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Linking inflammatory mediators and indicators of insulin resistance in anthropometry specified type 2 diabetic males
Inflammation associated with insulin resistance is a risk factor in the development of complications in Type 2 diabetes mellitus (T2DM). The study was conducted to assess the relationship between inflammatory mediators and insulin resistance, independent of lipid profile in anthropometry specified m...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Biomedical Informatics
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10465773/ https://www.ncbi.nlm.nih.gov/pubmed/37654824 http://dx.doi.org/10.6026/97320630018998 |
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author | Bonam, Venkata Ramesh Srinivasan, Abu Raghavan Manoj, Daniel Devaprasad |
author_facet | Bonam, Venkata Ramesh Srinivasan, Abu Raghavan Manoj, Daniel Devaprasad |
author_sort | Bonam, Venkata Ramesh |
collection | PubMed |
description | Inflammation associated with insulin resistance is a risk factor in the development of complications in Type 2 diabetes mellitus (T2DM). The study was conducted to assess the relationship between inflammatory mediators and insulin resistance, independent of lipid profile in anthropometry specified male Type 2 diabetics. 180 males having T2DM for more than 5yrs and on diabetic medication were chosen for the study and categorized into obese and overweight. Patients with thyroid or other endocrine disorders, kidney, muscle, liver, systemic, and inflammatory diseases were excluded from the study. Blood glucose, glycated hemoglobin, plasma insulin, and the inflammatory biomarkers namely hs-CRP, ferritin, haptoglobin, and adiponectin were evaluated. HOMA-IR and QUICKI were computed to assess insulin resistance. The study demonstrated significant changes in adiponectin and hsCRP in obese and overweight T2DM. However, Ferritin and Haptoglobin were insignificant. The entire biochemical study was carried out to demonstrate lipid profile independent associations. The significant insulin resistance associated with a substantial increase in hs-CRP levels and a pronounced decrease in the adiponectin levels suggests impending diabetic complications in anthropometry specified male T2DM. This could promote the use of personalised medicine to regulate levels of hs-CRP or to improve the secretion of adiponectin thereby countering insulin resistance in T2DM, independent of the lipid profile which is the novelty of our study. |
format | Online Article Text |
id | pubmed-10465773 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Biomedical Informatics |
record_format | MEDLINE/PubMed |
spelling | pubmed-104657732023-08-31 Linking inflammatory mediators and indicators of insulin resistance in anthropometry specified type 2 diabetic males Bonam, Venkata Ramesh Srinivasan, Abu Raghavan Manoj, Daniel Devaprasad Bioinformation Research Article Inflammation associated with insulin resistance is a risk factor in the development of complications in Type 2 diabetes mellitus (T2DM). The study was conducted to assess the relationship between inflammatory mediators and insulin resistance, independent of lipid profile in anthropometry specified male Type 2 diabetics. 180 males having T2DM for more than 5yrs and on diabetic medication were chosen for the study and categorized into obese and overweight. Patients with thyroid or other endocrine disorders, kidney, muscle, liver, systemic, and inflammatory diseases were excluded from the study. Blood glucose, glycated hemoglobin, plasma insulin, and the inflammatory biomarkers namely hs-CRP, ferritin, haptoglobin, and adiponectin were evaluated. HOMA-IR and QUICKI were computed to assess insulin resistance. The study demonstrated significant changes in adiponectin and hsCRP in obese and overweight T2DM. However, Ferritin and Haptoglobin were insignificant. The entire biochemical study was carried out to demonstrate lipid profile independent associations. The significant insulin resistance associated with a substantial increase in hs-CRP levels and a pronounced decrease in the adiponectin levels suggests impending diabetic complications in anthropometry specified male T2DM. This could promote the use of personalised medicine to regulate levels of hs-CRP or to improve the secretion of adiponectin thereby countering insulin resistance in T2DM, independent of the lipid profile which is the novelty of our study. Biomedical Informatics 2022-10-31 /pmc/articles/PMC10465773/ /pubmed/37654824 http://dx.doi.org/10.6026/97320630018998 Text en © 2022 Biomedical Informatics https://creativecommons.org/licenses/by/3.0/This is an Open Access article which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. This is distributed under the terms of the Creative Commons Attribution License. |
spellingShingle | Research Article Bonam, Venkata Ramesh Srinivasan, Abu Raghavan Manoj, Daniel Devaprasad Linking inflammatory mediators and indicators of insulin resistance in anthropometry specified type 2 diabetic males |
title | Linking inflammatory mediators and indicators of insulin resistance in anthropometry specified type 2 diabetic males |
title_full | Linking inflammatory mediators and indicators of insulin resistance in anthropometry specified type 2 diabetic males |
title_fullStr | Linking inflammatory mediators and indicators of insulin resistance in anthropometry specified type 2 diabetic males |
title_full_unstemmed | Linking inflammatory mediators and indicators of insulin resistance in anthropometry specified type 2 diabetic males |
title_short | Linking inflammatory mediators and indicators of insulin resistance in anthropometry specified type 2 diabetic males |
title_sort | linking inflammatory mediators and indicators of insulin resistance in anthropometry specified type 2 diabetic males |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10465773/ https://www.ncbi.nlm.nih.gov/pubmed/37654824 http://dx.doi.org/10.6026/97320630018998 |
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