Current experiments investigated whether a
ketogenic diet impacts neuropathy associated with
obesity and
prediabetes. Mice challenged with a
ketogenic diet were compared to mice fed a high-fat diet or a high-fat diet plus exercise. Additionally, an intervention switching to a
ketogenic diet following 8 weeks of high-fat diet was performed to compare how a control diet, exercise, or a
ketogenic diet affects
metabolic syndrome-induced neural complications. When challenged with a
ketogenic diet, mice had reduced bodyweight and fat mass compared to high-fat-fed mice, and were similar to exercised, high-fat-fed mice. High-fat-fed, exercised and ketogenic-fed mice had mildly elevated
blood glucose; conversely,
ketogenic diet-fed mice were unique in having reduced serum
insulin levels.
Ketogenic diet-fed mice never developed
mechanical allodynia contrary to mice fed a high-fat diet.
Ketogenic diet fed mice also had increased epidermal axon density compared all other groups. When a
ketogenic diet was used as an intervention, a
ketogenic diet was unable to reverse high-fat fed-induced metabolic changes but was able to significantly reverse a high-fat diet-induced
mechanical allodynia. As an intervention, a
ketogenic diet also increased epidermal axon density. In vitro studies revealed increased neurite outgrowth in sensory neurons from mice fed a
ketogenic diet and in neurons from normal diet-fed mice given
ketone bodies in the culture medium. These results suggest a
ketogenic diet can prevent certain complications of
prediabetes and provides significant benefits to peripheral axons and sensory dysfunction.