Elisa Villalobos

Sep 2, 2024 | dialnet.unirioja.es | Sonia Olivares |Elisa Villalobos |Gonzalez Blanco Gonzalez |González González |Isabel Zacarías

Ayuda Buscar en la ayuda Buscar en la ayuda Proceso de formulación y validación de las guías alimentarias para la población chilena Sonia Olivares C [1] ; Isabel Zacarías H [1] ; Carmen Gloria González G [1] ; Elisa Villalobos V [1] [1] Universidad de Chile Instituto de Nutrición y Tecnología de los Alimentos Localización: Revista chilena de nutrición, ISSN-e 0717-7518, Vol. 40, Nº. 3, 2013, págs. 262-268 Idioma: español Títulos paralelos: Development and validation process of food-based...

Jul 3, 2024 | joe.bioscientifica.com | Elisa Villalobos |Allende Miguelez-Crespo |Ruth Morgan |Lisa Ivatt

Keywords: glucocorticoids; steroids; transport; metabolism; obesity; homeostasisIntroductionGlucocorticoids are required to maintain glucose and lipid homeostasis in times of physiological stress, ensuring an adequate fuel supply for the body (Kuo et al. 2015). In key metabolic tissues such as adipose tissue, skeletal muscle and liver, glucocorticoids act to prevent glycolysis and instead promote gluconeogenesis (Kuo et al. 2013).

Jan 26, 2024 | biorxiv.org | Elisa Villalobos |Ruth Morgan |Allende Miguelez-Crespo |Lisa Ivatt

AbstractGlucocorticoids modulate glucose homeostasis, acting on metabolically active tissues such as liver, skeletal muscle, and adipose tissue. Intra-cellular regulation of glucocorticoid action in adipose tissue impacts metabolic responses to obesity. ATP-Binding Cassette Family C member 1 (ABCC1) is a transmembrane glucocorticoid transporter known to limit the accumulation of exogenously administered corticosterone in adipose tissue.

Sep 6, 2023 | nature.com | Daniel Natera |José Verdú-Díaz |Giorgio A. Tasca |Volker Straub |Elisa Villalobos

AbstractDuchenne muscular dystrophy is a genetic disease produced by mutations in the dystrophin gene characterized by early onset muscle weakness leading to severe and irreversible disability. The cellular and molecular consequences of the lack of dystrophin in humans are only partially known, which is crucial for the development of new therapies aiming to slow or stop the progression of the disease.