Chain length of saturated fatty acids regulates mitochondrial trafficking and
function in sensory neurons.
Authors Rumora AE, LoGrasso G, Haidar JA, Dolkowski JJ, Lentz SI, Feldman EL
Submitted By Submitted Externally on 1/24/2019
Status Published
Journal Journal of lipid research
Year 2019
Date Published 1/1/2019
Volume : Pages 60 : 58 - 70
PubMed Reference 30442656
Abstract Dyslipidemia associated with T2D leads to diabetic neuropathy, a complication
characterized by sensory neuronal dysfunction and peripheral nerve damage.
Sensory dorsal root ganglion (DRG) neurons are dependent on axonal mitochondrial
energy production facilitated by mitochondrial transport mechanisms that
distribute mitochondria throughout the axon. Because long-chain saturated FAs
(SFAs) damage DRG neurons and medium-chain SFAs are reported to improve neuronal
function, we evaluated the impact of SFA chain length on mitochondrial
trafficking, mitochondrial function, and apoptosis. DRG neurons were exposed to
SFAs with C12:0-C18:0 chain lengths and evaluated for changes in mitochondrial
trafficking, mitochondrial polarization, and apoptosis. DRG neurons treated with
C16:0 and C18:0 SFAs showed a significant decrease in the percentage of motile
mitochondria and velocity of mitochondrial trafficking, whereas C12:0 and C14:0
SFAs had no impact on motility. Treatment with C16:0 and C18:0 SFAs exhibited
mitochondrial depolarization correlating with impaired mitochondrial motility;
the C12:0- and C14:0-treated neurons retained mitochondrial polarization. The
reduction in mitochondrial trafficking and function in C16:0- and C18:0-treated
DRG neurons correlated with apoptosis that was blocked in C12:0 and C14:0 SFA
treatments. These results suggest that SFA chain length plays an important role
in regulating axonal mitochondrial trafficking and function in DRG neurons.