Name: | Description: | Size: | Format: | |
---|---|---|---|---|
138.73 KB | Adobe PDF |
Authors
Advisor(s)
Abstract(s)
Background
Obesity is reaching epidemic proportions worldwide, being characterised by long-term, low-grade inflammation with detrimental effects on virtually all physiological systems. Adipocyte dysfunction has been recently regarded as the instigator of the main metabolic disturbances observed in obesity and obesity-related comorbidities. Thus, the impact of this dysfunction upon major organic systems involved in obesity clearly needs to be determined.
Given the intimate cross-talk between adipocytes and immune cells, and the recent discovery that immune cells are a source of cathecolamines (CA), we propose that these amines constitute an important link between neuroendocrine and immune networks. Consequently, we need to better understand the role of CA in modulation of the immune response in inflammatory-associated diseases such as obesity.
Immune cell-derived CA alter a wide array of cell functions, including proliferation, differentiation, apoptosis and the pattern of cytokine expression, suggesting a crucial role in the inflammatory outcome. However, the exact mechanisms controlling the release of CA in obesity are not fully understood.