scholarly journals Protein acetylation in skeletal muscle mitochondria is involved in impaired fatty acid oxidation and exercise intolerance in heart failure

2018 ◽  
Vol 9 (5) ◽  
pp. 844-859 ◽  
Author(s):  
Masaya Tsuda ◽  
Arata Fukushima ◽  
Junichi Matsumoto ◽  
Shingo Takada ◽  
Naoya Kakutani ◽  
...  
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Exercise Intolerance ◽  
Acid Oxidation ◽  
Protein Acetylation ◽  
Muscle Mitochondria ◽  
Skeletal Muscle Mitochondria ◽  
Impaired Fatty Acid

65 Fatty acid oxidation in human skeletal muscle mitochondria determined by oxidative phosphorylation as a function of age

Mitochondrion ◽  
2007 ◽  
Vol 7 (6) ◽  
pp. 422-423
Author(s):  
George Kypriotakis ◽  
Bruce H. Cohen ◽  
Sumit Parikh ◽  
Douglas S. Kerr ◽  
Charles L. Hoppel ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acid ◽  
Oxidative Phosphorylation ◽  
Fatty Acid Oxidation ◽  
Human Skeletal Muscle ◽  
Acid Oxidation ◽  
Muscle Mitochondria ◽  
Skeletal Muscle Mitochondria

scholarly journals Fatty acid oxidation in cardiac and skeletal muscle mitochondria is unaffected by deletion of CD36

2007 ◽  
Vol 467 (2) ◽  
pp. 234-238 ◽  
Author(s):  
Kristen L. King ◽  
William C. Stanley ◽  
Mariana Rosca ◽  
Janos Kerner ◽  
Charles L. Hoppel ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Acid Oxidation ◽  
Muscle Mitochondria ◽  
Skeletal Muscle Mitochondria

Fatty acid oxidation in human skeletal-muscle mitochondria

1983 ◽  
Vol 11 (6) ◽  
pp. 728-729 ◽  
Author(s):  
KISHORCHANDRA GOHIL ◽  
DAVID A. JONES ◽  
RICHARD H. T. EDWARDS
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Human Skeletal Muscle ◽  
Acid Oxidation ◽  
Muscle Mitochondria ◽  
Skeletal Muscle Mitochondria

Saturated glucose uptake capacity and impaired fatty acid oxidation in hypertensive hearts before development of heart failure

2004 ◽  
Vol 287 (2) ◽  
pp. H760-H766 ◽  
Author(s):  
Nozomu Fujii ◽  
Takashi Nozawa ◽  
Akihiko Igawa ◽  
Bun-ichi Kato ◽  
Norio Igarashi ◽  
...  
Keyword(s):  
Heart Failure ◽  
Fatty Acid ◽  
Glucose Uptake ◽  
Fatty Acid Oxidation ◽  
Acid Oxidation ◽  
Uptake Capacity ◽  
Impaired Fatty Acid

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

2020 ◽  
Author(s):  
Junichi Matsumoto ◽  
Shingo Takada ◽  
Takaaki Furihata ◽  
Hideo Nambu ◽  
Naoya Kakutani ◽  
...  
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Fatty Acid ◽  
Protein Kinase ◽  
Fatty Acid Oxidation ◽  
Exercise Capacity ◽  
Knockout Mice ◽  
Neurotrophic Factor ◽  
Adenosine Monophosphate ◽  
Acid Oxidation

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

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