We found, unexpectedly, that glucosamine reduced mesangial expansion and expression of fibronectin and α-SMA in diabetic nephropathy, and decreased the number of α-SMA+ endothelial cells in the glomeruli, while renal function and expression of inflammatory factors and other genes associated with accumulation of extracellular matrix were not affected by glucosamine. This evidence concerns the gene ACTA1 and diabetic kidney disease.