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Tumour necrosis factor-α −308G/A polymorphism is associated with insulin secretory defects in Bangladeshi prediabetic/diabetic subjects

OBJECTIVES: Tumour necrosis factor (TNF)-α, an adipocytokine, is closely linked to impaired glucose tolerance (IGT) and insulin resistance (IR) in type 2 diabetes (T2D) subjects. The relationship between the polymorphisms in the TNF-α gene and IR in Bangladeshi prediabetes and T2D subjects has not y...

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Autores principales: Hossain, Muhammad M., Paul, Sunanda, Das, Manisha, Saha, Trissa, Faruque, Md O., Hassan, Zahid
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taibah University 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9073880/
https://www.ncbi.nlm.nih.gov/pubmed/35592794
http://dx.doi.org/10.1016/j.jtumed.2021.09.013
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author Hossain, Muhammad M.
Paul, Sunanda
Das, Manisha
Saha, Trissa
Faruque, Md O.
Hassan, Zahid
author_facet Hossain, Muhammad M.
Paul, Sunanda
Das, Manisha
Saha, Trissa
Faruque, Md O.
Hassan, Zahid
author_sort Hossain, Muhammad M.
collection PubMed
description OBJECTIVES: Tumour necrosis factor (TNF)-α, an adipocytokine, is closely linked to impaired glucose tolerance (IGT) and insulin resistance (IR) in type 2 diabetes (T2D) subjects. The relationship between the polymorphisms in the TNF-α gene and IR in Bangladeshi prediabetes and T2D subjects has not yet been fully identified. This study aims to reveal the association between TNF-α gene polymorphism and IR in hyperglycaemic patients of Bangladeshi origin. METHODS: In our study, 106 IGT, 100 T2D, and 109 healthy subjects of Bangladeshi origin were recruited to identify the impact of TNF-α gene polymorphism at position −308 with a G>A transition using PCR and subsequent restriction fragment length polymorphism (RFLP). RESULTS: The −308G>A TNF-α genotype frequency distribution within the control, IGT, and T2D groups showed a significant association (χ(2) = 21.077; P = 0.001), although allele frequency distribution within the groups showed a statistically non-significant difference (χ(2) = 1.696; P = 0.091). β-cell functional deficiency (HOMA-B%) was observed to be significantly (P = 0.034) lower in subjects with a variant genotype. In addition, our results indicate that the study subjects’ body mass index (BMI) and residence status were positively correlated (P ≤ 0.05) with −308G>A TNF-α gene polymorphism. CONCLUSIONS: Therefore, it can be concluded that −308G>A TNF-α gene polymorphism may have a causative relationship with lower insulin secretory capacity and higher BMI in Bangladeshi IGT and T2D populations, while the urban population's lifestyle might be associated with this polymorphism.
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spelling pubmed-90738802022-05-18 Tumour necrosis factor-α −308G/A polymorphism is associated with insulin secretory defects in Bangladeshi prediabetic/diabetic subjects Hossain, Muhammad M. Paul, Sunanda Das, Manisha Saha, Trissa Faruque, Md O. Hassan, Zahid J Taibah Univ Med Sci Original Article OBJECTIVES: Tumour necrosis factor (TNF)-α, an adipocytokine, is closely linked to impaired glucose tolerance (IGT) and insulin resistance (IR) in type 2 diabetes (T2D) subjects. The relationship between the polymorphisms in the TNF-α gene and IR in Bangladeshi prediabetes and T2D subjects has not yet been fully identified. This study aims to reveal the association between TNF-α gene polymorphism and IR in hyperglycaemic patients of Bangladeshi origin. METHODS: In our study, 106 IGT, 100 T2D, and 109 healthy subjects of Bangladeshi origin were recruited to identify the impact of TNF-α gene polymorphism at position −308 with a G>A transition using PCR and subsequent restriction fragment length polymorphism (RFLP). RESULTS: The −308G>A TNF-α genotype frequency distribution within the control, IGT, and T2D groups showed a significant association (χ(2) = 21.077; P = 0.001), although allele frequency distribution within the groups showed a statistically non-significant difference (χ(2) = 1.696; P = 0.091). β-cell functional deficiency (HOMA-B%) was observed to be significantly (P = 0.034) lower in subjects with a variant genotype. In addition, our results indicate that the study subjects’ body mass index (BMI) and residence status were positively correlated (P ≤ 0.05) with −308G>A TNF-α gene polymorphism. CONCLUSIONS: Therefore, it can be concluded that −308G>A TNF-α gene polymorphism may have a causative relationship with lower insulin secretory capacity and higher BMI in Bangladeshi IGT and T2D populations, while the urban population's lifestyle might be associated with this polymorphism. Taibah University 2021-11-12 /pmc/articles/PMC9073880/ /pubmed/35592794 http://dx.doi.org/10.1016/j.jtumed.2021.09.013 Text en © 2021 The Authors https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Original Article
Hossain, Muhammad M.
Paul, Sunanda
Das, Manisha
Saha, Trissa
Faruque, Md O.
Hassan, Zahid
Tumour necrosis factor-α −308G/A polymorphism is associated with insulin secretory defects in Bangladeshi prediabetic/diabetic subjects
title Tumour necrosis factor-α −308G/A polymorphism is associated with insulin secretory defects in Bangladeshi prediabetic/diabetic subjects
title_full Tumour necrosis factor-α −308G/A polymorphism is associated with insulin secretory defects in Bangladeshi prediabetic/diabetic subjects
title_fullStr Tumour necrosis factor-α −308G/A polymorphism is associated with insulin secretory defects in Bangladeshi prediabetic/diabetic subjects
title_full_unstemmed Tumour necrosis factor-α −308G/A polymorphism is associated with insulin secretory defects in Bangladeshi prediabetic/diabetic subjects
title_short Tumour necrosis factor-α −308G/A polymorphism is associated with insulin secretory defects in Bangladeshi prediabetic/diabetic subjects
title_sort tumour necrosis factor-α −308g/a polymorphism is associated with insulin secretory defects in bangladeshi prediabetic/diabetic subjects
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9073880/
https://www.ncbi.nlm.nih.gov/pubmed/35592794
http://dx.doi.org/10.1016/j.jtumed.2021.09.013
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