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Endurance training in obese humans improves glucose tolerance and mitochondrial fatty acid oxidation and alters muscle lipid content.
TLDR
The improved capacity for mitochondrial FA uptake and oxidation leads not only to a reduction in muscle lipid content but also a to change in the saturation status of lipids, which may, at least in part, provide a mechanism for the enhanced insulin action observed with endurance training in obese individuals. Expand
Is membrane transport of FFA mediated by lipid, protein, or both? Mechanisms and regulation of protein-mediated cellular fatty acid uptake: molecular, biochemical, and physiological evidence.
TLDR
This poster presents a probabilistic procedure to assess the response of the immune system to chemotherapy and its applications in the context of central nervous system disorders. Expand
Two phases of palmitate-induced insulin resistance in skeletal muscle: impaired GLUT4 translocation is followed by a reduced GLUT4 intrinsic activity.
We examined, in soleus muscle, the effects of prolonged palmitate exposure (0, 6, 12, 18 h) on insulin-stimulated glucose transport, intramuscular lipid accumulation and oxidation, activation ofExpand
Enhanced sarcolemmal FAT/CD36 content and triacylglycerol storage in cardiac myocytes from obese zucker rats.
TLDR
Cardiac myocytes from obese Zucker rats, a permanent relocation of FAT/CD36 to the sarcolemma is responsible for myocardial TAG accumulation, and these cardiac myocytes, although sensitive to contraction-like stimulation, were completely insensitive to insulin. Expand
Regulation of fatty acid transport by fatty acid translocase/CD36
TLDR
It is found that within minutes of beginning muscle contraction or being exposed to insulin FA transport is increased, and this increase is a result of the contraction- and insulin-induced translocation of FAT/CD36 from an intracellular depot to the cell surface. Expand
Greater Transport Efficiencies of the Membrane Fatty Acid Transporters FAT/CD36 and FATP4 Compared with FABPpm and FATP1 and Differential Effects on Fatty Acid Esterification and Oxidation in Rat
TLDR
In vivo, FAT/CD36 and FATP4 are the most effective fatty acid transporters, whereas FABPpm and FAT/ CD36 are key for stimulating fatty acids to oxidation and/or esterification and Fatty acid transporters failed to alter the rates of fatty acid esterization into triacylglycerols. Expand
Increased levels of peroxisome proliferator-activated receptor gamma, coactivator 1 alpha (PGC-1α) improve lipid utilisation, insulin signalling and glucose transport in skeletal muscle of lean and
TLDR
Increases in PGC-1α levels, similar to those that can be induced by physiological stimuli, altered intramuscular lipids and improved fatty acid oxidation, insulin signalling and insulin-stimulated glucose transport, are found, albeit to different extents in lean and diabetes-resistant muscle. Expand
Omega‐3 supplementation alters mitochondrial membrane composition and respiration kinetics in human skeletal muscle
TLDR
It is demonstrated that omega‐3 supplementation improves mitochondrial ADP kinetics, suggesting post‐translational modification of existing proteins. Expand
Additive effects of insulin and muscle contraction on fatty acid transport and fatty acid transporters, FAT/CD36, FABPpm, FATP1, 4 and 6
TLDR
Insulin and muscle contraction increase fatty acid transport into muscle by inducing the translocation of FAT/CD36 and FATP1 and whether these effects are additive, and whether other fatty acid transporters are also induced to translocate. Expand
In Vivo, Fatty Acid Translocase (CD36) Critically Regulates Skeletal Muscle Fuel Selection, Exercise Performance, and Training-induced Adaptation of Fatty Acid Oxidation*
TLDR
CD36 contributes to regulating fatty acid oxidation and adaptation in a mitochondrion-independent manner and has a key role in muscle fuel selection, exercise performance, and training-induced muscle FAO adaptation, challenging long held views of mechanisms involved in acute and adaptive regulation of Muscle FAO. Expand
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