Roy Chowdhury 2011 Mitochondrion
|Roy Chowdhury SK, Dobrowsky RT, Fernyhough P (2011) Nutrient excess and altered mitochondrial proteome and function contribute to neurodegeneration in diabetes. Mitochondrion 11:845-54.|
Abstract: Diabetic neuropathy is a major complication of diabetes that results in the progressive deterioration of the sensory nervous system. Mitochondrial dysfunction has been proposed to play an important role in the pathogenesis of the neurodegeneration observed in diabetic neuropathy. Our recent work has shown that mitochondrial dysfunction occurs in dorsal root ganglia (DRG) sensory neurons in streptozotocin (STZ) induced diabetic rodents. In neurons, the nutrient excess associated with prolonged diabetes may trigger a switching off of AMP kinase (AMPK) and/or silent information regulator T1 (SIRT1) signaling leading to impaired peroxisome proliferator-activated receptor γ coactivator-1 (PGC-1α) expression/activity and diminished mitochondrial activity. This review briefly summarizes the alterations of mitochondrial function and proteome in sensory neurons of STZ-diabetic rodents. We also discuss the possible involvement of AMPK/SIRT/PGC-1α pathway in other diabetic models and different tissues affected by diabetes.
• Keywords: Mitochondrial respiratory chain, Diabetic neuropathy, Dorsal root ganglia, PGC-1α, AMPK, SIRT • Bioblast editor: Plangger M • O2k-Network Lab: CA Winnipeg Banerji V, CA Winnipeg Fernyhough P
Labels: MiParea: Respiration Pathology: Diabetes, Neurodegenerative
Organism: Rat Tissue;cell: Nervous system Preparation: Homogenate
Coupling state: OXPHOS Pathway: N, CIV HRR: Oxygraph-2k