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解析脂质、肥胖和炎症之间的复杂三角关系。

Unraveling the complex relationship triad between lipids, obesity, and inflammation.

作者信息

Khan Shahida A, Ali Ashraf, Khan Sarah A, Zahran Solafa A, Damanhouri Ghazi, Azhar Esam, Qadri Ishtiaq

机构信息

Department of Applied Nutrition, King Fahd Medical Research Center, King Abdulaziz University, P.O. Box 80216, Jeddah 21589, Saudi Arabia.

Department of Medical Biotechnology, King Fahd Medical Research Center, King Abdulaziz University, P.O. Box 80216, Jeddah 21589, Saudi Arabia.

出版信息

Mediators Inflamm. 2014;2014:502749. doi: 10.1155/2014/502749. Epub 2014 Aug 28.

DOI:10.1155/2014/502749
PMID:25258478
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4166426/
Abstract

Obesity today stands at the intersection between inflammation and metabolic disorders causing an aberration of immune activity, and resulting in increased risk for diabetes, atherosclerosis, fatty liver, and pulmonary inflammation to name a few. Increases in mortality and morbidity in obesity related inflammation have initiated studies to explore different lipid mediated molecular pathways of attempting resolution that uncover newer therapeutic opportunities of anti-inflammatory components. Majorly the thromboxanes, prostaglandins, leukotrienes, lipoxins, and so forth form the group of lipid mediators influencing inflammation. Of special mention are the omega-6 and omega-3 fatty acids that regulate inflammatory mediators of interest in hepatocytes and adipocytes via the cyclooxygenase and lipoxygenase pathways. They also exhibit profound effects on eicosanoid production. The inflammatory cyclooxygenase pathway arising from arachidonic acid is a critical step in the progression of inflammatory responses. New oxygenated products of omega-3 metabolism, namely, resolvins and protectins, behave as endogenous mediators exhibiting powerful anti-inflammatory and immune-regulatory actions via the peroxisome proliferator-activated receptors (PPARs) and G protein coupled receptors (GPCRs). In this review we attempt to discuss the complex pathways and links between obesity and inflammation particularly in relation to different lipid mediators.

摘要

如今,肥胖处于炎症与代谢紊乱的交叉点,导致免疫活动异常,进而增加患糖尿病、动脉粥样硬化、脂肪肝和肺部炎症等疾病的风险。肥胖相关炎症导致的死亡率和发病率上升,促使人们开展研究,探索不同的脂质介导的分子途径,以寻求解决办法,从而发现抗炎成分的新治疗机会。主要来说,血栓素、前列腺素、白三烯、脂氧素等构成了影响炎症的脂质介质组。特别值得一提的是ω-6和ω-3脂肪酸,它们通过环氧化酶和脂氧合酶途径调节肝细胞和脂肪细胞中相关的炎症介质。它们对类花生酸的产生也有深远影响。由花生四烯酸引发的炎症性环氧化酶途径是炎症反应进展中的关键步骤。ω-3代谢产生的新的氧化产物,即消退素和保护素,作为内源性介质,通过过氧化物酶体增殖物激活受体(PPARs)和G蛋白偶联受体(GPCRs)发挥强大的抗炎和免疫调节作用。在这篇综述中,我们试图讨论肥胖与炎症之间的复杂途径和联系,特别是与不同脂质介质的关系。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8851/4166426/0e3152283587/MI2014-502749.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8851/4166426/0e3152283587/MI2014-502749.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8851/4166426/0e3152283587/MI2014-502749.001.jpg

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