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Acyl-CoA

About: Acyl-CoA is a research topic. Over the lifetime, 527 publications have been published within this topic receiving 25134 citations. The topic is also known as: Acyl Coenzyme A.


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Journal ArticleDOI
TL;DR: This review will focus on the human and mouse peroxisomal ACOT and acyltransferase enzymes identified to date and discuss their cellular localizations, emerging structural information and functions as auxiliary enzymes in peroxISomal metabolic pathways.

144 citations

Journal ArticleDOI
TL;DR: Altered fatty acid metabolism and the accumulation of triacylglycerol and lipid metabolites has been strongly associated with insulin resistance and diabetes, but it appears that converting fatty acids to acyl-CoAs and downstream metabolic intermediates increases cellular fatty acid uptake, probably by limiting efflux.
Abstract: Purpose of reviewThe aim of this review is to highlight the importance of fatty acid metabolism as a major determinant in fatty acid uptake. In particular, we emphasize how the activation, intracellular transport and downstream metabolism of fatty acids influence their uptake into cells.Recent findi

143 citations

Journal ArticleDOI
W Lysiak1, K. Lilly1, F DiLisa1, P P Toth1, Loran L. Bieber1 
TL;DR: It is demonstrated that carnitine can modulate the aliphatic short-chain acyl-CoA/CoA ratio in heart and liver mitochondria and indicate that the degree of modulation varies with theAliphatic acyl moiety.

140 citations

Journal ArticleDOI
TL;DR: Evidence suggests that cytosolic accumulation of this active form of lipid in muscle can lead to impaired insulin signaling, impaired enzyme activity, and insulin resistance, either directly or by conversion to other lipid intermediates that alter the activity of key kinases and phosphatases.
Abstract: A common observation in animal models and in humans is that accumulation of muscle triglyceride is associated with the development of insulin resistance. In animals, this is true of genetic models of obesity and nutritional models of insulin resistance generated by high-fat feeding, infusion of lipid, or infusion of glucose. Although there is a strong link between the accumulation of triglycerides (TG) in muscle and insulin resistance, it is unlikely that TG are directly involved in the generation of muscle insulin resistance. There are now other plausible mechanistic links between muscle lipid metabolites and insulin resistance, in addition to the classic substrate competition proposed by Randle's glucose-fatty acid cycle. The first step in fatty acid metabolism (oxidation or storage) is activation to the long-chain fatty acyl CoA (LCACoA). This review covers the evidence suggesting that cytosolic accumulation of this active form of lipid in muscle can lead to impaired insulin signaling, impaired enzyme activity, and insulin resistance, either directly or by conversion to other lipid intermediates that alter the activity of key kinases and phosphatases. Actions of fatty acids to bind specific nuclear transcription factors provide another mechanism whereby different lipids could influence metabolism.

139 citations

Journal ArticleDOI
TL;DR: The following effects of fatty acids and acyl-CoA thioesters on energy metabolism of mitochondria can now be assumed: inhibition of adenine nucleotide translocation, increased permeability to monovalent cations, and substrate effect.
Abstract: The following effects of fatty acids and acyl-CoA thioesters on energy metabolism of mitochondria can now be assumed: (1) Inhibition of adenine nucleotide translocation. This effect may increase the energy state of mitochondria respiring under state 3 conditions and decrease phosphorylation potential in the surrounding medium (the cytoplasm). (2) Increased permeability to monovalent cations. This may lead to a partial energy dissipation due to a futile recycling of K+ (or another cation), namely and energy-dependent uptake and a passive outflow. (3) True uncoupling due to increased permeability to protons. This effect probably occurs at high concentrations of fatty acids only. (4) Substrate effect. Fatty acids in the form of acyl-CoA are excellent respiratory substrates for mitochondria of most tissues. Their oxidation is coupled to the generation of high energy state of the mitochondrial membrane and, consequently, to ATP synthesis.

137 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
20232
202212
20218
20205
20193
20185