scholarly journals Cold tolerance of UCP1-ablated mice: A skeletal muscle mitochondria switch toward lipid oxidation with marked UCP3 up-regulation not associated with increased basal, fatty acid- or ROS-induced uncoupling or enhanced GDP effects

2010 ◽  
Vol 1797 (6-7) ◽  
pp. 968-980 ◽  
Author(s):  
Irina G. Shabalina ◽  
Joris Hoeks ◽  
Tatiana V. Kramarova ◽  
Patrick Schrauwen ◽  
Barbara Cannon ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acid ◽  
Lipid Oxidation ◽  
Cold Tolerance ◽  
Muscle Mitochondria ◽  
Skeletal Muscle Mitochondria

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

scholarly journals Associations of Mitochondrial Fatty Acid Oxidation with Body Fat in Premenopausal Women

2017 ◽  
Vol 2017 ◽  
pp. 1-7
Author(s):  
Jonathan L. Warren ◽  
Barbara A. Gower ◽  
Gary R. Hunter ◽  
Samuel T. Windham ◽  
Douglas R. Moellering ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acid ◽  
Body Fat ◽  
Fat Mass ◽  
Premenopausal Women ◽  
Muscle Mitochondria ◽  
Skeletal Muscle Mitochondria ◽  
Total Body Fat ◽  
Total Fat ◽  
Total Body

Higherin vivofatty acid (FA) oxidation rates have been reported in obese individuals compared to lean counterparts; however whether this reflects a shift in substrate-specific oxidative capacity at the level of the skeletal muscle mitochondria has not been examined. The purpose of this study was to test the hypothesis that in situ measures of skeletal muscle mitochondria FA oxidation would be positively associated with total body fat. Participants were 38 premenopausal women (BMI=26.5±4.3 kg/m2). Total and regional fat were assessed by dual-energy X-ray absorptiometry (DXA). Mitochondrial FA oxidation was assessed in permeabilized myofibers using high-resolution respirometry and a palmitoyl carnitine substrate. We found positive associations of total fat mass with State 3 (ADP-stimulated respiration) (r=0.379,p<0.05) and the respiratory control ratio (RCR, measure of mitochondrial coupling) (r=0.348,p<0.05). When participants were dichotomized by high or low body fat percent, participants with high total body fat displayed a higher RCR compared to those with low body fat (p<0.05). There were no associations between any measure of regional fat and mitochondrial FA oxidation independent of total fat mass. In conclusion, greater FA oxidation in obesity may reflect molecular processes that enhance FA oxidation capacity at the mitochondrial level.

scholarly journals Long-Chain Fatty Acid Combustion Rate Is Associated with Unique Metabolite Profiles in Skeletal Muscle Mitochondria

PLoS ONE ◽  
2010 ◽  
Vol 5 (3) ◽  
pp. e9834 ◽  
Author(s):  
Erin L. Seifert ◽  
Oliver Fiehn ◽  
Véronic Bezaire ◽  
David R. Bickel ◽  
Gert Wohlgemuth ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acid ◽  
Combustion Rate ◽  
Chain Fatty Acid ◽  
Long Chain Fatty Acid ◽  
Muscle Mitochondria ◽  
Skeletal Muscle Mitochondria ◽  
Metabolite Profiles ◽  
Long Chain

scholarly journals Cold Tolerance in Hypothyroid Rabbits: Role of Skeletal Muscle Mitochondria and Sarcoplasmic Reticulum Ca2+ ATPase Isoform 1 Heat Production

Endocrinology ◽  
2008 ◽  
Vol 149 (12) ◽  
pp. 6262-6271 ◽  
Author(s):  
Ana Paula Arruda ◽  
Luisa A. Ketzer ◽  
Mariana Nigro ◽  
Antonio Galina ◽  
Denise P. Carvalho ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Sarcoplasmic Reticulum ◽  
Cold Acclimation ◽  
Cold Tolerance ◽  
Heat Production ◽  
Cold Exposure ◽  
Muscle Enzymes ◽  
Muscle Mitochondria ◽  
Skeletal Muscle Mitochondria ◽  
Brown Adipose

Brown adipose tissue (BAT) is involved in rat and mice thermoregulation, and heat produced by BAT depends on the concerted action of thyroid hormones and catecholamines. Little is known about cold-induced thermogenesis in mammals that have little or no BAT, such as rabbits. In these animals, thermogenesis primarily occurs in skeletal muscle. In this work, we have studied the effect of cold acclimation (4 C for 10 d) in normal and hypothyroid rabbits. It is known that hypothyroid rats die after a few hours of cold exposure. We now show that, different from rats, hypothyroid rabbits sustain their body temperature and survive after 10 d cold exposure. When compared with rabbits kept at room temperature, the muscles of cold-exposed rabbits showed a dark red color characteristic of oxidative muscle fibers. According to this pattern, we observed that in both normal and hypothyroid rabbits, cold exposure promotes an increase in oxygen consumption by skeletal muscle mitochondria. Moreover, in red muscle, cold acclimation induces an increase in the expression and activity of sarcoplasmic reticulum Ca2+ ATPase isoform 1 (SERCA1), one of the muscle enzymes involved in heat production. We conclude that rabbit cold tolerance is probably related to increased muscle oxidative metabolism and heat production by SERCA1 and that these changes are not completely dependent on normal thyroid function.

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