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肥胖相关炎症中的单不饱和脂肪酸

Monounsaturated Fatty Acids in Obesity-Related Inflammation.

作者信息

Ravaut Gaetan, Légiot Alexandre, Bergeron Karl-F, Mounier Catherine

机构信息

CERMO-FC Research Center, Molecular Metabolism of Lipids Laboratory, Biological Sciences Department, University of Quebec in Montreal (UQAM), Montreal, QC H3C 3P8, Canada.

出版信息

Int J Mol Sci. 2020 Dec 30;22(1):330. doi: 10.3390/ijms22010330.

DOI:10.3390/ijms22010330
PMID:33396940
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7795523/
Abstract

Obesity is an important aspect of the metabolic syndrome and is often associated with chronic inflammation. In this context, inflammation of organs participating in energy homeostasis (such as liver, adipose tissue, muscle and pancreas) leads to the recruitment and activation of macrophages, which secrete pro-inflammatory cytokines. Interleukin-1β secretion, sustained C-reactive protein plasma levels and activation of the NLRP3 inflammasome characterize this inflammation. The Stearoyl-CoA desaturase-1 (SCD1) enzyme is a central regulator of lipid metabolism and fat storage. This enzyme catalyzes the generation of monounsaturated fatty acids (MUFAs)-major components of triglycerides stored in lipid droplets-from saturated fatty acid (SFA) substrates. In this review, we describe the molecular effects of specific classes of fatty acids (saturated and unsaturated) to better understand the impact of different diets (Western versus Mediterranean) on inflammation in a metabolic context. Given the beneficial effects of a MUFA-rich Mediterranean diet, we also present the most recent data on the role of SCD1 activity in the modulation of SFA-induced chronic inflammation.

摘要

肥胖是代谢综合征的一个重要方面,且常与慢性炎症相关。在这种情况下,参与能量稳态的器官(如肝脏、脂肪组织、肌肉和胰腺)发生炎症会导致巨噬细胞的募集和激活,巨噬细胞会分泌促炎细胞因子。白细胞介素-1β的分泌、持续的血浆C反应蛋白水平以及NLRP3炎性小体的激活是这种炎症的特征。硬脂酰辅酶A去饱和酶-1(SCD1)是脂质代谢和脂肪储存的核心调节因子。该酶催化单不饱和脂肪酸(MUFAs)的生成,单不饱和脂肪酸是储存在脂滴中的甘油三酯的主要成分,其由饱和脂肪酸(SFA)底物生成。在本综述中,我们描述了特定种类脂肪酸(饱和脂肪酸和不饱和脂肪酸)的分子效应,以便更好地理解不同饮食(西方饮食与地中海饮食)在代谢背景下对炎症的影响。鉴于富含单不饱和脂肪酸的地中海饮食的有益作用,我们还展示了关于SCD1活性在调节饱和脂肪酸诱导的慢性炎症中的作用的最新数据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1083/7795523/6ee6db73d7a1/ijms-22-00330-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1083/7795523/1d0e6a1d9cca/ijms-22-00330-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1083/7795523/0d1a6f1ed0ac/ijms-22-00330-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1083/7795523/6ee6db73d7a1/ijms-22-00330-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1083/7795523/1d0e6a1d9cca/ijms-22-00330-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1083/7795523/0d1a6f1ed0ac/ijms-22-00330-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1083/7795523/6ee6db73d7a1/ijms-22-00330-g003.jpg

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