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
[1]   The c-Jun NH2-terminal kinase promotes insulin resistance during association with insulin receptor substrate-1 and phosphorylation of Ser307 [J].
Aguirre, V ;
Uchida, T ;
Yenush, L ;
Davis, R ;
White, MF .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (12) :9047-9054
[2]   Adipose tissue recruitment of leukocytes [J].
Anderson, Emily K. ;
Gutierrez, Dario A. ;
Hasty, Alyssa H. .
CURRENT OPINION IN LIPIDOLOGY, 2010, 21 (03) :172-177
[3]   Tumor Necrosis Factor Receptor 1 Gain-of-Function Mutation Aggravates Nonalcoholic Fatty Liver Disease but Does Not Cause Insulin Resistance in a Murine Model [J].
Aparicio-Vergara, Marcela ;
Hommelberg, Pascal P. H. ;
Schreurs, Marijke ;
Gruben, Nanda ;
Stienstra, Rinke ;
Shiri-Sverdlov, Ronit ;
Kloosterhuis, Niels J. ;
de Bruin, Alain ;
van de Sluis, Bart ;
Koonen, Debby P. Y. ;
Hofker, Marten H. .
HEPATOLOGY, 2013, 57 (02) :566-576
[4]   Adipose tissue IL-6 content correlates with resistance to insulin activation of glucose uptake both in vivo and in vitro [J].
Bastard, JP ;
Maachi, M ;
Van Nhieu, JT ;
Jardel, C ;
Bruckert, E ;
Grimaldi, A ;
Robert, JJ ;
Capeau, J ;
Hainque, B .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2002, 87 (05) :2084-2089
[5]   Gene expression of tumor necrosis factor α and TNF-receptors, p55 and p75, in nonalcoholic steatohepatitis patients [J].
Crespo, J ;
Cayón, A ;
Fernández-Gil, P ;
Hernández-Guerra, M ;
Mayorga, M ;
Domínguez-Díez, A ;
Fernández-Escalante, JC ;
Pons-Romero, F .
HEPATOLOGY, 2001, 34 (06) :1158-1163
[6]   Tumor necrosis factor-α in sera of obese patients:: Fall with weight loss [J].
Dandona, P ;
Weinstock, R ;
Thusu, K ;
Abdel-Rahman, E ;
Aljada, A ;
Wadden, T .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1998, 83 (08) :2907-2910
[7]   Lipid and carbohydrate metabolism in mice with a targeted mutation in the IL-6 gene: absence of development of age-related obesity [J].
Di Gregorio, GB ;
Hensley, L ;
Lu, T ;
Ranganathan, G ;
Kern, PA .
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM, 2004, 287 (01) :E182-E187
[8]   Interleukin-1 in the pathogenesis and treatment of inflammatory diseases [J].
Dinarello, Charles A. .
BLOOD, 2011, 117 (14) :3720-3732
[9]   Type 2 diabetes as an inflammatory disease [J].
Donath, Marc Y. ;
Shoelson, Steven E. .
NATURE REVIEWS IMMUNOLOGY, 2011, 11 (02) :98-107
[10]   Cytokine production by islets in health and diabetes: cellular origin, regulation and function [J].
Donath, Marc Y. ;
Boeni-Schnetzler, Marianne ;
Ellingsgaard, Helga ;
Halban, Philippe A. ;
Ehses, Jan A. .
TRENDS IN ENDOCRINOLOGY AND METABOLISM, 2010, 21 (05) :261-267