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热量限制对高脂饮食喂养小鼠棕色脂肪组织中lipocalin-2及其受体表达的影响。

Effects of caloric restriction on the expression of lipocalin-2 and its receptor in the brown adipose tissue of high-fat diet-fed mice.

作者信息

Park Kyung-Ah, Jin Zhen, An Hyeong Seok, Lee Jong Youl, Jeong Eun Ae, Choi Eun Bee, Kim Kyung Eun, Shin Hyun Joo, Lee Jung Eun, Roh Gu Seob

机构信息

Department of Anatomy and Convergence Medical Science, Bio Anti-Aging Medical Research Center, Institute of Health Sciences, College of Medicine, Gyeongsang National University, Jinju 52727, Korea.

Department of Thoracic and Cardiovascular Surgery, Institute of Health Sciences, College of Medicine, Gyeongsang National University, Jinju 52727, Korea.

出版信息

Korean J Physiol Pharmacol. 2019 Sep;23(5):335-344. doi: 10.4196/kjpp.2019.23.5.335. Epub 2019 Aug 26.

DOI:10.4196/kjpp.2019.23.5.335
PMID:31496871
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6717793/
Abstract

Obesity causes inflammation and impairs thermogenic functions in brown adipose tissue (BAT). The adipokine lipocalin 2 (LCN2) has been implicated in inflammation and obesity. Herein, we investigated the protective effects of caloric restriction (CR) on LCN2-mediated inflammation and oxidative stress in the BAT of high-fat diet (HFD)-fed mice. Mice were fed a HFD for 20 weeks and then either continued on the HFD or subjected to CR for the next 12 weeks. CR led to the browning of the white fat-like phenotype in HFD-fed mice. Increased expressions of LCN2 and its receptor in the BAT of HFD-fed mice were significantly attenuated by CR. Additionally, HFD+CR-fed mice had fewer neutrophils and macrophages expressing LCN2 and iron-positive cells than HFD-fed mice. Further, oxidative stress and mitochondrial fission induced by a HFD were also significantly attenuated by CR. Our findings indicate that the protective effects of CR on inflammation and oxidative stress in the BAT of obese mice may be associated with regulation of LCN2.

摘要

肥胖会引发炎症,并损害棕色脂肪组织(BAT)的产热功能。脂肪因子lipocalin 2(LCN2)与炎症和肥胖有关。在此,我们研究了热量限制(CR)对高脂饮食(HFD)喂养小鼠BAT中LCN2介导的炎症和氧化应激的保护作用。小鼠先喂食HFD 20周,然后要么继续喂食HFD,要么在接下来的12周进行CR。CR导致HFD喂养小鼠白色脂肪样表型出现棕色化。CR显著减弱了HFD喂养小鼠BAT中LCN2及其受体表达的增加。此外,与HFD喂养小鼠相比,HFD+CR喂养小鼠中表达LCN2的中性粒细胞和巨噬细胞以及铁阳性细胞更少。此外,CR也显著减弱了HFD诱导的氧化应激和线粒体分裂。我们的研究结果表明,CR对肥胖小鼠BAT中炎症和氧化应激的保护作用可能与LCN2的调节有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/985b/6717793/31ad3bcd757a/kjpp-23-335-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/985b/6717793/31ad3bcd757a/kjpp-23-335-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/985b/6717793/31ad3bcd757a/kjpp-23-335-g004.jpg

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