Status of glucose metabolism including insulin resistance and beta cell function in overtly iron loaded Thalassemia patients

<p><strong>BACKGROUND <br /> </strong>Abnormality of glucose metabolism is a frequent complication in Thalassemia patients. Both insulin deficiency and insulin resistance has been proposed in its pathogenesis. Some form of abnormality in glucose metabolism is expected at an e...

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Main Authors: A Pan, SS Nag, BC Mondal, A Anindya Dasgupta, P Piyali Mitra
Format: Article
Language:English
Published: College of Medical Sciences 2015-06-01
Series:Journal of College of Medical Sciences-Nepal
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Online Access:http://nepjol.info/index.php/JCMSN/article/view/12774
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spelling doaj-51e12c1af0094df68dc990cbac14ff5f2020-11-25T00:13:44ZengCollege of Medical SciencesJournal of College of Medical Sciences-Nepal2091-06572091-06732015-06-01103293610.3126/jcmsn.v10i3.1277410050Status of glucose metabolism including insulin resistance and beta cell function in overtly iron loaded Thalassemia patientsA Pan0SS Nag1BC Mondal2A Anindya Dasgupta3P Piyali Mitra4College of Medical Sciences Department of Paediatrics, BharatpurDepartment of Pediatrics, Burdwan Medical College, BurdwanDepartment of Pediatrics, Burdwan Medical College, BurdwanDepartment of Biochemistry, Burdwan Medical College, BurdwanDepartment of Pathology, Burdwan Medical College, Burdwan<p><strong>BACKGROUND <br /> </strong>Abnormality of glucose metabolism is a frequent complication in Thalassemia patients. Both insulin deficiency and insulin resistance has been proposed in its pathogenesis. Some form of abnormality in glucose metabolism is expected at an earlier age in these patients in developing countries like India and Nepal where iron overload is excessive due to lack of chelation therapy.</p> <p><strong>MATERIALS AND METHODS <br /> </strong>Fasting serum glucose and fasting serum insulin (FSI) were measured in 40 beta-thalassemia major patients, 40 Ebeta- thalassemia patients and 40 controls, all aged between 5 and 12 years. 2 hours after an appropriate dose of oral glucose feed (Children ingested 1.75 g/kg body weight maximum 75 gram dissolved in 250 to 300 ml water) blood samples were drawn again to measure post prandial serum glucose. Iron overload was assessed by measuring liver size, spleen size, total amount of packed cells transfused and serum ferritin. Insulin resistance (IR), insulin sensitivity (%S) and beta cell functions (%B) were derived from the measured laboratory parameters using the latest version of Homeostatic Model Assessment (HOMA) calculator software.</p> <p><strong>RESULTS <br /> </strong>No one had impaired glucose metabolism or diabetes mellitus beta-thalassemia major patients showed evidence of insulin resistance in the form of significantly higher fasting serum insulin (p value 0.002), IR (p value 0.003), %B (p value 0.017) and significantly lower %S (0.002) when compared with controls. FSI showed positive correlation with total amount of packed cells received (r=0.372, p=0.018), serum ferritin (r=0.345, p=0.029) and spleen size (r=0.427, p=0.006). Similarly, IR also showed positive correlation with total amount of packed cells received (r=0.388, p=0.013), serum ferritin (r=0.336, p=0.034) and spleen size (r=0.425, p=0.005). %S showed negative correlation with all these parameters. %B didn&rsquo;t show any statistically significant correlation with these parameters.Ebeta- thalassemia patients didn&rsquo;t have any statistically significant difference in FSI, IR, %S and %B than controls.</p> <p><strong>CONCLUSION <br /> </strong>Insulin resistance develops as the earliest abnormality in glucose metabolism in overtly iron loaded beta thalassemia major patients at an early age. Ebeta- thalassemia patients with milder phenotype do not develop dysfunction of glucose metabolism at such an early age.</p><p>DOI: <a href="http://dx.doi.org/10.3126/jcmsn.v10i3.12774">http://dx.doi.org/10.3126/jcmsn.v10i3.12774</a></p> <p>Journal of College of Medical Sciences-Nepal, 2014, Vol-10, No-3, 29-36</p>http://nepjol.info/index.php/JCMSN/article/view/12774Glucose metabolism, Insulin resistance, Insulin sensitivity, Beta cell function, beta- thalassemia major, Ebeta- thalassemia
collection DOAJ
language English
format Article
sources DOAJ
author A Pan
SS Nag
BC Mondal
A Anindya Dasgupta
P Piyali Mitra
spellingShingle A Pan
SS Nag
BC Mondal
A Anindya Dasgupta
P Piyali Mitra
Status of glucose metabolism including insulin resistance and beta cell function in overtly iron loaded Thalassemia patients
Journal of College of Medical Sciences-Nepal
Glucose metabolism, Insulin resistance, Insulin sensitivity, Beta cell function, beta- thalassemia major, Ebeta- thalassemia
author_facet A Pan
SS Nag
BC Mondal
A Anindya Dasgupta
P Piyali Mitra
author_sort A Pan
title Status of glucose metabolism including insulin resistance and beta cell function in overtly iron loaded Thalassemia patients
title_short Status of glucose metabolism including insulin resistance and beta cell function in overtly iron loaded Thalassemia patients
title_full Status of glucose metabolism including insulin resistance and beta cell function in overtly iron loaded Thalassemia patients
title_fullStr Status of glucose metabolism including insulin resistance and beta cell function in overtly iron loaded Thalassemia patients
title_full_unstemmed Status of glucose metabolism including insulin resistance and beta cell function in overtly iron loaded Thalassemia patients
title_sort status of glucose metabolism including insulin resistance and beta cell function in overtly iron loaded thalassemia patients
publisher College of Medical Sciences
series Journal of College of Medical Sciences-Nepal
issn 2091-0657
2091-0673
publishDate 2015-06-01
description <p><strong>BACKGROUND <br /> </strong>Abnormality of glucose metabolism is a frequent complication in Thalassemia patients. Both insulin deficiency and insulin resistance has been proposed in its pathogenesis. Some form of abnormality in glucose metabolism is expected at an earlier age in these patients in developing countries like India and Nepal where iron overload is excessive due to lack of chelation therapy.</p> <p><strong>MATERIALS AND METHODS <br /> </strong>Fasting serum glucose and fasting serum insulin (FSI) were measured in 40 beta-thalassemia major patients, 40 Ebeta- thalassemia patients and 40 controls, all aged between 5 and 12 years. 2 hours after an appropriate dose of oral glucose feed (Children ingested 1.75 g/kg body weight maximum 75 gram dissolved in 250 to 300 ml water) blood samples were drawn again to measure post prandial serum glucose. Iron overload was assessed by measuring liver size, spleen size, total amount of packed cells transfused and serum ferritin. Insulin resistance (IR), insulin sensitivity (%S) and beta cell functions (%B) were derived from the measured laboratory parameters using the latest version of Homeostatic Model Assessment (HOMA) calculator software.</p> <p><strong>RESULTS <br /> </strong>No one had impaired glucose metabolism or diabetes mellitus beta-thalassemia major patients showed evidence of insulin resistance in the form of significantly higher fasting serum insulin (p value 0.002), IR (p value 0.003), %B (p value 0.017) and significantly lower %S (0.002) when compared with controls. FSI showed positive correlation with total amount of packed cells received (r=0.372, p=0.018), serum ferritin (r=0.345, p=0.029) and spleen size (r=0.427, p=0.006). Similarly, IR also showed positive correlation with total amount of packed cells received (r=0.388, p=0.013), serum ferritin (r=0.336, p=0.034) and spleen size (r=0.425, p=0.005). %S showed negative correlation with all these parameters. %B didn&rsquo;t show any statistically significant correlation with these parameters.Ebeta- thalassemia patients didn&rsquo;t have any statistically significant difference in FSI, IR, %S and %B than controls.</p> <p><strong>CONCLUSION <br /> </strong>Insulin resistance develops as the earliest abnormality in glucose metabolism in overtly iron loaded beta thalassemia major patients at an early age. Ebeta- thalassemia patients with milder phenotype do not develop dysfunction of glucose metabolism at such an early age.</p><p>DOI: <a href="http://dx.doi.org/10.3126/jcmsn.v10i3.12774">http://dx.doi.org/10.3126/jcmsn.v10i3.12774</a></p> <p>Journal of College of Medical Sciences-Nepal, 2014, Vol-10, No-3, 29-36</p>
topic Glucose metabolism, Insulin resistance, Insulin sensitivity, Beta cell function, beta- thalassemia major, Ebeta- thalassemia
url http://nepjol.info/index.php/JCMSN/article/view/12774
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