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Na1.8 神经元参与限制对膳食脂肪的急性反应。

Na1.8 neurons are involved in limiting acute phase responses to dietary fat.

机构信息

Division of Hypothalamic Research, Department of Internal Medicine, The University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas 75390, TX, USA.

Touchstone Diabetes Center, Department of Internal Medicine, The University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas 75390, TX, USA.

出版信息

Mol Metab. 2017 Oct;6(10):1081-1091. doi: 10.1016/j.molmet.2017.07.012. Epub 2017 Aug 4.


DOI:10.1016/j.molmet.2017.07.012
PMID:29031710
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5641637/
Abstract

OBJECTIVE AND METHODS: Metabolic viscera and their vasculature are richly innervated by peripheral sensory neurons. Here, we examined the metabolic and inflammatory profiles of mice with selective ablation of all Na1.8-expressing primary afferent neurons. RESULTS: While mice lacking sensory neurons displayed no differences in body weight, food intake, energy expenditure, or body composition compared to controls on chow diet, ablated mice developed an exaggerated inflammatory response to high-fat feeding characterized by bouts of weight loss, splenomegaly, elevated circulating interleukin-6 and hepatic serum amyloid A expression. This phenotype appeared to be directly mediated by the ingestion of saturated lipids. CONCLUSIONS: These data demonstrate that the Na1.8-expressing afferent neurons are not essential for energy balance but are required for limiting the acute phase response caused by an obesogenic diet.

摘要

目的和方法:代谢内脏及其脉管系统由外周感觉神经元丰富地支配。在这里,我们检查了选择性消融所有表达 Na1.8 的初级传入神经元的小鼠的代谢和炎症特征。

结果:与对照饮食的小鼠相比,缺乏感觉神经元的小鼠在体重、食物摄入、能量消耗或身体成分方面没有差异,但在高脂肪喂养时,消融的小鼠表现出过度的炎症反应,表现为体重减轻、脾肿大、循环白细胞介素-6 和肝血清淀粉样蛋白 A 表达升高。这种表型似乎直接由饱和脂肪的摄入介导。

结论:这些数据表明,表达 Na1.8 的传入神经元对于能量平衡不是必需的,但对于限制肥胖饮食引起的急性期反应是必需的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72dc/5641637/d1f2e442331b/figs2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72dc/5641637/bda242f8cb75/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72dc/5641637/a6484e3f41f6/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72dc/5641637/9714e9cde2f7/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72dc/5641637/a3b359d73ce0/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72dc/5641637/73862a93d906/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72dc/5641637/181c4bc0f0c5/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72dc/5641637/16f634d956b4/figs1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72dc/5641637/d1f2e442331b/figs2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72dc/5641637/bda242f8cb75/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72dc/5641637/a6484e3f41f6/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72dc/5641637/9714e9cde2f7/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72dc/5641637/a3b359d73ce0/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72dc/5641637/73862a93d906/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72dc/5641637/181c4bc0f0c5/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72dc/5641637/16f634d956b4/figs1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72dc/5641637/d1f2e442331b/figs2.jpg

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本文引用的文献

[1]
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Levels of Cocaine- and Amphetamine-Regulated Transcript in Vagal Afferents in the Mouse Are Unaltered in Response to Metabolic Challenges.

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