Delayed wound healing in diabetes is caused by neuropathy, vascular changes, and impaired cellular response to the injury. Macrophages are crucial in normal wound healing, and impaired functions of these cells have been shown in diabetes. beta-1,3-D-glucans stimulate macrophage function. This open-label study was performed to see if aminated beta-1,3-D-glucan (AG) stimulates wound healing in diabetes. Four groups (1-4) of diabetic db/db mice and one nondiabetic control group, db/+(5) were studied: group 1 (n=11): topical AG; group 2 (n=10): topical AG and subcutaneous insulin; group 3 (n=14): topical placebo and subcutaneous insulin; group 4 (n=10): diabetic control (placebo); group 5 (n=12): normal control (placebo). At the end of the experiments fasting blood glucose and A1C were (mean +/- SE) as follows: Group 1: 30.5 +/- 1.9 mmol/L and 11.3 +/- 0.6%; group 2: 12.0 +/- 1.7 mmol/L and 8.0 +/- 0.6%; group 3: 15.4 +/- 2.4 mmol/L and 7.4 +/- 0.3%; group 4: 32.6 +/- 2.6 mmol/L and 12.3 +/- 0.6%; group 5: 7.2 +/- 0.4 mmol/L and 3.9 +/- 0.04%, respectively. The closed wound area was the same in group 1 (AG alone) and group 2 (AG plus insulin) after 17 days, 57.3 +/- 4.7 vs. 50.1 +/- 4.9% (p=0.7). The results of these two groups were superior to group 3 (insulin treatment alone, 32.0 +/- 4.3%, p<0.001) and diabetic controls (38.2 +/- 5.1%, p=0.001). The macrophage-stimulant AG improves wound healing in db/db mice.