Document Detail


Adipocytokine orosomucoid integrates inflammatory and metabolic signals to preserve energy homeostasis by resolving immoderate inflammation.
MedLine Citation:
PMID:  20442402     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Orosomucoid (ORM), also called alpha-1 acid glycoprotein, is an abundant plasma protein that is an immunomodulator induced by stressful conditions such as infections. In this study, we reveal that Orm is induced selectively in the adipose tissue of obese mice to suppress excess inflammation that otherwise disturbs energy homeostasis. Adipose Orm levels were elevated by metabolic signals, including insulin, high glucose, and free fatty acid, as well as by the proinflammatory cytokine tumor necrosis factor-alpha, which is found in increased levels in the adipose tissue of morbid obese subjects. In both adipocytes and macrophages, ORM suppressed proinflammatory gene expression and pathways such as NF-kappaB and mitogen-activated protein kinase signalings and reactive oxygen species generation. Concomitantly, ORM relieved hyperglycemia-induced insulin resistance as well as tumor necrosis factor-alpha-mediated lipolysis in adipocytes. Accordingly, ORM improved glucose and insulin tolerance in obese and diabetic db/db mice. Taken together, our results suggest that ORM integrates inflammatory and metabolic signals to modulate immune responses to protect adipose tissue from excessive inflammation and thereby from metabolic dysfunction.
Authors:
Yun Sok Lee; Jin Woo Choi; Injae Hwang; Joo Won Lee; Jae Ho Lee; A Young Kim; Jin Young Huh; Young Jun Koh; Gou Young Koh; Hee Jung Son; Hiroaki Masuzaki; Kikuko Hotta; Assim A Alfadda; Jae Bum Kim
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-05-04
Journal Detail:
Title:  The Journal of biological chemistry     Volume:  285     ISSN:  1083-351X     ISO Abbreviation:  J. Biol. Chem.     Publication Date:  2010 Jul 
Date Detail:
Created Date:  2010-07-12     Completed Date:  2010-08-06     Revised Date:  2011-08-01    
Medline Journal Info:
Nlm Unique ID:  2985121R     Medline TA:  J Biol Chem     Country:  United States    
Other Details:
Languages:  eng     Pagination:  22174-85     Citation Subset:  IM    
Affiliation:
Institute of Molecular Biology and Genetics, Seoul National University, Seoul 151-742, Korea.
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MeSH Terms
Descriptor/Qualifier:
Adipocytes / drug effects,  enzymology,  pathology
Adipokines / genetics,  metabolism*
Adipose Tissue / drug effects,  metabolism,  pathology
Animals
CCAAT-Enhancer-Binding Proteins / metabolism
Cell Line
Cell Movement / drug effects
Diabetes Mellitus, Experimental / blood,  metabolism
Dietary Fats / administration & dosage,  pharmacology
Energy Metabolism* / drug effects
Feeding Behavior / drug effects
Homeostasis* / drug effects
Humans
Inflammation / blood,  metabolism*,  pathology
Insulin / metabolism
Insulin Resistance
Macrophages / cytology,  drug effects,  enzymology
Mice
Mice, Obese
Mitogen-Activated Protein Kinases / metabolism
NF-kappa B / metabolism
Orosomucoid / genetics,  metabolism*
Signal Transduction* / drug effects
Sterol Regulatory Element Binding Protein 1 / metabolism
Tumor Necrosis Factor-alpha / pharmacology
Chemical
Reg. No./Substance:
0/Adipokines; 0/CCAAT-Enhancer-Binding Proteins; 0/Dietary Fats; 0/NF-kappa B; 0/Orosomucoid; 0/Sterol Regulatory Element Binding Protein 1; 0/Tumor Necrosis Factor-alpha; 11061-68-0/Insulin; EC 2.7.11.24/Mitogen-Activated Protein Kinases
Comments/Corrections

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