| http://purl.uniprot.org/citations/31039008 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/31039008 | http://www.w3.org/2000/01/rdf-schema#comment | "Neurons uniquely antagonize fatty acid utilization by hydrolyzing the activated form of fatty acids, long chain acyl-CoAs, via the enzyme acyl-CoA thioesterase 7, Acot7. The loss of Acot7 results in increased fatty acid utilization in neurons and exaggerated stimulus-evoked behavior such as an increased startle response. To understand the contribution of Acot7 to seizure susceptibility, we generated Acot7 knockout (KO) mice and assayed their response to kainate-induced seizures. Acot7 KO mice exhibited potentiated behavioral and molecular indices of seizure severity following kainic acid administration, suggesting that fatty acid metabolism in neurons can be a critical regulator of neuronal activity. These data are consistent with the presentation of seizures in a human with genomic deletion of ACOT7 demonstrating the conservation of function across species. To further understand the metabolic complications arising from a deletion in Acot7, we subjected Acot7 KO mice to a high-fat diet. While the loss of Acot7 did not result in metabolic complications following a normal chow diet, a high-fat diet induced greater body weight gain, adiposity, and glucose intolerance in Acot7 KO mice. These data demonstrate that Acot7, a fatty acid metabolic enzyme highly enriched in neurons, regulates both brain-specific metabolic processes related to seizure susceptibility and the whole body response to dietary lipid."xsd:string |
| http://purl.uniprot.org/citations/31039008 | http://purl.org/dc/terms/identifier | "doi:10.1152/ajpendo.00537.2018"xsd:string |
| http://purl.uniprot.org/citations/31039008 | http://purl.uniprot.org/core/author | "Wolfgang M.J."xsd:string |
| http://purl.uniprot.org/citations/31039008 | http://purl.uniprot.org/core/author | "Ellis J.M."xsd:string |
| http://purl.uniprot.org/citations/31039008 | http://purl.uniprot.org/core/author | "Bowman C.E."xsd:string |
| http://purl.uniprot.org/citations/31039008 | http://purl.uniprot.org/core/author | "Selen Alpergin E.S."xsd:string |
| http://purl.uniprot.org/citations/31039008 | http://purl.uniprot.org/core/date | "2019"xsd:gYear |
| http://purl.uniprot.org/citations/31039008 | http://purl.uniprot.org/core/name | "Am J Physiol Endocrinol Metab"xsd:string |
| http://purl.uniprot.org/citations/31039008 | http://purl.uniprot.org/core/pages | "E941-E951"xsd:string |
| http://purl.uniprot.org/citations/31039008 | http://purl.uniprot.org/core/title | "Loss of ACOT7 potentiates seizures and metabolic dysfunction."xsd:string |
| http://purl.uniprot.org/citations/31039008 | http://purl.uniprot.org/core/volume | "317"xsd:string |
| http://purl.uniprot.org/citations/31039008 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/31039008 |
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