Related Experiment Video
Updated: Oct 8, 2026

High-resolution Respirometry to Measure Mitochondrial Function of Intact Beta Cells in the Presence of Natural Compounds
Published on: January 23, 2018
Exogenous pyruvate protects IMS32 Schwann cells from impairing the maturation process under hyperglycemia
Hideji Yako1, Sana Hattori1, Sayaka Iwamoto1
1Laboratory of Molecular Neuroscience and Neurology, Tokyo University of Pharmacy and Life Sciences, Horinouchi, Hachioji, Tokyo, 192-0392, Japan; Laboratory for Drug Target Discovery, Tokyo University of Pharmacy and Life Sciences, Horinouchi, Hachioji, Tokyo, 192-0392, Japan.
Abstract:
Peripheral neuropathy is a chronic common complication of diabetes mellitus. Continuous hyperglycemia induces metabolic disturbances and elicits oxidative stress. However, the impact of hyperglycemia on the maturation of Schwann cells is not fully understood. Therefore, we examined whether hyperglycemia affects the maturation process of IMS32 Schwann cells treated with forskolin, a Schwann cell maturation enhancer, using promoter assays and immunoblotting of Schwann cell markers such as MBP, CNPase, and GFAP. IMS32 cells exposed to high-glucose conditions showed decreased expression of these markers. Exogenous pyruvate plays a crucial role in maintaining glucose metabolism and reducing oxidative stress under hyperglycemic conditions. These decreases were prevented by pyruvate supplementation. Pyruvate treatment also prevented IMS32 cells from producing reactive oxygen species and from impairing mitochondrial membrane potential. These results indicate that hyperglycemia impairs Schwann cell maturation accompanied by mitochondrial dysfunction and oxidative stress, contributing to the development and progression of diabetic peripheral neuropathy.
