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表达 Nav1.8 的神经元控制小鼠的摄食、体重和肠道微生物群的日常波动。

Nav1.8-expressing neurons control daily oscillations of food intake, body weight and gut microbiota in mice.

机构信息

Microbiome, Nutrition and Health Unit, Institute of Agrochemistry and Food Technology, National Research Council (IATA-CSIC), Valencia, Spain.

Research Group Intracellular Pathogens: Biology and Infection, Department of Animal Production and Health, Veterinary Public Health and Food Science and Technology, Faculty of Veterinary Medicine, Cardenal Herrera-CEU University, Valencia, Spain.

出版信息

Commun Biol. 2024 Feb 22;7(1):219. doi: 10.1038/s42003-024-05905-3.

DOI:10.1038/s42003-024-05905-3
PMID:38388698
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10883928/
Abstract

Recent evidence suggests a role of sensory neurons expressing the sodium channel Nav1.8 on the energy homeostasis control. Using a murine diphtheria toxin ablation strategy and ad libitum and time-restricted feeding regimens of control or high-fat high-sugar diets, here we further explore the function of these neurons on food intake and on the regulation of gastrointestinal elements transmitting immune and nutrient sensing.The Nav1.8+ neuron ablation increases food intake in ad libitum and time-restricted feeding, and exacerbates daily body weight variations. Mice lacking Nav1.8+ neurons show impaired prandial regulation of gut hormone secretion and gut microbiota composition, and altered intestinal immunity.Our study demonstrates that Nav1.8+ neurons are required to control food intake and daily body weight changes, as well as to maintain physiological enteroendocrine and immune responses and the rhythmicity of the gut microbiota, which highlights the potential of Nav1.8+ neurons to restore energy balance in metabolic disorders.

摘要

最近的证据表明，表达钠离子通道 Nav1.8 的感觉神经元在能量稳态控制中发挥作用。在这里，我们使用鼠类白喉毒素消融策略以及自由摄食和限时进食方案，进一步研究了这些神经元对食物摄入以及调节传递免疫和营养感应的胃肠道元素的功能。Nav1.8+神经元消融会增加自由摄食和限时进食时的食物摄入，并加剧每日体重变化。缺乏 Nav1.8+神经元的小鼠表现出餐后胃肠激素分泌和肠道微生物组成的调节受损，以及肠道免疫改变。我们的研究表明，Nav1.8+神经元是控制食物摄入和每日体重变化、维持生理肠内分泌和免疫反应以及肠道微生物群节律所必需的，这突出了 Nav1.8+神经元在代谢紊乱中恢复能量平衡的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/88d3/10883928/f59204997e46/42003_2024_5905_Fig8_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/88d3/10883928/89c25e082a2a/42003_2024_5905_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/88d3/10883928/1691a2662467/42003_2024_5905_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/88d3/10883928/49ea6cebc960/42003_2024_5905_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/88d3/10883928/52d7ad498edb/42003_2024_5905_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/88d3/10883928/5e73eca16bd9/42003_2024_5905_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/88d3/10883928/f59204997e46/42003_2024_5905_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/88d3/10883928/b5caddfda926/42003_2024_5905_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/88d3/10883928/2e5b996c5e9d/42003_2024_5905_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/88d3/10883928/89c25e082a2a/42003_2024_5905_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/88d3/10883928/1691a2662467/42003_2024_5905_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/88d3/10883928/49ea6cebc960/42003_2024_5905_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/88d3/10883928/52d7ad498edb/42003_2024_5905_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/88d3/10883928/5e73eca16bd9/42003_2024_5905_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/88d3/10883928/f59204997e46/42003_2024_5905_Fig8_HTML.jpg

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