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Iron Profile and Glycaemic Control in Patients with Type 2 Diabetes Mellitus

Iron overload is increasingly being connected to insulin resistance in Type 2 Diabetes Mellitus (T2DM) patients. Free iron causes the assembly of reactive oxygen species that invariably steer the body’s homeostasis towards oxidative stress-mediated diabetic complications. This study aims to assess t...

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Autores principales: Misra, Gunjan, Bhatter, Surendra Kumar, Kumar, Ajai, Gupta, Varsha, Khan, Mohd Y.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5635795/
https://www.ncbi.nlm.nih.gov/pubmed/29083385
http://dx.doi.org/10.3390/medsci4040022
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author Misra, Gunjan
Bhatter, Surendra Kumar
Kumar, Ajai
Gupta, Varsha
Khan, Mohd Y.
author_facet Misra, Gunjan
Bhatter, Surendra Kumar
Kumar, Ajai
Gupta, Varsha
Khan, Mohd Y.
author_sort Misra, Gunjan
collection PubMed
description Iron overload is increasingly being connected to insulin resistance in Type 2 Diabetes Mellitus (T2DM) patients. Free iron causes the assembly of reactive oxygen species that invariably steer the body’s homeostasis towards oxidative stress-mediated diabetic complications. This study aims to assess the serum iron, total iron binding capacity (TIBC), and percentage transferrin saturation (Tsat) of 150 subjects divided into three groups (I,II,III) of 50. Healthy individuals (controls) constituted Group I. Group II consisted of T2DM patients with optimal glycaemic control. T2DM patients with suboptimal glycaemic control formed group III. Mean serum free iron concentration was 105.34 ± 3.5, 107.33 ± 3.45, and 125.58 ± 3.45 μg/dL in Group I, Group II, and Group III, respectively. Mean serum TIBC concentration in Group I, Group II, and Group III was 311.39 ± 5.47, 309.63 ± 6.1, and 284.2 ± 3.18μg/dL, respectively. Mean serum transferrin saturation (%) in Group I, Group II, and Group III was 34.17 ± 1.21, 35.02 ± 1.2, and 44.39 ± 1.07, respectively. The difference between TIBC, mean serum free iron concentration, and transferrin saturation between Group I and Group III (for all, p values <0.001), as well as between Group II and Group III (p values 0.0012, 0.0015, and <0.0001, respectively) was statistically significant. The fasting plasma glucose values of Groups II and III were significantly higher than those of Group I, (p < 0.0001). Glycated haemoglobin (HbA1c) values were also shown to increase from Group I to II and then III, and the increase was highly significant (all p values <0.0001). Thus, decreased glycaemic control and an increase in the glycation of haemoglobin was the key to elevation in serum iron values and alterations in other parameters. However, a significant correlation was absent between serum iron and HbA1c (r = 0.05) and transferrin saturation (r = 0.0496) in Group III.
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spelling pubmed-56357952017-10-26 Iron Profile and Glycaemic Control in Patients with Type 2 Diabetes Mellitus Misra, Gunjan Bhatter, Surendra Kumar Kumar, Ajai Gupta, Varsha Khan, Mohd Y. Med Sci (Basel) Article Iron overload is increasingly being connected to insulin resistance in Type 2 Diabetes Mellitus (T2DM) patients. Free iron causes the assembly of reactive oxygen species that invariably steer the body’s homeostasis towards oxidative stress-mediated diabetic complications. This study aims to assess the serum iron, total iron binding capacity (TIBC), and percentage transferrin saturation (Tsat) of 150 subjects divided into three groups (I,II,III) of 50. Healthy individuals (controls) constituted Group I. Group II consisted of T2DM patients with optimal glycaemic control. T2DM patients with suboptimal glycaemic control formed group III. Mean serum free iron concentration was 105.34 ± 3.5, 107.33 ± 3.45, and 125.58 ± 3.45 μg/dL in Group I, Group II, and Group III, respectively. Mean serum TIBC concentration in Group I, Group II, and Group III was 311.39 ± 5.47, 309.63 ± 6.1, and 284.2 ± 3.18μg/dL, respectively. Mean serum transferrin saturation (%) in Group I, Group II, and Group III was 34.17 ± 1.21, 35.02 ± 1.2, and 44.39 ± 1.07, respectively. The difference between TIBC, mean serum free iron concentration, and transferrin saturation between Group I and Group III (for all, p values <0.001), as well as between Group II and Group III (p values 0.0012, 0.0015, and <0.0001, respectively) was statistically significant. The fasting plasma glucose values of Groups II and III were significantly higher than those of Group I, (p < 0.0001). Glycated haemoglobin (HbA1c) values were also shown to increase from Group I to II and then III, and the increase was highly significant (all p values <0.0001). Thus, decreased glycaemic control and an increase in the glycation of haemoglobin was the key to elevation in serum iron values and alterations in other parameters. However, a significant correlation was absent between serum iron and HbA1c (r = 0.05) and transferrin saturation (r = 0.0496) in Group III. MDPI 2016-12-09 /pmc/articles/PMC5635795/ /pubmed/29083385 http://dx.doi.org/10.3390/medsci4040022 Text en © 2016 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC-BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Misra, Gunjan
Bhatter, Surendra Kumar
Kumar, Ajai
Gupta, Varsha
Khan, Mohd Y.
Iron Profile and Glycaemic Control in Patients with Type 2 Diabetes Mellitus
title Iron Profile and Glycaemic Control in Patients with Type 2 Diabetes Mellitus
title_full Iron Profile and Glycaemic Control in Patients with Type 2 Diabetes Mellitus
title_fullStr Iron Profile and Glycaemic Control in Patients with Type 2 Diabetes Mellitus
title_full_unstemmed Iron Profile and Glycaemic Control in Patients with Type 2 Diabetes Mellitus
title_short Iron Profile and Glycaemic Control in Patients with Type 2 Diabetes Mellitus
title_sort iron profile and glycaemic control in patients with type 2 diabetes mellitus
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5635795/
https://www.ncbi.nlm.nih.gov/pubmed/29083385
http://dx.doi.org/10.3390/medsci4040022
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