Elevated hemoglobin A1 in streptozotocin diabetic rats and in rats on sucrose and galactose-enriched diets.

Increased hemoglobin A1 (HbA1) occurs in diabetes mellitus as a direct consequence of hyperglycemia, which causes postsynthetic modification of hemoglobin proportional to blood glucose concentration. Glycosylation of hemoglobin is demonstrable also in vitro, not only by glucose, but with other reducing sugars such as galactose. The purpose of this study was to show that increased HbA1 could be induced by feeding rats a diet enriched either by galactose or sucrose. A third experimental group consisted of rats made diabetic by injection of streptozotocin. Exposure to a diet of 40% galactose resulted in a diabetes-like state with polyuria, weight loss, muscle atrophy, fat depletion, bilateral cataracts, peripheral neuropathy and significantly elevated HbA1. Blood glucose levels were not elevated and after four months of galactose feeding there was hypoglycemia. Total HbA1 was determined by a microcolumn chromatographic procedure, recently made available for clinical use. Increased HbA1 was also found in rats which received a diet of 68% sucrose for several months. The highest values of HbA1 were determined in streptozotocin diabetic rats and there was significant correlation with plasma glucose concentration. Development of experimental models for increased HbA1 by dietary exposure makes it possible to relate increases in HbA1 to measured amounts of sugar included in the diet. Increased HbA1 in galactosemic and diabetic rats provides a biochemical marker which may be correlated with the evolving morphologic changes such as basement membrane thickening occurring in certain tissues in diabetes mellitus.