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Submitted on May 16, 2006
Accepted on December 1, 2006
Else Kröner-Fresenius-Center for Nutritional Medicine of the Technical University Munich, Germany; German Diabetes Clinic, German Diabetes Center, Leibniz Center at Heinrich-Heine-University Düsseldorf, D-40225 Düsseldorf, Germany
* To whom correspondence should be addressed. E-mail: nutritional.medicine{at}wzw.tum.de.
Context: Adipocytes are known to release a variety of factors that may contribute to the pro-inflammatory state characteristic for obesity. This secretory function is considered to provide the basis for obesity-related complications such as type 2 diabetes and atherosclerosis.
Objective: To get a better insight into possible underlying mechanisms we investigated the effect of adipocyte size on adipokine production and secretion.
Design, Patients and Main Outcome Measures: Protein secretion and mRNA expression in cultured adipocytes separated according cell size from 30 individuals undergoing elective plastic surgery were investigated.
Results: The mean adipocyte volume of the 4 fractions ranged from 205±146pl to 983±87pl. There were strong linear correlations for the secretion of adipokines over time. Secretion of leptin, IL-6, IL-8, TNF-
, MCP-1, IP-10, MIP-1
, G-CSF, IL-1ra, and adiponectin was positively correlated with cell size. After correction for cell surface, there was still a significant difference between fraction IV (very large) and fraction I (small cells), for leptin, IL-6, IL-8, MCP-1 and G-CSF. In contrast, anti-inflammatory factors such as IL-1ra and adiponectin lost their association size after correction for cell surface area comparing fraction I and IV. In addition, there was a decrease of IL-10 secretion with increasing cell size.
Conclusions: The results clearly suggest that adipocyte size is an important determinant of adipokine secretion. There seems to be a differential expression of pro- and anti-inflammatory factors with increasing adipocyte size resulting in a shift towards dominance of pro-inflammatory adipokines largely due to a dysregulation of hypertrophic, very large cells.
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