Department of Molecular Pathology, Hirosaki University Graduate School of Medicine
Department of Molecular Pathology, Hirosaki University Graduate School of Medicine
Department of Molecular Pathology, Hirosaki University Graduate School of Medicine
Department of Molecular Pathology, Hirosaki University Graduate School of Medicine
抄録
Accumulating evidence supports that proinflammatory processes are implicated in the establishment
of characteristic pathology in diabetic vascular and neurological complications. Altered cellular signaling during
inflammatory processes is a new target for the treatment of diabetic complications and there appear to be some
attempts to explore the eff ects of thiazolidinedione, a ligand of peroxisome proliferating activator receptor( PPAR)-γ
for not only the treatment of diabetes itself but for the application to diabetic complications. We therefore explored the
eff ects of PPAR-γ agonist, pioglitazone, on the experimental model of diabetic neuropathy. We found that pioglitazone
signifi cantly improved nerve conduction velocities and depressed protein kinase C activity. This is a new area for the
exploration of eff ective treatment of diabetic complications that pose a considerable socioeconomic burden in the current
world.