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Department of Pediatrics and Adolescent Medicine, University of Ulm (P.F.-P., K.-M.D., M.W.), D-89075 Ulm, Germany; and Department of Diabetes Biology, Novo Nordisk A/S (H.T.), DK-2760 Måloev, Denmark
Address all correspondence and requests for reprints to: Martin Wabitsch, M.D., Department of Pediatrics and Adolescent Medicine, University of Ulm, Prittwitzstrasse 43, 89075 Ulm, Germany. E-mail: martin.wabitsch{at}medizin.uni-ulm.de.
Adipose tissue mass is reflected by the volume and the number of adipocytes and is subject to homeostatic regulation involving cell death mechanisms. In this study we have investigated the mechanisms of apoptosis in human preadipocytes and adipocytes that may play a role in the regulation of adipose tissue mass. We found that death receptors (CD95, TNF-related apoptosis-inducing ligand receptors 1 and 2, and TNF receptor 1) are expressed in human fat cells and that apoptosis can be induced by specific ligands. Sensitivity to apoptosis could be stimulated by an inhibitor of biosynthesis. In addition, inhibition of auto-/paracrine action of IGF-I dramatically sensitizes human adipocytes for death ligand-induced apoptosis. Phosphoinositide 3-kinase and, to a weaker extent, p38 MAPK are involved in IGF-I-mediated survival. IGF-I protects human fat cells from apoptosis by maintaining the expression of antiapoptotic proteins, Bcl-xL and Fas-associated death domain-like IL-1-converting enzyme inhibitory protein. In conclusion, we identified mechanisms of apoptosis induction in human fat cells. We furthermore demonstrate that human fat cells protect themselves from apoptosis by IGF-I in an auto-/paracrine manner.
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