Acyl-CoA metabolism and partitioning
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Acyl-CoA metabolism and partitioning. / Grevengoed, Trisha J; Klett, Eric L; Coleman, Rosalind A.
I: Annual Review of Nutrition, Bind 34, 2014, s. 1-30.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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TY - JOUR
T1 - Acyl-CoA metabolism and partitioning
AU - Grevengoed, Trisha J
AU - Klett, Eric L
AU - Coleman, Rosalind A
PY - 2014
Y1 - 2014
N2 - Long-chain fatty acyl-coenzyme As (CoAs) are critical regulatory molecules and metabolic intermediates. The initial step in their synthesis is the activation of fatty acids by one of 13 long-chain acyl-CoA synthetase isoforms. These isoforms are regulated independently and have different tissue expression patterns and subcellular locations. Their acyl-CoA products regulate metabolic enzymes and signaling pathways, become oxidized to provide cellular energy, and are incorporated into acylated proteins and complex lipids such as triacylglycerol, phospholipids, and cholesterol esters. Their differing metabolic fates are determined by a network of proteins that channel the acyl-CoAs toward or away from specific metabolic pathways and serve as the basis for partitioning. This review evaluates the evidence for acyl-CoA partitioning by reviewing experimental data on proteins that are believed to contribute to acyl-CoA channeling, the metabolic consequences of loss of these proteins, and the potential role of maladaptive acyl-CoA partitioning in the pathogenesis of metabolic disease and carcinogenesis.
AB - Long-chain fatty acyl-coenzyme As (CoAs) are critical regulatory molecules and metabolic intermediates. The initial step in their synthesis is the activation of fatty acids by one of 13 long-chain acyl-CoA synthetase isoforms. These isoforms are regulated independently and have different tissue expression patterns and subcellular locations. Their acyl-CoA products regulate metabolic enzymes and signaling pathways, become oxidized to provide cellular energy, and are incorporated into acylated proteins and complex lipids such as triacylglycerol, phospholipids, and cholesterol esters. Their differing metabolic fates are determined by a network of proteins that channel the acyl-CoAs toward or away from specific metabolic pathways and serve as the basis for partitioning. This review evaluates the evidence for acyl-CoA partitioning by reviewing experimental data on proteins that are believed to contribute to acyl-CoA channeling, the metabolic consequences of loss of these proteins, and the potential role of maladaptive acyl-CoA partitioning in the pathogenesis of metabolic disease and carcinogenesis.
KW - Acyl Coenzyme A
KW - Animals
KW - Cell Membrane
KW - Coenzyme A Ligases
KW - Endoplasmic Reticulum
KW - Fatty Acid Transport Proteins
KW - Gene Expression Regulation
KW - Humans
KW - Lipid Metabolism
KW - Models, Biological
KW - Protein Isoforms
KW - Protein Transport
U2 - 10.1146/annurev-nutr-071813-105541
DO - 10.1146/annurev-nutr-071813-105541
M3 - Journal article
C2 - 24819326
VL - 34
SP - 1
EP - 30
JO - Annual Review of Nutrition
JF - Annual Review of Nutrition
SN - 0199-9885
ER -
ID: 146698774