Fas activation in adipocytes impairs insulin-stimulated glucose uptake by reducing Akt |
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Authors: | Stephan Wueest Reto A. Rapold Eugen J. Schoenle |
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Affiliation: | a Division of Pediatric Endocrinology and Diabetology, University Children’s Hospital, CH-8032 Zurich, Switzerland b Zurich Center for Integrative Human Physiology, University of Zurich, CH-8057 Zurich, Switzerland |
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Abstract: | Fas (CD95) belongs to the superfamily of the tumor necrosis factor (TNF) receptors. Besides its key role in apoptosis, Fas contributes to non-apoptotic pathways such as cell proliferation and inflammation. In 3T3-L1 adipocytes, activation of Fas by Fas ligand decreased insulin-stimulated glucose uptake, without affecting cell viability. This decrease in glucose uptake was accompanied by reduced protein expression and diminished phosphorylation of Akt. Similarly, insulin-stimulated glucose incorporation and protein levels of Akt were increased in isolated adipocytes from Fas deficient mice when compared to wild-type mice. In conclusion, Fas activation in adipocytes decreases Akt expression and thereby impairs insulin sensitivity. |
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Keywords: | AFasKO, adipocyte-specific Fas knockout Fas-def, Fas deficient |
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