Mice given a high fat and rich carbohydrate (54% kcal from fat, 25% kcal from CHO) diet eventually display clinical symptoms of prediabetes, including obesity, hyperglycemia, and mechanical allodynia. Previous work from our group has shown that mice allowed to voluntarily exercise while fed a high-fat diet develop mechanical allodynia over the first 6 weeks, but then have their mechanical allodynia return to control levels during weeks 6-12 from the continued exercise. The present work examined whether a ‘ketogenic’ diet (∼90% kcal from fat, <1% kcal from CHO) similarly alters metabolic-related sensory changes. Our goal was to understand how dietary fat processing impacts the metabolic status as it relates to, as well as to better understand the function of the peripheral nervous system. Ketogenic diet-fed mice develop similar metabolic changes similar to of high fat exercised mice, with increased body weight, fat mass, and blood glucose, though all are less than that of high-fat sedentary animals. Unlike mice on a high fat diet, ketogenic fed mice never develop mechanical allodynia, suggesting the adaption to metabolic fuel sources may be key in the development of mechanical allodynia. Mice fed a high fat diet display increased sensory and motor conduction velocities compared to ketogenic and control mice. Ketogenic-diet fed mice had mildly increased peripheral nerve fiber density in the epidermis of the hind paw compared to normal chow and high at fed mice, suggesting a ketogenic diet may be beneficial to sensory axon growth in the epidermis. Together, these results suggest that a ketogenic diet does not lead to changes in sensory function similar to high-fat fed mice, and mirrors many of the sensory and metabolic changes that are corrected by exercise in in high-fat fed mice.
© 2017 Published by Elsevier Inc.