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Voluntary Exercise Modifies Olfactory Circuits in Control‐ and Fat‐Fed Mice

Consumption of a fatty diet causes loss of olfactory sensory neurons (OSNs), loss of olfactory discrimination assessed by olfactometry and electroolfactogram, and increased inflammation in the olfactory epithelium. Because of potential anti‐inflammatory properties of voluntary exercise, we hypothesized it could mitigate the detrimental effects of a fatty diet on the olfactory system. Mice with reporters for the olfactroy receptor M72 (Olfr160) and those with resistance to diet‐induced obesity (Kv1.3−/−) were challenged with control (CF) vs. moderately‐high fat (MHF) diet for 6 months upon weaning, with (running wheel; RW) and without access (sedentary; SED) to a Med Associates vertical wireless running wheel and sensor. MHF/RW mice (n=10; mean 7 month body weight = 40.1 g) gained less body weight than MHF/SED (n=10; 33.3 g, p<0.001) and were able to clear plasma glucose as efficiently as CF/SED mice. Although mice of all treatment groups ran at the same velocity, those provided MHF diet (distance run/day = 11.2 km) increased running distance compared to both CF‐fed WT (n=10) and Kv1.3−/− (n=5) mice (6.85 km/day and 8.29 km/day respectively; p=0.02). Actogram analysis demonstrated that CF‐fed Kv1.3−/− and MHF/RW spend 20.2% and 28.3%, respectively, more time running and exhibit shorter pauses in running activity than CF/RW. Whole‐mount brain images were examined to evaluate M72 staining as quantified by the pixel density of the lateral glomerulus and projections. MHF/RW M72 pixel density was twice as much as MHF/SED mice, but CF/RW pixel density was 31.6% lower than that of CF/SED mice. Our results indicate that in addition to combating weight gain and glucose intolerance, voluntary exercise may reduce the detrimental effects of a MHF diet on olfaction, but exercise may also affect the olfactory system independent of diet composition.