Levels of 4-1BB transcripts and soluble 4-1BB protein are elevated in the adipose tissue of human obese subjects and are associated with inflammatory and metabolic parameters

Background: 4-1BB, a member of the TNF receptor superfamily, has a role in various inflammatory pathologies through its interaction with 4-1BB ligand. We previously demonstrated that it participates in initiating and promoting obesity-induced adipose inflammation in a rodent model. Objective: In thi...

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Bibliographic Details
Published in:	International Journal of Obesity Vol. 38; no. 8; pp. 1075 - 1082
Main Authors:	Tu, T H, Kim, C-S, Kang, J-H, Nam-Goong, I S, Nam, C W, Kim, E S, Kim, Y I, Choi, J I, Kawada, T, Goto, T, Park, T, Yoon Park, J H, Choi, M-S, Yu, R
Format:	Journal Article
Language:	English
Published:	London Nature Publishing Group UK 01-08-2014 Nature Publishing Group
Subjects:	4-1BB Ligand - metabolism 631/250/256 692/53 692/699/2743/2037 692/699/2743/393 Adipocytes Adipocytes - metabolism Adipose tissue Adipose Tissue - immunology Adipose Tissue - metabolism Adipose tissues Biological and medical sciences Biomarkers Body fat Body Mass Index Body size Cells, Cultured Complications and side effects Enzyme-Linked Immunosorbent Assay Epidemiology Female Genetic aspects Health Promotion and Disease Prevention Humans Immunoassay Inflammation Inflammation - immunology Inflammation - metabolism Insulin resistance Internal Medicine Lymphocytes Lymphocytes T Male Medical sciences Medicine Medicine & Public Health Metabolic Diseases Metabolic disorders Metabolic syndrome Metabolism Miscellaneous Monocytes Nutrition Obesity Obesity - immunology Obesity - metabolism Obesity - physiopathology original-article Other metabolic disorders Parameters Proteins Public Health Real-Time Polymerase Chain Reaction Rodents Solubility Therapeutic targets Tumor necrosis factor Tumor Necrosis Factor Receptor Superfamily, Member 9 - metabolism Tumor necrosis factor receptors South Korea metabolic syndrome adipose tissue inflammation Endocrinopathy Human Obesity Adipose tissue Nutrition Nutrition disorder Cardiovascular disease Metabolic diseases Inflammation Soluble form Metabolism Metabolic syndrome Protein Association Messenger RNA Nutritional status
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Summary:	Background: 4-1BB, a member of the TNF receptor superfamily, has a role in various inflammatory pathologies through its interaction with 4-1BB ligand. We previously demonstrated that it participates in initiating and promoting obesity-induced adipose inflammation in a rodent model. Objective: In this study, we examined whether 4-1BB is related to obesity-induced adipose inflammation and metabolic parameters in humans. Methods: A total of 50 subjects, 25 obese (body mass index (BMI)⩾25 kg m −2 ) and 25 lean (BMI<23 kg m −2 ) participated in the study. The levels of 4-1BB transcripts and soluble 4-1BB protein (s4-1BB) in subcutaneous adipose tissue were measured by quantitative real-time PCR and enzyme-linked immunosorbent assay, respectively. Inflammatory and metabolic parameters were measured by enzymatic analysis and immunoassay. Results: Obese subjects had higher levels of both 4-1BB transcripts and s4-1BB protein in subcutaneous adipose tissue than lean controls, and the levels were correlated with BMI and the expression of inflammatory markers, as well as with serum metabolic parameters. Moreover, s4-1BB was released from human adipocytes, and elicited chemotactic responses from human monocytes/T cells as well as enhancing their inflammatory activity, indicating that it may promote human adipose inflammation. Discussion: Our data demonstrate that elevated levels of 4-1BB transcripts and s4-1BB in adipose tissue are closely associated with obesity-induced inflammation and metabolic dysregulation. They suggest that both 4-1BB transcripts and s4-1BB could serve as novel biomarkers and/or therapeutic targets for obesity-induced inflammation and metabolic syndrome in humans.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	0307-0565 1476-5497
DOI:	10.1038/ijo.2013.222