There is an interesting article published in September about how thalassemia sufferers report problems with hypoglycemia including myself. The article discusses diabetes as a complication from iron overload, bit focuses instead on a calculation for energy consumption. The author states the following:
The role of beta thalassemia instability in altered metabolic change relative to poor diabetic control has not been entirely resolved and needs additional structural study for clarification. In this work, the author calculated the required energy for HbATable 1.
The molecular weight and the energy required for HbA1C formation in controls and beta thalassemia cases
CategoryMolecular weight (MW)Required energy per unit (RE; cal) Beta and beta (normal)64,5001.085 Beta and beta+48,633<MW<64,5001.085<RE<1.439 Beta and beta048,6331.439 Beta+ and beta+32,766<MW<64,5001.085<RE<2.136 Beta+ and beta032,766<MW<48,6331.439<RE<2.136 Beta0 and beta032,766N/Aa
Each beta globin subunit consists of 146 amino acids and has a molecular weight of 15,867 Da. These data were used for the calculation of molecular weight in each type of beta thalassemia.
There are two beta globin chains in Hb. Each beta globin chain is coded by a beta globin gene. Beta+ refers to a partial deletion of the beta globin gene, resulting in partial disappearance of the beta globin chain. Beta0 refers to a total deletion of the beta globin gene, resulting in the total disappearance of the beta globin chain.
a Although the required energy per unit in this category can be calculated, it must not exist; if there is no beta globin, then there must be no HbA1C.
1C per unit in beta thalassemia and found that the energy required is slightly different from that required in normal Hb and might have very little effect on the pathophysiological process."
In conclusion, the author states:
According to this study, the energy range required for any type of beta thalassemia is greater than that required in normal Hb. Hence, it might be expressed that beta thalassemia significantly increased complications due to energy consumption during HbA1C formation in poor-control diabetic cases. Indeed, in previous studies, the risk for thrombotic episodes as a diabetic complication in beta thalassemia patients has been confirmed to increase ([Borgna Pignatti et al., 1998] and [Moratelli et al., 1998]). The present study confirms the fact that beta thalassemia patients in developing countries may be at risk for endocrine deficiencies at younger ages (Gulati, Bhatia, & Agarwal, 200).
I am very happy to see that research is being done toward what some of us "feel" is right but can't explain. Just because something hasn't been explained or correlated, doesn't invalidate it. Science is about discovery, and I learn something new every month.
You can find the full article here:
1: J Diabetes Complications. 2007 Sep-Oct;21(5):338-40.
Links Beta thalassemia and energy consumption in hemoglobin A1C formation: a model. Wiwanitkit V.
Department of Laboratory Medicine, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.
wviroj@yahoo.com
Hemoglobin (Hb) A1C is the nonenzymatic glycated product of the Hb beta chain at the valine terminal residue. Recently, the nature of energy-consuming reaction in HbA1C formation was reported, and this was proposed as an underlying pathophysiology for poor nutritional status, muscle loss, and functional impairment in poor-control diabetic patients. Here, the author focuses on energy change in HbA1C formation in the case of beta thalassemia. According to this study, the energy range required for any type of beta thalassemia is greater than that required for normal Hb. Hence, it might be expressed that beta thalassemia did significantly increase complications due to energy consumption during HbA1C formation in poor-control diabetic cases.
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