In addition, glycated hemoglobin (HbA1c) of diabetes rats was also increased up to 6.0%, indicating that the body could not control blood glucose, resulting in the elevation of blood glucose and reduced insulin secretion. The exposure of hemoglobin to the high levels of blood glucose could cause non-enzymatic glycation of hemoglobin resulting in higher percentage of glycosylated hemoglobin in all the diabetic rats (Siddiqui et al., 2010). After 3 months of treatment with experimental diets, all treatment groups of diabetic rats fed with RBBO, except for the metformin group, showed significant improvement on fasting blood glucose (FBG), non-fasting blood glucose (NFBG), glycated hemoglobin (HbA1c), and serum insulin concentration. Although the reduction of blood glucose and elevation of serum insulin level in RBBO supplemented groups did not reach the normal values, the STZ-induced diabetic rats supplemented with RBBO perhaps recovered and increased pancreatic β-cells and granulation to nearly normal condition which indicated by the improvement of hyperglycemia in RBBO supplemented diabetes rats. In addition, the greatest value of GLUT4 was observed in normal rats (NC; NR) and RBBO supplemented group compared to the DMC group, p < 0.05 (Figure1).