scholarly journals Skeletal Muscle-Specific Keap1 Disruption Modulates Fatty Acid Utilization and Enhances Exercise Capacity in Female Mice

Redox Biology ◽  
2021 ◽  
pp. 101966
Author(s):  
Takahiro Onoki ◽  
Yoshihiro Izumi ◽  
Masatomo Takahashi ◽  
Shohei Murakami ◽  
Daisuke Matsumaru ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acid ◽  
Exercise Capacity ◽  
Fatty Acid Utilization ◽  
Female Mice

AMPKα is critical for enhancing skeletal muscle fatty acid utilization during in vivo exercise in mice

2015 ◽  
Vol 29 (5) ◽  
pp. 1725-1738 ◽  
Author(s):  
Joachim Fentz ◽  
Rasmus Kjøbsted ◽  
Jesper B. Birk ◽  
Andreas B. Jordy ◽  
Jacob Jeppesen ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acid ◽  
Fatty Acid Utilization

scholarly journals Enhanced Muscle Strength in Dyslipidemic Mice and Its Relation to Increased Capacity for Fatty Acid Oxidation

2021 ◽  
Vol 22 (22) ◽  
pp. 12251
Author(s):  
Marta Tomczyk ◽  
Alicja Braczko ◽  
Patrycja Jablonska ◽  
Adriana Mika ◽  
Kamil Przyborowski ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acid ◽  
Muscle Strength ◽  
Fatty Acid Oxidation ◽  
Exercise Capacity ◽  
Citrate Synthase ◽  
Adenine Nucleotides ◽  
Acid Oxidation ◽  
Skeletal Muscle Function ◽  
Knock Out

Dyslipidemia is commonly linked to skeletal muscle dysfunction, accumulation of intramyocellular lipids, and insulin resistance. However, our previous research indicated that dyslipidemia in apolipoprotein E and low-density lipoprotein receptor double knock-out mice (ApoE/LDLR -/-) leads to improvement of exercise capacity. This study aimed to investigate in detail skeletal muscle function and metabolism in these dyslipidemic mice. We found that ApoE/LDLR -/- mice showed an increased grip strength as well as increased troponins, and Mhc2 levels in skeletal muscle. It was accompanied by the increased skeletal muscle mitochondria numbers (judged by increased citrate synthase activity) and elevated total adenine nucleotides pool. We noted increased triglycerides contents in skeletal muscles and increased serum free fatty acids (FFA) levels in ApoE/LDLR -/- mice. Importantly, Ranolazine mediated inhibition of FFA oxidation in ApoE/LDLR -/- mice led to the reduction of exercise capacity and total adenine nucleotides pool. Thus, this study demonstrated that increased capacity for fatty acid oxidation, an adaptive response to dyslipidemia leads to improved cellular energetics that translates to increased skeletal muscle strength and contributes to increased exercise capacity in ApoE/LDLR -/- mice.

Altered carnitine metabolism in spontaneously hypertensive rats

1985 ◽  
Vol 249 (2) ◽  
pp. E183-E186 ◽  
Author(s):  
K. A. Foster ◽  
B. O'Rourke ◽  
D. K. Reibel
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acid ◽  
Spontaneously Hypertensive Rats ◽  
Elevated Serum ◽  
Total Serum ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Fatty Acid Utilization ◽  
Carnitine Metabolism ◽  
Wistar Kyoto

Carnitine metabolism was examined in spontaneously hypertensive rats (SHR). Carnitine levels were elevated by 25% in hypertrophied hearts of 10- and 15-wk-old SHR when compared with Wistar-Kyoto (WKy) controls. This elevation was associated with a greater than 25% increase in total serum carnitine. The elevated serum carnitine does not appear to be due to increased mobilization from skeletal muscle because carnitine levels were elevated by 25% in gastrocnemius and diaphragm of SHR. Elevated serum carnitine is also not a result of reduced urinary excretion because daily urinary carnitine output was increased by 150% in SHR. These findings suggest that the most likely mechanism for increased serum carnitine is increased carnitine synthesis by the liver. The changes in carnitine metabolism in SHR appear to occur between 5 and 10 wk of age, because the carnitine levels in serum and organs were comparable in 5-wk-old WKy and SHR. The observed alterations in tissue and serum carnitine levels may result in altered fatty acid utilization in SHR.

Cytoplasmic fatty acid-binding protein facilitates fatty acid utilization by skeletal muscle

2003 ◽  
Vol 178 (4) ◽  
pp. 367-371 ◽  
Author(s):  
J. F. C. Glatz ◽  
F. G. Schaap ◽  
B. Binas ◽  
A. Bonen ◽  
G. J. Van Der Vusse ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acid ◽  
Fatty Acid Binding Protein ◽  
Binding Protein ◽  
Fatty Acid Binding ◽  
Fatty Acid Utilization ◽  
Acid Binding Protein

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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