scholarly journals Resistin Is More Abundant in Liver Than Adipose Tissue and Is Not Up-Regulated by Lipopolysaccharide

2009 ◽  
Vol 94 (8) ◽  
pp. 3051-3057 ◽  
Author(s):  
Ewa Szalowska ◽  
Marieke G. L. Elferink ◽  
Annemiek Hoek ◽  
Geny M. M. Groothuis ◽  
Roel J. Vonk

Context: Resistin is an adipokine correlated with inflammatory markers and is predictive for cardiovascular diseases. There is evidence that serum resistin levels are elevated in obese patients; however, the role of resistin in insulin resistance and type 2 diabetes remains controversial. Objective: We addressed the question of whether inflammation may induce expression of resistin in organs involved in regulation of total body energy metabolism, such as liver and adipose tissue (AT). Methods: Human liver tissue, sc AT, and omentum were cultured in the absence/presence of lipopolysaccharide (LPS). The resistin and cytokine mRNA and protein expression levels were determined by real-time PCR, ELISA, and Multiplex Technology, respectively. The localization of resistin in human liver was analyzed by immunohistochemistry. Results: Resistin gene and protein expression was significantly higher in liver than in AT. Exposure of human AT and liver tissue in culture to LPS did not alter resistin concentration; however, concentrations of IL-1β, IL-6, and TNFα were significantly increased in these tissues. In liver, resistin colocalizes with markers for Kupffer cells, for a subset of endothelial and fibroblast-like cells. Conclusions: High level of resistin gene and protein expression in liver compared to AT implies that resistin should not be considered only as an adipokine in humans. LPS-induced inflammation does not affect resistin protein synthesis in human liver and AT. This suggests that elevated serum resistin levels are not indicative for inflammation of AT or liver in a manner similar to known inflammatory markers such as IL-1β, IL-6, or TNFα.

2011 ◽  
Vol 46 (2) ◽  
pp. 65-72 ◽  
Author(s):  
Yoshifumi Matsuura ◽  
Hiroshi Yagi ◽  
Sachiko Matsuda ◽  
Osamu Itano ◽  
Koichi Aiura ◽  
...  

1983 ◽  
Vol 48 (6) ◽  
pp. 791-796 ◽  
Author(s):  
M J Iqbal ◽  
M L Wilkinson ◽  
P J Johnson ◽  
R Williams

2009 ◽  
Vol 8 (4) ◽  
pp. 1672-1681 ◽  
Author(s):  
Cathrin Seibert ◽  
Brian R. Davidson ◽  
Barry J. Fuller ◽  
Laurence H. Patterson ◽  
William J. Griffiths ◽  
...  

2006 ◽  
Vol 32 (5) ◽  
pp. 649-657 ◽  
Author(s):  
Christiano Bittencourt Machado ◽  
Wagner Coelho de Albuquerque Pereira ◽  
Mahmoud Meziri ◽  
Pascal Laugier

2005 ◽  
Vol 29 (7) ◽  
pp. 715-717 ◽  
Author(s):  
D. M. Shakleya ◽  
J. C. Kraner ◽  
J. A. Kaplan ◽  
P. S. Callery

2009 ◽  
Vol 81 (9) ◽  
pp. 3321-3328 ◽  
Author(s):  
Yaohua Wang ◽  
Jennifer Hong ◽  
Erik N. K. Cressman ◽  
Edgar A. Arriaga

Endocrinology ◽  
2010 ◽  
Vol 151 (7) ◽  
pp. 3169-3180 ◽  
Author(s):  
Manjunath Ramanjaneya ◽  
Jing Chen ◽  
James E. Brown ◽  
Gyanendra Tripathi ◽  
Manfred Hallschmid ◽  
...  

Nesfatin-1 is a recently identified anorexigenic peptide derived from its precursor protein, nonesterified fatty acid/nucleobindin 2 (NUCB2). Although the hypothalamus is pivotal for the maintenance of energy homeostasis, adipose tissue plays an important role in the integration of metabolic activity and energy balance by communicating with peripheral organs and the brain via adipokines. Currently no data exist on nesfatin-1 expression, regulation, and secretion in adipose tissue. We therefore investigated NUCB2/nesfatin-1 gene and protein expression in human and murine adipose tissue depots. Additionally, the effects of insulin, dexamethasone, and inflammatory cytokines and the impact of food deprivation and obesity on nesfatin-1 expression were studied by quantitative RT-PCR and Western blotting. We present data showing NUCB2 mRNA (P < 0.001), nesfatin-1 intracellular protein (P < 0.001), and secretion (P < 0.01) were significantly higher in sc adipose tissue compared with other depots. Also, nesfatin-1 protein expression was significantly increased in high-fat-fed mice (P < 0.01) and reduced under food deprivation (P < 0.01) compared with controls. Stimulation of sc adipose tissue explants with inflammatory cytokines (TNFα and IL-6), insulin, and dexamethasone resulted in a marked increase in intracellular nesfatin-1 levels. Furthermore, we present evidence that the secretion of nesfatin-1 into the culture media was dramatically increased during the differentiation of 3T3-L1 preadipocytes into adipocytes (P < 0.001) and after treatments with TNF-α, IL-6, insulin, and dexamethasone (P < 0.01). In addition, circulating nesfatin-1 levels were higher in high-fat-fed mice (P < 0.05) and showed positive correlation with body mass index in human. We report that nesfatin-1 is a novel depot specific adipokine preferentially produced by sc tissue, with obesity- and food deprivation-regulated expression.


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