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缺乏内源性 TRPV1 的小鼠表达较低水平的产热蛋白,并且易患饮食诱导的肥胖和代谢功能障碍。

Mice lacking endogenous TRPV1 express reduced levels of thermogenic proteins and are susceptible to diet-induced obesity and metabolic dysfunction.

机构信息

Molecular Signaling Laboratory, School of Pharmacy, University of Wyoming, Laramie, WY, USA.

出版信息

FEBS Lett. 2021 Jul;595(13):1768-1781. doi: 10.1002/1873-3468.14105. Epub 2021 May 30.

DOI:10.1002/1873-3468.14105
PMID:33977527
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8277693/
Abstract

Transient receptor potential vanilloid subfamily 1 (TRPV1) is a non-selective cation channel protein expressed in neuronal and non-neuronal cells. Although TRPV1 is implicated in thermogenesis and diet-induced obesity (DIO), its precise role remains controversial. TRPV1 mice are protected from DIO, while TRPV1 activation enhances thermogenesis to prevent obesity. To reconcile this, we fed wild-type and TRPV1 mice for 32 weeks with normal chow or a high-fat diet and analyzed the weight gain, metabolic activities, and thermogenic protein expression in white and brown fats. TRPV1 mice became obese, exhibited reduced locomotor activity, reduced energy expenditure, enhanced hepatic steatosis, and decreased thermogenic protein expression in adipose tissues. Our data reveal that lack of TRPV1 does not prevent obesity, but rather enhances metabolic dysfunction.

摘要

瞬时受体电位香草酸亚型 1(TRPV1)是一种非选择性阳离子通道蛋白,存在于神经元和非神经元细胞中。尽管 TRPV1 与产热和饮食诱导的肥胖(DIO)有关,但它的确切作用仍存在争议。TRPV1 敲除小鼠可预防 DIO,而 TRPV1 的激活可增强产热以预防肥胖。为了解决这个问题,我们用正常饲料或高脂肪饲料喂养野生型和 TRPV1 敲除小鼠 32 周,并分析白色和棕色脂肪中的体重增加、代谢活动和产热蛋白表达。TRPV1 敲除小鼠变得肥胖,表现出运动活性降低、能量消耗减少、肝脂肪变性增强以及脂肪组织中产热蛋白表达减少。我们的数据表明,缺乏 TRPV1 并不能预防肥胖,反而会增强代谢功能障碍。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a8d/8277693/e7702c47f4ed/nihms-1703984-f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a8d/8277693/3b2e48d5ecd2/nihms-1703984-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a8d/8277693/d3b1699d6e82/nihms-1703984-f0002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a8d/8277693/7e622184a653/nihms-1703984-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a8d/8277693/f2750861a919/nihms-1703984-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a8d/8277693/e7702c47f4ed/nihms-1703984-f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a8d/8277693/3b2e48d5ecd2/nihms-1703984-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a8d/8277693/d3b1699d6e82/nihms-1703984-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a8d/8277693/a1a60570ad32/nihms-1703984-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a8d/8277693/7e622184a653/nihms-1703984-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a8d/8277693/f2750861a919/nihms-1703984-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a8d/8277693/e7702c47f4ed/nihms-1703984-f0006.jpg

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