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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: AMP-Activated Protein Kinases, Aminoimidazole Carboxamide, Analysis of Variance, Animals, Blotting, Western, Cell Line, Tumor, DNA Primers, Gene Expression Regulation, Glucose, Glucose Transporter Type 4, Male, Monocarboxylic Acid Transporters, Muscle Proteins, Muscle, Skeletal, Rats, Rats, Wistar, Reverse Transcriptase Polymerase Chain Reaction, Ribonucleotides.
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Does aMP-activated protein kinase regulate the expression of monocarboxylate transporter 4 in skeletal muscle? Context: The aim of this study was to determine the effect of 5-aminoimidazole-4-carboxamide-1-β-D-ribofuranoside (AICAR), an AMP-activated protein kinase (AMPK) activator, on monocarboxylate transporter 4 (MCT4) expression in rat skeletal muscle and a prototypic embryonal rhabdomyosarcoma cell line (RD cells). We examined the alteration in Glucose transporter 4 (GLUT4) and MCT4 mRNA levels by quantitative real-time PCR. Alteration in GLUT4 and MCT4 protein levels was examined by Western blotting. In an in vivo study, AICAR increased MCT4 mRNA and protein levels in a fiber-type specific manner. In an in vitro study, AICAR increased MCT4 mRNA and protein levels. Moreover, AICAR-induced MCT4 expression was blocked by Compound C, an AMPK inhibitor.
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In this study, we found that AMPK activation induced expression of MCT4 in RD cells and rat skeletal muscle in a fiber-type specific manner. These results indicate the possible involvement of an AMPK-mediated pathway associated with MCT4 expression in skeletal muscle. Final Decision: yes