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肥胖代谢并发症中核受体介导的脂肪组织信号传导

Adipose tissue signaling by nuclear receptors in metabolic complications of obesity.

作者信息

Jacobi David, Stanya Kristopher J, Lee Chih-Hao

机构信息

Department of Genetics and Complex Diseases; Department of Nutrition; Division of Biological Sciences; Harvard School of Public Health; Boston, MA USA.

出版信息

Adipocyte. 2012;1(1):4-12. doi: 10.4161/adip.19036.

DOI:10.4161/adip.19036
PMID:22916336
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3423221/
Abstract

In recent years white adipose tissue inflammation has been recognized to be associated with obesity. Adipocytes and adipose tissue associated macrophages (ATMs) secrete bioactive molecules, including adipokines, chemokines/cytokines and free fatty acids that modulate the development of low-grade inflammation and insulin resistance responsible for obesity-related metabolic and cardiovascular diseases. Nuclear receptors, notably peroxisome-proliferator-activated receptors, are sensors of dietary lipids and control transcriptional programs of key metabolic and inflammatory pathways in adipocytes and macrophages. This review focuses on mechanisms by which nuclear receptors maintain white adipose tissue homeostasis. The identification of ATMs as active players in the initiation of chronic inflammation and the links between inflammatory signaling and metabolic dysfunction will be presented, followed by discussion of recent evidence for nuclear receptors in ATM function, with an emphasis on the paracrine interaction between adipocytes and ATMs.

摘要

近年来,白色脂肪组织炎症已被认为与肥胖有关。脂肪细胞和脂肪组织相关巨噬细胞(ATM)分泌生物活性分子,包括脂肪因子、趋化因子/细胞因子和游离脂肪酸,这些分子调节导致肥胖相关代谢和心血管疾病的低度炎症和胰岛素抵抗的发展。核受体,尤其是过氧化物酶体增殖物激活受体,是膳食脂质的传感器,并控制脂肪细胞和巨噬细胞中关键代谢和炎症途径的转录程序。本综述重点关注核受体维持白色脂肪组织稳态的机制。将介绍ATM作为慢性炎症起始的活跃参与者的鉴定以及炎症信号与代谢功能障碍之间的联系,随后讨论核受体在ATM功能方面的最新证据,重点是脂肪细胞与ATM之间的旁分泌相互作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7c0/3661120/e4e9e28357ef/adip-1-4-g4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7c0/3661120/4205bb490b31/adip-1-4-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7c0/3661120/8dd2a37186b3/adip-1-4-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7c0/3661120/9f41753ca84e/adip-1-4-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7c0/3661120/e4e9e28357ef/adip-1-4-g4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7c0/3661120/4205bb490b31/adip-1-4-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7c0/3661120/8dd2a37186b3/adip-1-4-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7c0/3661120/9f41753ca84e/adip-1-4-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7c0/3661120/e4e9e28357ef/adip-1-4-g4.jpg

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