In This Issue of Diabetes

摘要

Oral L-serine may offer a new strategy for the treatment of diabetic neuropathy (DN), according to a report in this issue of Diabetes. The new study by Othman et al. (p. 1035) builds on the group's earlier work that focused on hereditary sensory and autonomic neuropathy type 1 (HSAN1). HSAN1 is a rare neuropathy that is caused by 1-deoxysphingolipids (1-deoxySLs), which are neurotoxic. Oral L-serine supplementation reduced the concentration of 1-deoxySLs in HSAN1 patients and in mouse models of HSAN1. The treatment also protected mice from developing neuropathy. Using a rodent model of diabetes, the new report explored the impact of L-serine supplementation in the setting of hyperglycemia. The experimental animals were given a standard diet or one enriched with L-serine. To assess various aspects of DN, thermal and mechanical tests of DN were conducted, measures of nerve conduction velocity were collected, and epidermal nerve fiber density was measured. In addition, the sphingoid base composition of extracted lipids was also examined. The results of these experiments showed that diabetic rats that received the serine-enriched diet had lower plasma 1 -deoxySLs relative to those that received the standard diet. Rats on the enriched diet also showed more favorable DN phenotypes. They had more favorable sensory nerve function and nerve conduction measures, and they exhibited improvements in the percentage of large-diameter fibers/axons. The authors also observed a very strong negative correlation between plasma 1 -deoxySLs and nerve conduction velocity. The results of this new report suggest that further research on the effects of L-serine supplementation on DN is warranted. Future work in this area may be particularly important given the lack of adequate treatments that are currently available for this condition.