The prevalence of diabetic nephropathy, a serious complication of diabetes, has been increasing worldwide. Therefore, there is an urgent need to identify a new therapeutic target to prevent diabetic nephropathy. "Nutrient-sensing" pathways are generally well conserved among eukaryotes. Accumulating evidence indicates that alteration of nutrient-sensing pathways and subsequent impairment of cell function in insulin-sensitive organs of mammals are involved in the pathogenesis of type 2 diabetes. According to recent reports, nutrient-sensing in the kidney also seems to be altered under diabetic conditions. In this review, we discuss the possibility that nutrient-sensing pathways can be a therapeutic target for diabetic nephropathy and suggest future directions for research.