The IGF-I axis has been implicated in the development of renal complications of diabetes. The glomerulosclerosis of diabetes is characterized by cell proliferation and accumulation of extra-cellular matrix in the mesangium. This suggests that there may be an intrinsic defect of mesangial cell behavior. The non-obese diabetic mice (NOD) develop glomerular lesions early after the onset of diabetes. To study the role of the IGF-I axis in a model of spontaneous diabetes, we developed new lines of mesangial cells derived from these animals. We examined the IGF-I receptor, IGF-I production, and IGF-I binding proteins of NOD mouse cells and compared them to controls. We previously demonstrated the presence of IGF-I receptors and the synthesis of IGF-I in glomerular mesangial cells. Preliminary studies suggest that NOD mesangial cells differ substantially from normal cells with respect to the IGF axis.
