Dietary fructose intake has increased, with its link to diabetes there is a need to understand the metabolism of fructose by cells other than those of the liver and gut (Tappy & Rosset, 2019). Investigations into the central nervous system have shown many areas of the brain efficiently metabolise fructose and express key fructolytic enzymes e.g. fructokinase (Oppelt et al., 2017). Specifically, fructose enabled sustained conduction of smaller diameter axons of the optic nerve due to fructokinase expression, in contrast to larger diameter axons which do not express fructokinase (Meakin et al., 2007). This study aimed to investigate the link between fructokinase expression and differences in fibre subtype fructose metabolism of the peripheral sciatic nerve. Previously we have shown that only the C fibres, not A fibres, efficiently metabolise fructose (Rich & Brown, 2018). All procedures were carried out in accordance with the Animals (Scientific Procedures) Act 1986, Schedule 1. Adult male CD-1 mice were euthanised by cervical dislocation and decapitated. Sciatic nerves (n=6) were dissected, placed in liquid nitrogen and cut into longitudinal and transverse sections for immunohistochemistry processing. Sections were co-stained with fluorescent antibodies against fructokinase and a protein specific to each cell type: neurofilament 200 (A fibres), peripherin (C fibres) and S100β (Schwann cells). Images were taken using confocal microscopy. Sciatic nerves were also placed in a perfusion chamber, superfused with aerated aCSF. The A fibre compound action potential was evoked with supra-maximal stimuli at a baseline frequency of 1Hz, high frequency stimulation (HFS) was defined as 100Hz. The area under the normalised CAP amplitude vs. time (NCAP.mins) reflected axon conduction, expressed as mean SD (Rich & Brown, 2018). Co-localisation of fructokinase with neurofilament revealed fructokinase expression by A fibres but not C fibres or Schwann cells. A fibre conduction was maintained when HFS was imposed during the supply of 20mM fructose (442 44.8 NCAP.mins n=4) whilst the addition of 200µM cinnamate (lactate transport blocker) or reducing the concentration of fructose to 10mM prevented sustained conduction (133.2 18 NCAP.mins n=4 and 82.4 20.4 NCAP.mins n=4, respectively). This is in accord with our previous finding that A fibres indirectly benefit from fructose in the form of Schwann cell supplied lactate (Rich & Brown 2018). Expression of fructokinase only by A fibres, despite little direct use of fructose, suggests fructokinase is not essential for efficient metabolism of fructose by the sciatic, in contrast to the optic nerve. Interestingly, maintenance of A fibre conduction requires Schwann cells to provide lactate, derived from fructose or glycogen, highlighting metabolic interactions between axons and glia of the peripheral nervous system.