Person:
Martín Fernández, Beatriz

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First Name
Beatriz
Last Name
Martín Fernández
Affiliation
Universidad Complutense de Madrid
Faculty / Institute
Medicina
Department
Area
Fisiología
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UCM identifierORCIDScopus Author IDWeb of Science ResearcherIDDialnet ID

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Now showing 1 - 5 of 5
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    A Proteomic Approach to Determine Changes in Proteins Involved in the Myocardial Metabolism in Left Ventricles of Spontaneously Hypertensive Rats
    (Cellular Physiology and Biochemistry, 2010) Zamorano León, José Javier; Modrego, Javier; Mateos Cáceres, Petra; Macaya Miguel, Carlos; Martín Fernández, Beatriz; Miana, María; Heras Jiménez, Natalia De Las; Cachofeiro Ramos, María Victoria; Lahera Julia, Vicente; López Farre, Antonio José
    Different works have suggested that in the hypertrophied heart the energy metabolic pathway shifts to glycolysis. Our aim was to evaluate using proteomics the expression of proteins associated with different energetic metabolic pathways in hypertrophied left ventricles of spontaneously hypertensive rats (SHR). Methods: 24-weeks-old SHR with stable hypertension and established left ventricle hypertrophy were used. Normotensive Wistar Kyoto rats were used as control. Proteins from left ventricles were analyzed by 2-dimensional electrophoresis and identified by comparison with a virtual rat heart proteomic map and mass spectrometry. Results: Enoyl-CoA hydratase expression, an enzyme involved in fatty acid β-oxidation, was reduced whereas the expression of other β-oxidation enzymes, 3-ketoacyl-CoA thiolase and the mitochondrial precursor of acyl-CoA thioester hydrolase, was increased in the hypertrophied left ventricles. The expression of two enzymes involved in the first steps of glycolysis, fructose bisphosphate aldolase and triosephosphate isomerase, was reduced in the left ventricle of SHR. Pyruvate dehydrogenase expression, enzyme involved in glucose oxidation, was enhanced in the hypertrophied ventricles whereas proteins of the tricarboxylic acid cycle were not modified. Proteins involved in the mitochondrial oxidative phosphorylation were overexpressed whereas the α-subunit of the mitochondrial precursor of ATP synthase was downexpressed. Conclusions: Several proteins involved in the main energy metabolic pathways were up and downexpressed. Moreover, our results seem to suggest that probably neither fatty acid β-oxidation nor glycolysis are the only sources for energy in the hypertrophied left ventricle.
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    Project number: 46
    Flipped classroom exprés y gamificación para fomentar el aprendizaje autónomo en grupos numerosos
    (2016) Vicente Torres, María Ángeles; Colino Matilla, Asunción; Comas Rengifo, María Dolores; Martín Fernández, Beatriz
    El objetivo de este proyecto ha sido fomentar el aprendizaje autónomo de un grupo numeroso de estudiantes universitarios de primer curso, con distintos conocimientos iniciales, para mejorar tanto sus hábitos de estudio como sus calificaciones. Para ello hemos diseñado una modificación de la metodología de enseñanza inversa que denominamos “enseñanza inversa exprés” que permite extender esta metodología a grupos con elevado número de alumnos y a varias unidades temáticas, de manera que sea asumible el aumento de carga de trabajo por los profesores. Tras su aplicación, la metodología de enseñanza inversa exprés ha demostrado mejoras en el aprendizaje, la motivación y la integración de los estudiantes, así como en la opinión que manifiestan sobre la calidad de la enseñanza recibida. Por tanto consideramos que es muy recomendable su aplicación principalmente en las asignaturas de primer curso para perfeccionar los hábitos de estudio de los estudiantes
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    Changes in cardiac energy metabolic pathways in overweighed rats fed a high-fat diet
    (European Journal of Nutrition, 2013) Modrego, Javier; Heras Jiménez, Natalia De Las; Zamorano León, José Javier; Mateos Cáceres, Petra; Martín Fernández, Beatriz; Valero Muñoz, María; Lahera Julia, Vicente; López Farré, Vicente
    Background: Heart produces ATP through long-chain fatty acids beta oxidation. Purpose: To analyze whether in ventricular myocardium, high-fat diet may modify the expression of proteins associated with energy metabolism before myocardial function was affected. Methods: Wistar Kyoto rats were divided into two groups: (a) rats fed standard diet (control; n = 6) and (b) rats fed high-fat diet (HFD; n = 6). Proteins from left ventricles were analyzed by two-dimensional electrophoresis, mass spectrometry and Western blotting. Results: Rats fed with HFD showed higher body weight, insulin, glucose, leptin and total cholesterol plasma levels as compared with those fed with standard diet. However, myocardial functional parameters were not different between them. The protein expression of 3-ketoacyl-CoA thiolase, acyl-CoA hydrolase mitochondrial precursor and enoyl-CoA hydratase, three long-chain fatty acid β-oxidation-related enzymes, and carnitine-O-palmitoyltransferase I was significantly higher in left ventricles from HFD rats. Protein expression of triosephosphate isomerase was higher in left ventricles from HFD rats than in those from control. Two α/β-enolase isotypes and glyceraldehyde-3-phosphate isomerase were significantly increased in HFD rats as compared with control. Pyruvate and lactate contents were similar in HFD and control groups. Expression of proteins associated with Krebs cycle and mitochondrial oxidative phosphorylation was higher in HFD rats. Conclusions: Expression of proteins involved in left ventricle metabolic energy was enhanced before myocardial functionality was affected in rats fed with HFD. These findings may probably indicate higher cardiac energy requirement due to weight increase by HFD.
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    Low Phytanic Acid-Concentrated DHA Prevents Cognitive Deficit and Regulates Alzheimer Disease Mediators in an ApoE−/− Mice Experimental Model
    (Nutrients, 2018) Ruiz-Roso Guerra, María Belén; Echeverry Alzate, Víctor; Ruiz-Roso Calvo De La Mora, Baltasar; Quintela, José; Ballesteros Rodrigálvarez, Sandra María; Lahera Julia, Vicente; Heras Jiménez, Natalia De Las; López Moreno, José Antonio; Martín Fernández, Beatriz
    Alzheimer’s disease (AD) is the main cause of dementia and cognitive impairment. It has been associated with a significant diminution of omega-3 polyunsaturated fatty acid docosahexaenoic acid (DHA) levels in the brain. Clinical trials with DHA as a treatment in neurological diseases have shown inconsistent results. Previously, we reported that the presence of phytanic acid (PhA) in standard DHA compositions could be blunting DHA’s beneficial effects. Therefore, we aimed to analyze the effects of a low PhA-concentrated DHA and a standard PhA-concentrated DHA in Apolipoprotein E knockout (ApoE
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    Proanthocyanidins Maintain Cardiac Ionic Homeostasis in Aldosterone-Induced Hypertension and Heart Failure
    (International Journal of Molecular Sciences, 2021) Heras Jiménez, Natalia De Las; Galiana, Adrián; Ballesteros Rodrigálvarez, Sandra; Olivares Álvaro, Elena; Fuller, Peter J.; Lahera Julia, Vicente; Martín Fernández, Beatriz; Ballesteros Rodrigálvarez, Sandra María
    Excess aldosterone promotes pathological remodeling of the heart and imbalance in cardiac ion homeostasis of sodium, potassium and calcium. Novel treatment with proanthocyanidins in aldosterone-treated rats has resulted in downregulation of cardiac SGK1, the main genomic aldosterone-induced intracellular mediator of ion handling. It therefore follows that proanthocyanidins could be modulating cardiac ion homeostasis in aldosterone-treated rats. Male Wistar rats received aldosterone (1 mg kg−1 day−1) +1% NaCl for three weeks. Half of the animals in each group were simultaneously treated with the proanthocyanidins-rich extract (80% w/w) (PRO80, 5 mg kg−1 day−1). PRO80 prevented cardiac hypertrophy and decreased calcium content. Expression of ion channels (ROMK, NHE1, NKA and NCX1) and calcium transient mediators (CAV1.2, pCaMKII and oxCaMKII) were reduced by PRO80 treatment in aldosterone-treated rats. To conclude, our data indicate that PRO80 may offer an alternative treatment to conventional MR-blockade in the prevention of aldosterone-induced cardiac pathology.