Demystifying Diabetic Neuropathy

In some communities, nearly half of all people with type 2 diabetes will develop nerve damage and peripheral neuropathy (1). And although medications and therapies can mitigate symptoms, the underlying factors that trigger the development of neuropathy are not yet fully understood. Notably, current treatments cannot effectively prevent peripheral neuropathy; even good blood glucose control only partially prevents its onset (2). But what if predictive – and modifiable – metabolic factors existed?

A recent study has discovered a link between a number of specific lipid biomarkers and the development of neuropathy in people with type 2 diabetes (3). The retrospective study used mass spectrometry to analyze 10-year-old serum samples from 69 patients with type 2 diabetes. For each participant, the researchers generated a serum lipidomic profile featuring 435 lipid species from 18 classes. The team noticed a pattern in the lipidomic profiles of those who went on to develop neuropathy – as identified by the Michigan Neuropathy Screening Instrument (MNSI) examination – compared with those who did not. Specifically, participants with a high MNSI index had significantly decreased medium-chain acylcarnitines, increased total free fatty acids, decreased phosphatidylcholines, and increased lysophosphatidylcholines.

The authors noted that neuropathy did not seem to affect the abundance of other lipid classes. They also indicated that the overall findings indicate that lipid changes may be related to impaired mitochondrial β-oxidation, which is notable because it suggests that conventional medications for lowering lipid levels may not effectively treat neuropathy.