Metabolic inflammation: role of cytokines in the crosstalk between adipose tissue and liver

被引:52
作者
Gerner, Romana R. [1 ]
Wieser, Verena [1 ]
Moschen, Alexander R. [1 ]
Tilg, Herbert [1 ]
机构
[1] Med Univ Innsbruck, Dept Internal Med Gastroenterol Endocrinol & Meta, A-6020 Innsbruck, Austria
关键词
inflammation; non-alcoholic fatty liver disease; metabolism; adipocytokines; insulin resistance; adipose tissue inflammation; TUMOR-NECROSIS-FACTOR; INDUCED INSULIN-RESISTANCE; IL-1 RECEPTOR ANTAGONIST; FACTOR-ALPHA; INTERLEUKIN-1; RECEPTOR; WEIGHT-LOSS; NONALCOHOLIC STEATOHEPATITIS; ADHESION MOLECULES; GENE-EXPRESSION; PROTECTS MICE;
D O I
10.1139/cjpp-2013-0050
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
The innate immune system and its major mediators, i.e., cytokines, are increasingly recognized as being of crucial importance in metabolic inflammation as observed in morbid obesity and type 2 diabetes (T2D). Morbid obesity is commonly associated with adipose tissue inflammation. Adipose tissue inflammation is characterized by an increased expression of various pro-inflammatory cytokines such as tumor necrosis factor-alpha, interleukin-1 and -6, and by a rather heterogenous cellular infiltrate including monocytes/macrophages, neutrophils, B lymphocytes, T lymphocytes, and others. It has been demonstrated that in patients with severe obesity and fatty liver disease, expression of these pro-inflammatory cytokines in adipose tissue is 100-1000 times higher compared with that in the liver. Therefore, the adipose tissue can be considered in the state of severe obesity as the "cytokine factory" of the body. Rapid weight loss almost entirely eliminates pro-inflammatory cytokines in the adipose tissue, and therefore provides a very potent anti-inflammatory strategy. In conclusion, there is increasing evidence that peripheral tissues such as the adipose tissue may affect disease processes in target organs such as the liver, pancreas, heart, or blood vessels, and may therefore significantly contribute to chronic inflammation as observed in obesity and T2D.
引用
收藏
页码:867 / 872
页数:6
相关论文
共 59 条
[11]   Release of interleukins and other inflammatory cytokines by human adipose tissue is enhanced in obesity and primarily due to the nonfat cells [J].
Fain, John N. .
INTERLEUKINS, 2006, 74 :443-477
[12]   RETRACTED: Obesity-Induced Increase in Tumor Necrosis Factor-α Leads to Development of Colon Cancer in Mice (Retracted article. See vol. 153, pg. 871, 2017) [J].
Flores, Marcelo B. S. ;
Rocha, Guilherme Z. ;
Damas-Souza, Danilo M. ;
Osorio-Costa, Felipe ;
Dias, Marilia M. ;
Ropelle, Eduardo R. ;
Camargo, Juliana A. ;
de Carvalho, Rita B. ;
Carvalho, Hernandes F. ;
Saad, Mario J. A. ;
Carvalheira, Jose B. C. .
GASTROENTEROLOGY, 2012, 143 (03) :741-+
[13]  
GRANOWITZ EV, 1991, J BIOL CHEM, V266, P14147
[14]   IRS-1-mediated inhibition of insulin receptor tyrosine kinase activity in TNF-alpha- and obesity-induced insulin resistance [J].
Hotamisligil, GS ;
Peraldi, P ;
Budavari, A ;
Ellis, R ;
White, MF ;
Spiegelman, BM .
SCIENCE, 1996, 271 (5249) :665-668
[15]   ADIPOSE EXPRESSION OF TUMOR-NECROSIS-FACTOR-ALPHA - DIRECT ROLE IN OBESITY-LINKED INSULIN RESISTANCE [J].
HOTAMISLIGIL, GS ;
SHARGILL, NS ;
SPIEGELMAN, BM .
SCIENCE, 1993, 259 (5091) :87-91
[16]   Interleukin-1 Receptor-Associated Kinase-3 Is a Key Inhibitor of Inflammation in Obesity and Metabolic Syndrome [J].
Hulsmans, Maarten ;
Geeraert, Benjamine ;
De Keyzer, Dieuwke ;
Mertens, Ann ;
Lannoo, Matthias ;
Vanaudenaerde, Bart ;
Hoylaerts, Marc ;
Benhabiles, Nora ;
Tsatsanis, Christos ;
Mathieu, Chantal ;
Holvoet, Paul .
PLOS ONE, 2012, 7 (01)
[17]   Deletion of PPARγ in adipose tissues of mice protects against high fat diet-induced obesity and insulin resistance [J].
Jones, JR ;
Barrick, C ;
Kim, KA ;
Lindner, J ;
Blondeau, B ;
Fujimoto, Y ;
Shiota, M ;
Kesterson, RA ;
Kahn, BB ;
Magnuson, MA .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2005, 102 (17) :6207-6212
[18]   Lack of interleukin-1α or interleukin-1β inhibits transformation of steatosis to steatohepatitis and liver fibrosis in hypercholesterolemic mice [J].
Kamari, Yehuda ;
Shaish, Aviv ;
Vax, Einav ;
Shemesh, Shay ;
Kandel-Kfir, Michal ;
Arbel, Yaron ;
Olteanu, Sarita ;
Barshack, Iris ;
Dotan, Shahar ;
Voronov, Elana ;
Dinarello, Charles A. ;
Apte, Ron N. ;
Harats, Dror .
JOURNAL OF HEPATOLOGY, 2011, 55 (05) :1086-1094
[19]   MCP-1 contributes to macrophage infiltration into adipose tissue, insulin resistance, and hepatic steatosis in obesity [J].
Kanda, Hajime ;
Tateya, Sanshiro ;
Tamori, Yoshikazu ;
Kotani, Ko ;
Hiasa, Ken-ichi ;
Kitazawa, Riko ;
Kitazawa, Sohei ;
Miyachi, Hitoshi ;
Maeda, Sakan ;
Egashira, Kensuke ;
Kasuga, Masato .
JOURNAL OF CLINICAL INVESTIGATION, 2006, 116 (06) :1494-1505
[20]   THE EXPRESSION OF TUMOR-NECROSIS-FACTOR IN HUMAN ADIPOSE-TISSUE - REGULATION BY OBESITY, WEIGHT-LOSS, AND RELATIONSHIP TO LIPOPROTEIN-LIPASE [J].
KERN, PA ;
SAGHIZADEH, M ;
ONG, JM ;
BOSCH, RJ ;
DEEM, R ;
SIMSOLO, RB .
JOURNAL OF CLINICAL INVESTIGATION, 1995, 95 (05) :2111-2119