Adipocytes and/or adipose tissue release a variety of pro-infl ammatory cytokines and chemokines including interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α). In the absence of an acute infl ammatory process a substantial amount of interleukin-6 (IL-6) is produced by WAT. IL-6 secretion from visceral adipose tissue is three times stronger than from subcutaneous adipose tissue. Plasma IL-6 levels correlate with obesity and have been thought to be implicated in insulin resistance and its complications. Data from human muscle exercise studies have indicated that IL-6 produced by skeletal muscles might improve insulin sensitivity rather than induce insulin resistance. However, these results are under discussion. As for IL-6, obesity is associated with an overexpression of TNF-α. TNF-α expression in WAT was initially demonstrated in rodents to be markedly increased in obese models, and TNF-α was thought to be a mediator of insulin resistance. However, human studies about the role of TNF-α in insulin resistance yielded controversy results.
Produced in E. coli. The extracellular domain of human TNF-α (tumor necrosis factor-α) (aa 85-223) is fused at the N-terminus to a linker peptide (8 aa) and a FLAG®-tag., ≥95% (SDS-PAGE), ELISA | Print as PDF
Produced in E. coli. The extracellular domain of mouse TNF-α (tumor necrosis factor-α) (aa 77-235) is fused at the N-terminus to a linker peptide (8 aa) and a FLAG®-tag., ≥90% (SDS-PAGE), ELISA | Print as PDF
Produced in CHO cells. The extracellular domain of human TNF-α (aa 85-233) is fused at the N-terminus to the Fc portion of human IgG1 and a linker peptide (20 aa)., ≥90% (SDS-PAGE) | Print as PDF