CADMOULD 3D-F V2.0 (c) SIMCON 64 Bit
Installation 1.1. System requirements:. 64bit operating system. 1.3. CADMOULD 3D-F V2.0. SIMCON V2.0.5.IL-6 release from epithelial cells: a possible missing link between adipose tissue inflammation and atherosclerosis.
In type 2 diabetes and obesity, obesity-related inflammation has a central role in atherogenesis. Whether the proatherogenic activity of T cells is attributed to increased production of proinflammatory cytokines and/or due to a dysfunctional conversion of monocytes into inflammatory cells is a matter of debate. Because adipose tissue is now recognized as an active endocrine organ, we investigated the production of adipocytokines from human adipocytes and the effects of proinflammatory cytokines on the release of monocyte chemoattractant protein 1 (MCP-1) from adipocytes. Omental fat samples were obtained from 11 patients with type 2 diabetes and severe obesity undergoing bariatric surgery. The release of cytokines (tumor necrosis factor-alpha, TNF-alpha; interleukin [IL]-1beta, IL-1beta; IL-6, IL-6; and transforming growth factor-beta1, TGF-beta1) was analyzed by means of ELISA from isolated adipocytes incubated alone or with phorbol 12-myristate 13-acetate (PMA). MCP-1 release was determined in adipocytes stimulated by PMA alone or with IL-6. Both the basal release of cytokines and the release after PMA stimulation of adipocytes were increased in comparison with the levels observed in samples from control subjects. The release of IL-6 was significantly increased in adipocytes from patients with type 2 diabetes and obesity. The release of IL-6 after PMA and IL-6 treatment was significantly increased compared with that after PMA treatment alone, but there was no additive effect of both stimuli. MCP-1 release was increased after PMA treatment compared with that observed after incubation of isolated adipocytes with medium alone. IL-6 addition induced a marked and statistically significant increase in MCP-1 release after PMA treatment. This increase was significantly greater than the release induced by PMA treatment alone. In conclusion, we show that the release of IL-6 from human adipocytes is increased by hyperglycemia and that this increase might be involved in the recruitment of inflammatory cells and the production of MCP-1. This process
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