The Sense of Smell Impacts Metabolic Health and Obesity

The Sense of Smell Impacts Metabolic Health and Obesity
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DOI:
10.1016/j.cmet.2017.06.015
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发表时间:
2017-07-05
期刊:
影响因子:
29
通讯作者:
Dillin, Andrew
Dillin, Andrew
中科院分区:
生物学1区
文献类型:
--
作者:
Riera, Celine E.;Tsaousidou, Eva;Dillin, Andrew

文献摘要

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嗅觉输入有助于协调食物的欣赏和选择,但它们在全身生理和能量平衡中的作用知之甚少。在这里,我们证明了成熟的嗅觉感觉神经元(OSNs)的条件消融后的小鼠对饮食诱导的肥胖症具有抵抗力,伴随着棕色和腹股沟脂肪库产热增加。在肥胖症发作后嗅觉的急剧丧失不仅消除了体重的进一步增加,而且改善了脂肪量和胰岛素抵抗。减少的嗅觉输入刺激交感神经活动,导致白色和棕色脂肪细胞上的β-肾上腺素能受体活化以促进脂解。相反,OSN中IGF 1受体的条件性消融增强了小鼠的嗅觉表现,并导致肥胖和胰岛素抵抗增加。这些发现揭示了嗅觉系统在响应感觉和激素信号控制能量稳态方面的新的双向功能。
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 beta-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.