March 5, 2020

A Low-Fat Diet May Help Reverse Diabetic Nerve Damage

A new study in Disease Models & Mechanisms by Drs. O'Brien, Guo, Eid, Rumora and Hinder indicates that dietary interventions in mice centered on fats help reverse diabetic neuropathy.

Drs. Phillipe O’Brien, Kai Guo, Stephanie Eid, Amy Rumora and Lucy Hinder found that a low-fat diet can reverse diabetic neuropathy (nerve damage) caused by the buildup of saturated fats in nerves. This work, conducted in mouse models, provides preliminary evidence that making dietary adjustments in humans could similarly improve nerve pain.

Drs. O'Brien and Feldman
Drs. Phillipe O'Brien and Eva Feldman.

“These findings are extremely relevant to diabetes patients,” explained Dr. Eva Feldman, director of the NeuroNetwork for Emerging Therapies at Michigan Medicine. “They demonstrate that saturated triglyceride fats accumulate in nerves, but that the process may be reversible. It also advocates dietary interventions in patients centered on fats, as well as their glucose regulating medication.”

Disease Models & Mechanisms First Person Interview with Drs. O'Brien, Guo, Eid, Rumora and Hinder

The NeuroNetwork scientists conducted a comprehensive study in nerves to identify which fats correlate with neuropathy in both prediabetes and diabetes mouse models. Mice were initially fed a high-fat diet of saturated fats to mimic unhealthy, high-calorie fatty diets in humans. When their metabolism began to suffer and they developed neuropathy, the fats in their nerves were studied. The mice were then switched to a low-fat diet, similar to a dietary intervention program in humans, and when their metabolism recovered, the fats in their nerves were examined again.

The study found that saturated triglyceride fats, the bad type of fat, were particularly elevated in damaged nerves compared to other fats, but that their levels dropped after the mice were switched to the low-fat diet. The study also identified an enzyme, DGAT2, that catalyzes the final step in triglyceride synthesis, as a key participant in neuropathy. DGAT2 levels were found to be higher in damaged nerves from diabetes patients with poor metabolic health compared to diabetes patients with well-regulated metabolism.

Dr. Feldman and her research team at the NeuroNetwork for Emerging Therapies continue to pursue this line of investigation. In addition to hyperglycemia (high blood sugar), they are examining the effect of obesity on neuropathy and other neurological diseases.

portrait of Dr. Eva Feldman

Eva Feldman, MD, PhD

James W. Albers Distinguished University Professor of Neurology
Russell N. DeJong Professor of Neurology
Director, NeuroNetwork for Emerging Therapies
Director, ALS Center of Excellence