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Acta Physiologica 2011; Volume 202, Supplement 685
Scandinavian Physiological Society's Annual Meeting
8/12/2011-8/14/2011
Bergen, Norway
CYTOKINE SECRETION FROM ADIPOCYTES IS REGULATED BY VITAMIN D VIA THE NF-B PATHWAY
Abstract number: 8.1.40
MUTT1 SJ, KARHU1 T, LEHENKARI1 P, SAARNIO1 J, JARVELIN1 MR, HERZIG1 KH
1Institute of Biomedicine, Department of Physiology and Biocenter of Oulu, Faculty of Medicine, PO BOX 5000, Aapistie 7, Oulu University, 90014 Oulu, Finland; Email: [email protected]
Background:
Adipose tissue inflammation is an important pathological process in obese people leading to insulin resistance, diabetes and cardiovascular disease. An inverse correlation of vitamin D (vitD) levels and BMI has been observed, in particular with abdominal obesity. During weight gain adipose tissue increases the secretion of inflammatory mediators (lik e IL-6). VitD deficiency is now recognized as a pandemic, and associated with numerous adverse general health outcomes such as an increased mortality rate. In the Nordic latitudes we are additionally lacking cutaneous vitD production during winter. Thus, we hypothesize that vitD inhibits cytokine secretion from adipocytes via a direct inhibition of NF-kB.
Methods:
We utilized two different models of human adipocytes: Mesenchymal stem cells (hMSCs) were differentiated into adipocytes and mature adipocytes isolated from fat tissue biopsies we re stimulated with lipopolysaccharide (LPS 10 ng/ml) ± vitD [10-6 to 10-10 M] for 24 hrs. IL-6 secretion was measured in cell culture supernatant by ELISA, RNA and cell lysate analyzed for NF-kB subunits and its regulating proteins.
Results:
LPS dose dependently stimulated IL-6 secretion from hMSC adipocytes and mature adipocytes. Incubation with vitD significantly reduced LPS stimulated IL-6 (32% at 10-6M) and inhibit ed NF-kB.
Conclusion:
Our data demonstrate that vitD inhibits LPS induced IL-6 release in both hMSC differentiated adipocytes and mature adipocytes via NF-kB inhibition. Our results suggest that sufficient vitD levels would be beneficial for reducing the inflammatory load in the obese population reducing the risks of known co-morbidities of obesity. Supported in part by the Academy of Finland.
To cite this abstract, please use the following information:
Acta Physiologica 2011; Volume 202, Supplement 685 :8.1.40