
id | pubmed-3505654 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-35056542012-12-04 Adipocytokine Levels in Genetically High Risk for Type 2 Diabetes in the Indian Population: A Cross-Sectional Study Bose, K. Subhash Chandra Gupta, Shachin K. Vyas, Prerna Exp Diabetes Res Research Article Introduction. In view of the noteworthy role of adipocytokines in the onset of insulin resistance and diabetes in gene-knockout-rat-model-cell-line studies we aimed to study the influence of genetic predisposition for diabetes on adipocytokine levels and their role in building insulin-resistance-like environment well before the onset of diabetes; thus a hypothesis can be drawn on their role in developing diabetes in high risk population. Methods. Ages between 18 and 22 years were selected and divided into three groups. Group I (n = 81): control group with no family history of diabetes. Group II (n = 157): with one of their parents with history of type 2 diabetes. Group III (n = 47): with both parents having history of type 2 diabetes. In all the groups we estimated fasting plasma glucose, insulin and adipocytokines like adiponectin, leptin, TNF-α, and IL-6. Results. Of all adipocytokines we observed significantly lower levels of adiponectin (8.7 ± 1 μg/mL in group III and 9.5 ± 1.3 μg/mL group II) when compared to control (11.0 ± 1.2 μg/mL; P < 0.01) and it has strong correlation with family history of diabetes with Pearson's coefficient of −0.502. Linear regression analysis showed significant negative association with HOMA-IR (P < 0.01) and logistic regression analysis showed highest association with parental diabetes (P < 0.01; OR .260, 95% CI .260–.468). Conclusion. Genetic predisposition for diabetes may influence adiponectin gene expression leading to decrease in its plasma concentration, which might play a key role in developing diabetes in near future. Hindawi Publishing Corporation 2012 2012-11-14 /pmc/articles/PMC3505654/ /pubmed/23213322 http://dx.doi.org/10.1155/2012/386524 Text en Copyright © 2012 K. Subhash Chandra Bose et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Bose, K. Subhash Chandra Gupta, Shachin K. Vyas, Prerna Adipocytokine Levels in Genetically High Risk for Type 2 Diabetes in the Indian Population: A Cross-Sectional Study |
title | Adipocytokine Levels in Genetically High Risk for Type 2 Diabetes in the Indian Population: A Cross-Sectional Study |
title_full | Adipocytokine Levels in Genetically High Risk for Type 2 Diabetes in the Indian Population: A Cross-Sectional Study |
title_fullStr | Adipocytokine Levels in Genetically High Risk for Type 2 Diabetes in the Indian Population: A Cross-Sectional Study |
title_full_unstemmed | Adipocytokine Levels in Genetically High Risk for Type 2 Diabetes in the Indian Population: A Cross-Sectional Study |
title_short | Adipocytokine Levels in Genetically High Risk for Type 2 Diabetes in the Indian Population: A Cross-Sectional Study |
title_sort | adipocytokine levels in genetically high risk for type 2 diabetes in the indian population: a cross-sectional study |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3505654/ https://www.ncbi.nlm.nih.gov/pubmed/23213322 http://dx.doi.org/10.1155/2012/386524 |
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