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Submitted on June 28, 2004
Accepted on November 15, 2004
B and IKK-
Pathway To Regulate The Release Of Pro-Inflammatory Cytokines From Human Adipose Tissue And Skeletal Muscle, In Vitro
Department of Obstetrics and Gynaecology, The University of Melbourne and Mercy Perinatal Research Centre, Mercy Hospital for Women, East Melbourne, Victoria, Australia 3002
* To whom correspondence should be addressed. E-mail: mlappas{at}unimelb.edu.au.
There is much evidence to indicate a role for adipocytokines in insulin resistance and/or Type 2 diabetes mellitus. In experimental models, oral salicylates, through their ability to interfere with the nuclear factor 
B (NF-B) transcription pathway, have been demonstrated to reverse insulin resistance. The aim of this study was to investigate whether or not NF-B regulates the release of adipocytokines in human adipose tissue and skeletal muscle. Human subcutaneous adipose tissue and skeletal muscle (obtained from normal pregnant women) were incubated in the absence (control) or presence of two NF-B inhibitors sulfasalazine (0.2.5, 2.5 and 5 mM) and BAY 11-7082 (25, 50 and 100 µM). After an 18 h incubation, the tissues were collected and NF-B p65 DNA binding activity, and IKK-
and IR- protein expression was assessed by ELISA and Western blotting, respectively. The incubation medium was collected and the release of TNF-
, IL-6 and IL-8, resistin, adiponectin and leptin was quantified by ELISA. Treatment of adipose tissue and skeletal muscle with sulfasalazine and BAY 11-7082 significantly inhibited the release of IL-6, IL-8 and TNF-, NF-B p65 DNA binding activity and IKK- protein expression (P < 0.05; Newman Keuls). There was no effect sulfasalazine and BAY 11-7082 on resistin, adiponectin and leptin release. Both sulfasalazine and BAY 11-7082 increased the adipose tissue and skeletal muscle expression of IR-. The data presented in this study demonstrate that the IKK-/NF-B transcription pathway is a key regulator of IL-6, IL-8 and TNF- release from adipose tissue and skeletal muscle. Control of the IKK-/NF-B pathway may therefore provide an alternative therapeutic strategy for regulating aberrant cytokine release, and therefore alleviating insulin resistance in Type 2 diabetes mellitus.
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