Search

Your search keyword '"Buque, Xabier"' showing total 10 results
Start Over Author "Buque, Xabier"
10 results on '"Buque, Xabier"'

1. FRI-153 High prevalence of steatotic liver disease and systemic inflammation in hereditary fructose intolerance (HFI) patients independent of age, BMI and the presence of metabolic syndrome.

Author

Delgado, Teresa Cardoso, Cano, Ainara, Mercado-Gómez, Maria, Buque, Xabier, Alonso, Cristina, Serrano-Macia, Marina, Alcalde, Carlos, Belanger-Quintana, Amaya, Cañedo-Villarroya, Elvira, Hualde, Leticia Ceberia, Chumillas-Calzada, Silvia, Correcher, Patricia, García-Arenas, Dolores, Gómez, Igor, Hernández, Tomáz, Izquierdo-García, Elsa, Chicano, Dámaris Martínez, Morales, Montserrat, Pedrón-Giner, Consuelo, and Jáuregui, Estrella Petrina

Published
2024
Full Text
View/download PDF

2. FRI-343-YI APAP induced liver damage is prevented by activation of PPARgamma and PPAR-alpha.

Author

Gomez-Jauregui, Paul, Gonzalez-Romero, Francisco, Santos, Beatriz Gómez, Apodaka-Biguri, Maider, Buque, Xabier, Crespo, Maria, Mora, Alfonso, Mesquita, Mariana, Aurrekoetxea, Igor, Delgado, Igotz, Nieva-Zuluaga, Ane, de Gauna, Mikel Ruiz, Fernández-Puertas, Idoia, Sainz-Ramírez, Natalia, Alfaro-Jiménez, Kendall, Irizar, María Esther, Iglesias, Ainhoa, Cubero, Francisco Javier, Sabio, Guadalupe, and Zubiaga, Ana

Published
2024
Full Text
View/download PDF

4. THU-210 Dysfunctional activation of the DNA damage response is associated with MASLD progression through an E2F2-dependent mechanism.

Author

Santos, Beatriz Gómez, Fernández-Puertas, Idoia, Gomez-Jauregui, Paul, Sainz-Ramírez, Natalia, Alfaro-Jiménez, Kendall, Castillero, Estibaliz, Nieva-Zuluaga, Ane, Apodaka-Biguri, Maider, Aurrekoetxea, Igor, Delgado, Igotz, Lopategi, Aritz, Iglesias, Ainhoa, González, Lorena Mosteiro, Olartekoetxea, Gaizka Errazti, Gaztambide, Sonia, González, Luis A. Castaño, Bujanda, Luis, Banales, Jesus Maria, Buque, Xabier, and Zubiaga, Ana

Published
2024
Full Text
View/download PDF

5. FRI-472-YI Mitochondrial metabolism is disrupted by ciprofloxacin preventing cholangiocarcinoma cell proliferation.

Author

de Gauna, Mikel Ruiz, Alfaro-Jiménez, Kendall, Nieva-Zuluaga, Ane, Apodaka-Biguri, Maider, Markaide, Enara, Izquierdo-Sánchez, Laura, Rae, Colin, González-Romero, Francisco, Gomez-Jauregui, Paul, Sainz-Ramírez, Natalia, Santos, Beatriz Gómez, Buque, Xabier, Aurrekoetxea, Igor, Delgado, Igotz, Fernández-Puertas, Idoia, Iglesias, Ainhoa, Rourke, Colm O., Rodrigues, Pedro Miguel, Andersen, Jesper, and Calvisi, Diego

Published
2024
Full Text
View/download PDF

6. Liver osteopontin is required to prevent the progression of age‐related nonalcoholic fatty liver disease.

Author

Gómez‐Santos, Beatriz, Saenz de Urturi, Diego, Nuñez‐García, Maitane, Gonzalez‐Romero, Francisco, Buque, Xabier, Aurrekoetxea, Igor, Gutiérrez de Juan, Virginia, Gonzalez‐Rellan, Maria J., García‐Monzón, Carmelo, González‐Rodríguez, Águeda, Mosteiro, Lorena, Errazti, Gaizka, Mifsut, Patricia, Gaztambide, Sonia, Castaño, Luis, Martin, Cesar, Nogueiras, Rubén, Martinez‐Chantar, María L., Syn, Wing‐Kin, and Aspichueta, Patricia

Subjects
*FATTY liver, *OSTEOPONTIN, *ANIMAL models for aging, *LIVER, *LIPID metabolism, *P53 antioncogene, *LIVER cells
Abstract

Osteopontin (OPN), a senescence‐associated secretory phenotype factor, is increased in patients with nonalcoholic fatty liver disease (NAFLD). Cellular senescence has been associated with age‐dependent hepatosteatosis. Thus, we investigated the role of OPN in the age‐related hepatosteatosis. For this, human serum samples, animal models of aging, and cell lines in which senescence was induced were used. Metabolic fluxes, lipid, and protein concentration were determined. Among individuals with a normal liver, we observed a positive correlation between serum OPN levels and increasing age. This correlation with age, however, was absent in patients with NAFLD. In wild‐type (WT) mice, serum and liver OPN were increased at 10 months old (m) along with liver p53 levels and remained elevated at 20m. Markers of liver senescence increased in association with synthesis and concentration of triglycerides (TG) in 10m OPN‐deficient (KO) hepatocytes when compared to WT hepatocytes. These changes in senescence and lipid metabolism in 10m OPN‐KO mice liver were associated with the decrease of 78 kDa glucose‐regulated protein (GRP78), induction of ER stress, and the increase in fatty acid synthase and CD36 levels. OPN deficiency in senescent cells also diminished GRP78, the accumulation of intracellular TG, and the increase in CD36 levels. In 20m mice, OPN loss led to increased liver fibrosis. Finally, we showed that OPN expression in vitro and in vivo was regulated by p53. In conclusion, OPN deficiency leads to earlier cellular senescence, ER stress, and TG accumulation during aging. The p53‐OPN axis is required to inhibit the onset of age‐related hepatosteatosis. [ABSTRACT FROM AUTHOR]

Published
2020
Full Text
View/download PDF

7. FRI-094-Targeting NEDDylation protects liver from acute drug-induced damage.

Author

Simón, Jorge, Ramos, David Fernández, de Juan, Virginia Gutiérrez, Serrano-Macia, Marina, Goikoetxea, Naroa, Urturi, Diego Saenz de, Agudo, Rubén Rodríguez, Otsoa, Fernando Lopitz, de Davalillo, Sergio López, Buque, Xabier, Varela-Rey, Marta, Fernández-Tussy, Pablo, Aspichueta, Patricia, Delgado, Teresa Cardoso, and Martínez-Chantar, María Luz

Subjects
*LIVER
Published
2019
Full Text
View/download PDF

8. FRI-343-NEDDylation inhibition as a new potential therapy of non-alcoholic fatty liver disease.

Author

Serrano-Macia, Marina, Azkargorta, Mikel, Simón, Jorge, Otsoa, Fernando Lopitz, Delgado, Teresa Cardoso, Ramos, David Fernández, de Juan, Virginia Gutiérrez, Varela-Rey, Marta, Goikoetxea, Naroa, Tussy, Pablo Fernández, Apichueta, Patricia, Urturi, Diego Saenz de, Buque, Xabier, Iruzubieta, Paula, Crespo, Javier, Lu, Shelly C., Mato, José M., Elortza, Felix, and Martínez-Chantar, María Luz

Subjects
*FATTY liver, *CHOLINE
Published
2019
Full Text
View/download PDF

9. PS-015-Role of methylation-controlled J-protein, endogenous repressor of the mitochondrial respiratory chain, in cholestatic liver disease.

Author

Iruzubieta, Paula, Barbier-Torres, Lucía, Goikoetxea, Naroa, Delgado, Teresa Cardoso, Ramos, David Fernández, Varela-Rey, Marta, Juan, Virginia Gutiérrez de, Tussy, Pablo Fernández, Zubiete-Franco, Imanol, Simón, Jorge, Congregado, Daniela Mestre, Otsoa, Fernando Lopitz, Santos, Beatriz Gómez, Buque, Xabier, López-Hoyos, Marcos, Apichueta, Patricia, Mato, José M., Anguita, Juan, Rincón, Mercedes, and Crespo, Javier

Subjects
*LIVER diseases, *MITOCHONDRIAL membranes, *BILE ducts, *THERAPEUTICS, *DEOXYCHOLIC acid
Published
2019
Full Text
View/download PDF

10. Atorvastatin provides a new lipidome improving early regeneration after partial hepatectomy in osteopontin deficient mice.

Author

Nuñez-Garcia, Maitane, Gomez-Santos, Beatriz, Saenz de Urturi, Diego, Mestre, Daniela, Gonzalez-Romero, Francisco, Buque, Xabier, Gutiérrez-de Juan, Virginia, Martinez-Chantar, María Luz, Syn, Wing-Kin, Fresnedo, Olatz, and Aspichueta, Patricia

Abstract

Osteopontin (OPN), a multifunctional cytokine that controls liver glycerolipid metabolism, is involved in activation and proliferation of several liver cell types during regeneration, a condition of high metabolic demands. Here we investigated the role of OPN in modulating the liver lipidome during regeneration after partial-hepatectomy (PH) and the impact that atorvastatin treatment has over regeneration in OPN knockout (KO) mice. The results showed that OPN deficiency leads to remodeling of phosphatidylcholine and triacylglycerol (TG) species primarily during the first 24 h after PH, with minimal effects on regeneration. Changes in the quiescent liver lipidome in OPN-KO mice included TG enrichment with linoleic acid and were associated with higher lysosome TG-hydrolase activity that maintained 24 h after PH but increased in WT mice. OPN-KO mice showed increased beta-oxidation 24 h after PH with less body weight loss. In OPN-KO mice, atorvastatin treatment induced changes in the lipidome 24 h after PH and improved liver regeneration while no effect was observed 48 h post-PH. These results suggest that increased dietary-lipid uptake in OPN-KO mice provides the metabolic precursors required for regeneration 24 h and 48 h after PH. However, atorvastatin treatment offers a new metabolic program that improves early regeneration when OPN is deficient. [ABSTRACT FROM AUTHOR]

Published
2018
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results