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Unwrapping the mechanisms of ceramide and fatty acid-initiated signals leading to immune-inflammatory responses in obesity
The International Journal of Biochemistry & Cell Biology ( IF 3.4 ) Pub Date : 2021-04-14 , DOI: 10.1016/j.biocel.2021.105972
Salih Kucuk 1 , Jennifer Niven 1 , Jorge Caamano 2 , Simon W Jones 1 , Dolores Camacho-Muñoz 3 , Anna Nicolaou 4 , Claudio Mauro 1
Affiliation  

Obesity is considered a global epidemic developed in part as a consequence of the overconsumption of high fat diets. One of the main negative outcomes of obesity is the development of low-grade chronic systemic inflammation, induced by dysregulated immune responses, which can lead to multiple obesity-related diseases. Ceramides are a group of bioactive lipids known to be elevated in obesity and obesity-associated conditions, including cardiovascular disease and type II diabetes. Ceramides may be key players in promoting an obesity–induced inflammatory environment due to their ability to activate key pathways such as Toll-like receptor 4 (TLR4) and NLR pyrin domain containing receptor 3 (Nlrp3), while studies have shown that inhibition of ceramide synthesis gives rise to an anti-inflammatory environment. N-3 polyunsaturated fatty acids (n-3 PUFA) have been of interest due to their anti-inflammatory actions and shown to have beneficial effects in obesity-related diseases. This review will highlight the impact of ceramides in promoting an obesity-induced inflammatory microenvironment and discuss how n-3 PUFA could potentially counteract these responses and have a regulatory effect promoting immune homeostasis.



中文翻译:

揭示神经酰胺和脂肪酸引发的信号导致肥胖症免疫炎症反应的机制

肥胖症被认为是一种全球性流行病,部分原因是高脂肪饮食的过度消费。肥胖的主要负面结果之一是由免疫反应失调引起的低度慢性全身炎症的发展,这可能导致多种肥胖相关疾病。神经酰胺是一组已知在肥胖和肥胖相关疾病(包括心血管疾病和 II 型糖尿病)中升高的生物活性脂质。神经酰胺可能是促进肥胖诱导的炎症环境的关键因素,因为它们能够激活关键通路,例如 Toll 样受体 4 (TLR4) 和 NLR pyrin 结构域受体 3 (Nlrp3),而研究表明抑制神经酰胺合成产生抗炎环境。N-3 多不饱和脂肪酸 (n-3 PUFA) 因其抗炎作用而受到关注,并显示对肥胖相关疾病具有有益作用。这篇综述将强调神经酰胺在促进肥胖引起的炎症微环境方面的影响,并讨论 n-3 PUFA 如何可能抵消这些反应并具有促进免疫稳态的调节作用。

更新日期:2021-04-19
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