Hemoglobin AIc levels in insulin-dependent and -independent diabetes mellitus.

Unusual increases in the minor hemoglobin components (Hb AIa, b, c) known 
to be elevated in diabetes mellitus were found in states of 
relative or absolute insulinopenia: diabetic ketoacidosis, steroid- induced diabetes, insulin-dependent diabetes 
in cystic-fibrosis patients, and cystic fibrosis occurring in infants who have 
a marked suppression of insulin secretion. In ketoacidotic diabetics, it required 
at least a month for high Hb AI levels (16.9 +/- 
2.6 per cent) to stabilize at nonacidotic levels (12.8 +/- 0.3 
per cent), suggesting that decreases occur only as new red cells 
form under conditions less favorable to Hb AI synthesis. Abnormal amounts 
os Hb A and Hb AI resisted removal from diabetic red-cell 
membranes by low ionic buffers but yielded to hypotonic Tris buffer. 
Their removal resulted in simultaneous elution of peripheral and integral membrane 
proteins. It is suggested that Hb so firmly bound could reduce 
membrane elasticity and cell deformability, characteristics so vital to normal red 
cell movement through the microvasculature. 