Autor segons l'article: Rodríguez-Calvo R; Vázquez-Carrera M; Masana L; Neumann D
Departament: Medicina i Cirurgia
Autor/s de la URV: Masana Marín, Luis
Paraules clau: Uncoupling protein 3 Transcription regulation Signaling pathway Reverse transcription polymerase chain reaction Real time polymerase chain reaction Protein expression Peroxisome proliferator activated receptor gamma Peroxisome proliferator activated receptor alpha Peroxisome proliferator activated receptor Palmitic acid Oxidative stress Mouse models Metabolic regulation Messenger rna Lipid storage Kinase inhibitors Insulin resistance Insulin Hydroxymethylglutaryl coenzyme a reductase kinase Human cell Human Heart muscle cell Glucose transporter 4 Glucose transport Gene expression Fatty-acid-metabolism Down-regulation Diabetic heart Cultured cardiomyocytes Controlled study Cell stimulation Cell protection Cd36 antigen Article Ampk Adipocyte Activated receptor-alpha 5 amino 4 imidazolecarboxamide riboside
Resum: Here we studied the impact of 5-aminoimidazole-4-carboxamide riboside (AICAR), a well-known AMPK activator, on cardiac metabolic adaptation. AMPK activation by AICAR was confirmed by increased phospho-Thr172-AMPK and phospho-Ser79-ACC protein levels in HL-1 cardiomyocytes. Then, cells were exposed to AICAR stimulation for 24 h in the presence or absence of the AMPK inhibitor Compound C, and the mRNA levels of the three PPARs were analyzed by real-time RT-PCR. Treatment with AICAR induced gene expression of all three PPARs, but only the Ppara and Pparg regulation were dependent on AMPK. Next, we exposed HL-1 cells to high palmitate/high insulin (HP/HI) conditions either in presence or in absence of AICAR, and we evaluated the expression of selected PPAR-targets genes. HP/HI induced insulin resistance and lipid storage was accompanied by increased Cd36, Acot1, and Ucp3 mRNA levels. AICAR treatment induced the expression of Acadvl and Glut4, which correlated to prevention of the HP/HI-induced intramyocellular lipid build-up, and attenuation of the HP/HI-induced impairment of glucose uptake. These data support the hypothesis that AICAR contributes to cardiac metabolic adaptation via regulation of transcriptional mechanisms. © 2015 Ricardo Rodríguez-Calvo et al.
Àrees temàtiques: Pharmacology (medical) Odontología Medicine, research & experimental Medicina ii Medicina i Farmacia Economia Drug discovery Ciências biológicas iii Ciências biológicas ii Ciências biológicas i
Accès a la llicència d'ús: https://creativecommons.org/licenses/by/3.0/es/
Adreça de correu electrònic de l'autor: luis.masana@urv.cat
Identificador de l'autor: 0000-0002-0789-4954
Data d'alta del registre: 2023-02-19
Versió de l'article dipositat: info:eu-repo/semantics/publishedVersion
Enllaç font original: https://www.hindawi.com/journals/ppar/2015/785783/
URL Document de llicència: http://repositori.urv.cat/ca/proteccio-de-dades/
Referència a l'article segons font original: Ppar Research. 2015
Referència de l'ítem segons les normes APA: Rodríguez-Calvo R; Vázquez-Carrera M; Masana L; Neumann D (2015). AICAR Protects against High Palmitate/High Insulin-Induced Intramyocellular Lipid Accumulation and Insulin Resistance in HL-1 Cardiac Cells by Inducing PPAR-Target Gene Expression. Ppar Research, 2015(), -. DOI: 10.1155/2015/785783
DOI de l'article: 10.1155/2015/785783
Entitat: Universitat Rovira i Virgili
Any de publicació de la revista: 2015
Tipus de publicació: Journal Publications
Repositori URV