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Acta Physiologica Congress

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Acta Physiologica 2012; Volume 206, Supplement 693
Joint FEPS and Spanish Physiological Society Scientific Congress 2012
9/8/2012-9/11/2012
Santiago de Compostela, Spain


P53 MEDIATES THE ADIPOGENIC EFFECT OF GHRELIN
Abstract number: P168

Porteiro1 B, Martinez2 G, Velasquez3 D, Vidal2 A, Lopez2 M, Dieguez2 C, Nogueiras2 R

1Physiology, University of Santiago,
2Physiology, University of Santiago de Compostela,
3Phisiology, University of Santiago de Compostela

Objectives: 

Ghrelin is a 28-residue peptide hormone from the stomach and acts as the endogenous ligand to GH secretagogue receptor (GHS-R), which is expressed in the brain and peripheral tissues. Ghrelin promotes feeding in rodents, which results in increased body weight and adiposity. p53, one of the most important defenders against tumor development, has also an important role in glucose and lipid metabolism. Previous studies have demonstrated that p53 regulates the orexigenic action of ghrelin. The aim of this study was to investigate if p53 regulates the adipogenic role of ghrelin

Materials: 

Ghrelin was injected intraperitoneally for seven days in wild-type and p53 null mice. For the biochemical analisys of the tissues (liver and white adipose tissue), real-time PCR and western blot were performed.

Results: 

Ghrelin increased body weight gain in wild-type mice. As expected, however, we failed to find this effect in p53 deficient mice. At biochemical level, ghrelin increased the expression of lipogenic enzymes in white adipose tissue of wild type mice, but failed to do so in adipose tissue of p53 null mice. These results were reflected in decreased adipogenic protein levels of ACC and FAS. In the liver, this effects were partial since ACC levels are increased in both wild-type and p53 null mice but FAS levels were stimulated only in wild-type mice

Conclusions: 

Our current data demonstrate that p53 is crucial for the adipogenic effect of ghrelin in adipose tissue.

To cite this abstract, please use the following information:
Acta Physiologica 2012; Volume 206, Supplement 693 :P168

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