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Adiponectin downregulates CD163 whose cellular and soluble forms are elevated in obesity
D Sporrer1, M Weber, J Wanninger
1Department of Internal Medicine I, Regensburg University Hospital, Regensburg, Germany.
European Journal of Clinical Investigation
|June 4, 2009
Summary
Soluble CD163 (sCD163) is elevated in obesity and type 2 diabetes (T2D). While adiponectin reduces CD163 in vitro, inflammatory factors like IL-6 may be more significant in vivo for this immune marker.
Area of Science:
- Immunology
- Metabolic Diseases
- Cell Biology
Background:
- CD163 is a macrophage receptor; its soluble form (sCD163) is a marker of inflammation.
- Obesity is linked to chronic inflammation and reduced adiponectin, an anti-inflammatory adipokine.
- Adiponectin, AICAR, and metformin activate AMP-kinase, known for anti-inflammatory effects.
Purpose of the Study:
- To investigate the influence of adiponectin and AMP-kinase activating drugs on monocytic CD163.
- To determine cellular and soluble CD163 levels in obesity and type 2 diabetes (T2D).
Main Methods:
- Monocytes were treated with adiponectin, AICAR, or metformin.
- Monocytes and serum were collected from T2D patients, overweight, and normal-weight controls.
- Cellular CD163 was analyzed by immunoblot; sCD163 was quantified using ELISA in cell supernatants and patient serum.
Main Results:
- Adiponectin decreased cellular and surface CD163 in vitro; metformin and AICAR also downregulated CD163.
- Monocytic CD163 levels were higher in T2D and obese individuals.
- Serum sCD163 was significantly elevated in obese and T2D patients, correlating positively with IL-6.
Conclusions:
- Monocytic and systemic sCD163 are elevated in T2D and obesity.
- Adiponectin reduces CD163 in vitro, but obesity-related factors like IL-6 may play a more critical role in vivo.
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