The peripheral nervous system is composed of long sensory and motor neurons, which are impacted by a number of genetic and environmental conditions. In particular, one of the most prevalent peripheral nerve disorders is diabetic neuropathy, leading to sequelae that become exacerbated by aging and are complicated to manage without effective treatments. Our laboratory has been engaged in studies of the peripheral nervous system and associated Schwann cells, focusing on genetic neuropathies and traumatic nerve injury. While there are important distinctions between diabetic and genetic neuropathy, progress in the field has developed a congruence of pathological mechanisms involving metabolic perturbations affecting axoglial homeostasis. For example, recent identification of neuropathy caused by mutations in the SORD gene confirmed the mechanistic role of increased sorbitol levels that are also observed in diabetic neuropathy. Our own work has focused on Schwann cell gene networks that are involved in development, regeneration, and homeostasis. We are currently engaged in a study of EPA and DHA in a mouse model of neuropathy, and these have shown beneficial effects in models of peripheral nerve injury and diabetic neuropathy. We would also welcome the opportunity to develop synergistic interactions with other members of the Wisconsin Diabetes Research Center working with neuropathy models, particularly mouse models of neuropathy involving a high fat diet since this recapitulates the major factors driving diabetic neuropathy, which is less associated with hyperglycemia per se.