1976
DOI: 10.1172/jci108534
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Red cell age-related changes of hemoglobins AIa+b and AIc in normal and diabetic subjects.

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Cited by 168 publications
(81 citation statements)
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“…Because erythropoietin accelerates the production of new erythrocytes and the proportion of young erythrocytes in peripheral blood must increase after erythropoietin administration. HbA 1c is the product of the chemical condensation of hemoglobin and glucose, and the glycated rate of just-produced young erythrocytes is reported to be lower than that of old cells (26). Therefore, it seems that the decrease of HbA 1c levels relative to PG or GA in HD patients who have diabetes and are treated with erythropoietin might be due to the increasing proportion of young erythrocytes over old erythrocytes in peripheral blood of those patients (11).…”
Section: Discussionmentioning
confidence: 99%
“…Because erythropoietin accelerates the production of new erythrocytes and the proportion of young erythrocytes in peripheral blood must increase after erythropoietin administration. HbA 1c is the product of the chemical condensation of hemoglobin and glucose, and the glycated rate of just-produced young erythrocytes is reported to be lower than that of old cells (26). Therefore, it seems that the decrease of HbA 1c levels relative to PG or GA in HD patients who have diabetes and are treated with erythropoietin might be due to the increasing proportion of young erythrocytes over old erythrocytes in peripheral blood of those patients (11).…”
Section: Discussionmentioning
confidence: 99%
“…Glucose was unequivocally identified to generate the most abundant HbA 1 fraction HbA 1c , which was shown to be an Amadori product formed by the irreversible binding of glucose to the β -N-terminal valine residues of globin chains, rearranged into 1-deoxy-1-N-valyl-fructose [8 -12] and present in the ring form [13] . This process was demonstrated to occur during the 120-day lifespan of the erythrocytes [14] , glycated Hb content being higher in older than in younger red blood cells [15,16] . Although mentioned in 1966 [6] , the intermediary formation of a labile Schiff base (labile HbA 1c , Hb pre-A 1c ) preceding the Amadori rearrangement and the formation of the characteristic keto-amine linkage was formally described in 1981 only [17] .…”
Section: The Times Of Pioneers and Discoveriesmentioning
confidence: 99%
“…4,5 However, normal RBC life span has been reported to have a wide range of values regardless of the method used, [6][7][8] and there are also studies suggesting that RBC life span may depend on glycemic control, although evidence for this is conflicting. [9][10][11][12][13] It is also possible that heterogeneity in other features of red cell physiology, such as membrane glucose transport 14 and loss of Hb from older RBCs, 15 may influence the relationship between blood glucose and HbA1c.…”
Section: Introductionmentioning
confidence: 99%