Dietary cholesterol effects on adipose tissue inflammation.
Dietary cholesterol effects on adipose tissue inflammation.
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DOI：
10.1097/mol.0000000000000260
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发表时间：
2016-02
影响因子：
4.4
通讯作者：
Parks JS
中科院分区：
文献类型：
--
作者：
Chung S;Parks JS
脂肪组织是调节全身能量平衡的重要内分泌和免疫器官。在肥胖的发病机制中，脂肪细胞肥大伴随着AT炎症，阻碍AT等组织的胰岛素敏感性和内分泌功能。随着脂肪细胞的肥大，脂肪细胞的胆固醇与甘油三酯(TG)成比例地积累。最近的研究表明，饮食中的胆固醇会导致脂肪细胞胆固醇的增加。然而，饮食中的胆固醇是如何在脂肪细胞中积累及其代谢影响的，目前还知之甚少。本文综述了脂肪细胞胆固醇平衡的最新研究进展，并着重介绍了膳食胆固醇在AT胆固醇平衡、炎症和全身能量代谢中的作用。脂肪细胞内胆固醇平衡的紊乱改变了细胞内胆固醇的分布，并调节了脂肪细胞的胰岛素和促炎信号。脂肪细胞的胆固醇水平是由膳食中从富含甘油三酯的脂蛋白摄取的胆固醇和细胞内的胆固醇流出到高密度脂蛋白之间的平衡来维持的。最近的动物研究证实了饮食胆固醇在促进AT炎症中的关键作用，从而恶化了肥胖介导的代谢并发症。最近的研究证实，高饮食胆固醇是AT炎症和功能障碍的增强剂。减少饮食中过量的胆固醇摄入被认为是一种简单但新颖的方法，可以减轻肥胖相关的代谢性疾病。
Adipose tissue (AT) is a critical endocrine and immunological organ that regulates systemic energy homeostasis. During the pathogenesis of obesity, adipocyte hypertrophy is accompanied by AT inflammation, impeding insulin sensitivity and endocrine function of AT and other tissues. Adipocyte cholesterol accumulates in proportion to triglyceride (TG) as adipocytes undergo hypertrophy. Recent studies suggest that dietary cholesterol contributes to increased adipocyte cholesterol. However, how dietary cholesterol accumulates in adipocytes and its metabolic consequences are poorly understood. This review summarizes recent advances in knowledge of adipocyte cholesterol balance and highlights the emerging role of dietary cholesterol in AT cholesterol balance, inflammation, and systemic energy metabolism. Perturbation of cholesterol balance in adipocytes alters intracellular cholesterol distribution and modulates adipocyte insulin and proinflammatory signaling. Adipocyte cholesterol levels are maintained by a balance between dietary cholesterol uptake from TG-enriched lipoproteins and cellular cholesterol efflux to high density lipoprotein. Recent animal studies established a critical role for dietary cholesterol in promoting AT inflammation, thereby worsening obesity-mediated metabolic complications. Recent studies identified high dietary cholesterol as a potentiator of AT inflammation and dysfunction. Reducing excessive dietary cholesterol intake is suggested as a simple, but novel, way to attenuate obesity-associated metabolic diseases.