The Sense of Smell Impacts Metabolic Health and Obesity

Publication date: 5 July 2017
Source:Cell Metabolism, Volume 26, Issue 1
Author(s): Celine E. Riera, Eva Tsaousidou, Jonathan Halloran, Patricia Follett, Oliver Hahn, Mafalda M.A. Pereira, Linda Engström Ruud, Jens Alber, Kevin Tharp, Courtney M. Anderson, Hella Brönneke, Brigitte Hampel, Carlos Daniel de Magalhaes Filho, Andreas Stahl, Jens C. Brüning, Andrew Dillin
Olfactory inputs help coordinate food appreciation and selection, but their role in systemic physiology and energy balance is poorly understood. Here we demonstrate that mice upon conditional ablation of mature olfactory sensory neurons (OSNs) are resistant to diet-induced obesity accompanied by increased thermogenesis in brown and inguinal fat depots. Acute loss of smell perception after obesity onset not only abrogated further weight gain but also improved fat mass and insulin resistance. Reduced olfactory input stimulates sympathetic nerve activity, resulting in activation of β-adrenergic receptors on white and brown adipocytes to promote lipolysis. Conversely, conditional ablation of the IGF1 receptor in OSNs enhances olfactory performance in mice and leads to increased adiposity and insulin resistance. These findings unravel a new bidirectional function for the olfactory system in controlling energy homeostasis in response to sensory and hormonal signals.

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Teaser

Riera et al. unravel a new bidirectional function for the olfactory system in energy homeostasis. Ablation of olfactory sensory neurons (OSNs) in mice protects them from diet-induced obesity accompanied by increased thermogenesis, while loss of IGF1 signaling in OSNs leads to increased adiposity and insulin resistance.


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