Sabio lab

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Tag: lipid metabolism (page 1 of 3)

CICERONE program 2018 for Masters and advanced undergraduate students

Though the CICERONE Program, our group is open to master and advanced undergraduate students for extending their scientific training through hands-on experience in our laboratory during the summer recess. In addition to carrying out a supervised research project, the students will also attend CNIC seminars.

The aim of the program is to give university students first-hand knowledge of biomedical research so that they can make more informed choices about the possibility of pursuing a scientific career.

To apply, you must register at CNIC website before 6 April 2018.

Link Size
.pdf 2018 Guidelines 190 KB
Application form
.pdf Call extract from BOE 169 KB

For the 2018 call, we are offering tehe following research project:

  • Role of p38MAPK in metabolic diseases: Metabolic syndrome is a medical disorder defined by the co‐occurrence of obesity, impaired glucose tolerance, dyslipidemia and hypertension. Stress activated protein kinases have been shown to control both obesity by itself and diabetes associated to obesity. These stress kinases are activated by several MAPK activated kinases (MKK). We want to investigate the role of MKK3 in this process and the molecular mechanism by which this kinase could affect diabetes.

¿Quién dirige la orquesta en la obesidad? (15 March 2018)

On Thursday 15 March 2018, at the XIV Congress of the Spanish Society for the Study of the Obesity (SEEDO) Guadalupe Sabio (Centro Nacional de Investigaciones Cardiovasculares Carlos III) and Amaia Rodríguez Murueta-Goyena (Clínica Universidad de Navarra) will debate about which is the main organ orchestrating the diseases caused by obesity.

SEEDO 2018

Pharmacological stimulation of p53 with low-dose doxorubicin ameliorates diet-induced nonalcoholic steatosis and steatohepatitis

Begoña Porteiro, Marcos F. Fondevila, Xabier Buque, Maria J. Gonzalez-Rellan, Uxia Fernandez, Alfonso Mora, Daniel Beiroa, Ana, Senra, Rosalia Gallego, Johan Fernø, Miguel López, Guadalupe Sabio, Carlos Dieguez, Patricia Aspichueta & Rubén Nogueiras.

Recent reports have implicated the p53 tumor suppressor in the regulation of lipid metabolism. We hypothesized that the pharmacological activation of p53 with low-dose doxorubicin, which is widely used to treat several types of cancer, may have beneficial effects on nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH).

Hematoxylin&eosin and oil red O staining of liver sections.

We used long-term pharmacological activation of p53 by i.p. or oral administration of low-dose doxorubicin in different animal models of NAFLD (high fat diet containing 45% and 60% kcal fat) and NASH (methionine- and choline-deficient diet and choline deficiency combined with high fat diet). We also administered doxorubicin in mice lacking p53 in the liver and in two human hepatic cells lines (HepG2 and THLE2).

The attenuation of liver damage was accompanied by the stimulation of fatty acid oxidation and decrease of lipogenesis, inflammation, and ER stress. The effects of doxorubicin were abrogated in mice with liver-specific ablation of p53. Finally, the effects of doxorubicin on lipid metabolism found in animal models were also present in two human hepatic cells lines, in which the drug stimulated fatty acid oxidation and inhibited de novo lipogenesis at doses that did not cause changes in apoptosis or cell viability.

These data provide new evidence for targeting p53 as a strategy to treat liver disease


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