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Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
Published on: June 3, 2016
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Chemerin activation in human obesity.
Shwu-Shin Chang1,2, Dan Eisenberg2,3, Lei Zhao1,2
1Division of Hematology, Stanford University School of Medicine, Stanford, California, USA.
Obesity (Silver Spring, Md.)
|May 26, 2016
Summary
Chemerin, an inflammatory adipokine, is activated in obesity. Its processing in adipose tissue leads to novel degraded forms in plasma, correlating with obesity.
Area of Science:
- Biochemistry
- Endocrinology
- Metabolic Research
Background:
- Chemerin is an inflammatory adipokine regulated by proteolytic cleavage.
- Its activity is dependent on specific C-terminal forms, with chem157S being the most potent.
Purpose of the Study:
- To investigate the activation status of chemerin in patients with obesity.
- To characterize different chemerin forms in human obesity.
Main Methods:
- Utilized specific ELISAs for various chemerin forms.
- Employed a pan-chemerin ELISA for comprehensive analysis.
- Mass spectrometry was used to identify C-terminal truncations.
Main Results:
- Plasma chemerin levels were significantly elevated in obese patients compared to lean controls.
- Increased unattributed chemerin and C-terminal truncation were observed in obese plasma.
- Adipose tissue showed distinct chemerin profiles, with higher chem157S and presence of chem155A in omental tissue.
Conclusions:
- Chemerin activation occurs in the adipose tissue of individuals with obesity.
- Further C-terminal processing of chemerin during its release from adipose tissue generates novel degraded forms in plasma.
- These novel plasma chemerin forms are associated with obesity.
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