Obesity is linked to cognitive deficits in humans, and consumption of a high-fat diet disrupts neurogenesis and neuronal function in animals. However, whether high fat intake alters sensory processing is unknown. Fadool and colleagues now show that, in mice, a high-fat diet leads to long-lasting structural and functional changes in the olfactory system.
Long-term obesity was induced by administration of high-fat diets to an obesity-prone (C57BL/6J) and obesity-resistant (Kv1.3(-/-)) line of mice. They were compared with late-onset, genetic-induced obesity in MC4R(-/-) mice in which diabetes secondarily precipitates after disruption of the hypothalamic axis. Marked loss of olfactory sensory neurons and their axonal projections were observed after exposure to a fatty diet. Mice maintained on fatty diets learned reward-reinforced behaviors more slowly, had deficits in reversal learning demonstrating behavioral inflexibility, and exhibited reduced olfactory discrimination.
When obese mice were removed from their high-fat diet to regain normal body weight and fasting glucose, olfactory dysfunctions persisted. The authors concluded that chronic energy imbalance is associated with long-term structural and functional changes in the olfactory sensory system. Currently, 65% of Americans are overweight, leading to well-supported cardiovascular and cognitive declines. A follow-up study in human subjects is warranted.

Thiebaud N, Johnson MC, Butler JL, Bell GA, Ferguson KL, Fadool AR, Fadool JC, Gale AM, Gale DS, Fadool DA: Hyperlipidemic diet causes loss of ofactory sensory neurons, reduces olfactory discrimination, and disrupts odor-reversal learning. J. Neuroscience 34(20):6970-6984 (2014).


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