Brain-Derived Neurotrophic Factor Improves Impaired Fatty Acid Oxidation Via the Activation of Adenosine Monophosphate-Activated Protein Kinase-ɑ – Proliferator-Activated Receptor-r Coactivator-1ɑ Signaling in Skeletal Muscle of Mice With Heart Failure

Background: We recently reported that treatment with rhBDNF (recombinant human brain-derived neurotrophic factor) improved the reduced exercise capacity of mice heart failure (HF) after myocardial infarction (MI). Since BDNF is to enhance fatty acid oxidation, we herein conducted an in vivo investigation determine whether improvement due enhancement oxidation skeletal muscle via AMPKα-PGC1α (adenosine monophosphate-activated protein kinase-ɑ–proliferator-activated receptor-r coactivator-1ɑ) axis. Methods: MI and sham operations were C57BL/6J mice. Two weeks postsurgery, randomly divided into groups treated or vehicle for 2 weeks. signaling mitochondrial content evaluated by Western blotting transmission electron microscopy. Fatty β-oxidation was examined high-resolution respirometry using permeabilized fiber. BDNF-knockout 5-aminoimidazole-4-carboxamide-1-beta-d-riboruranoside, activator AMPK. Results: The significantly increased expressions phosphorylated AMPKα PGC1α intermyofibrillar density lowered rhBDNF-treated dysfunction 5-aminoimidazole-4-carboxamide-1-beta-d-riboruranoside. Conclusions: Beneficial effects on HF are mediated through activation muscle. may become a therapeutic option improve as alternative adjunct training.