We are analyzing https://link.springer.com/article/10.1186/1471-2091-13-23.

Title:
Metabolomic profiling reveals a role for CPT1c in neuronal oxidative metabolism | BMC Biochemistry
Description:
Background Carnitine Palmitoyltransferase-1c (CPT1c) is a neuron specific homologue of the carnitine acyltransferase family of enzymes. CPT1 isoenzymes transfer long chain acyl groups to carnitine. This constitutes a rate setting step for mitochondrial fatty acid beta-oxidation by facilitating the initial step in acyl transfer to the mitochondrial matrix. In general, neurons do not heavily utilize fatty acids for bioenergetic needs and definitive enzymatic activity has been unable to be demonstrated for CPT1c. Although there are studies suggesting an enzymatic role of CPT1c, its role in neurochemistry remains elusive. Results In order to better understand how CPT1c functions in neural metabolism, we performed unbiased metabolomic profiling on wild-type (WT) and CPT1c knockout (KO) mouse brains. Consistent with the notion that CPT1c is not involved in fatty acid beta-oxidation, there were no changes in metabolites associated with fatty acid oxidation. Endocannabinoids were suppressed in the CPT1c KO, which may explain the suppression of food intake seen in CPT1c KO mice. Although products of beta-oxidation were unchanged, small changes in carnitine and carnitine metabolites were observed. Finally, we observed changes in redox homeostasis including a greater than 2-fold increase in oxidized glutathione. This indicates that CPT1c may play a role in neural oxidative metabolism. Conclusions Steady-state metabolomic analysis of CPT1c WT and KO mouse brains identified a small number of metabolites that differed between CPT1c WT and KO mice. The subtle changes in a broad range of metabolites in vivo indicate that CPT1c does not play a significant or required role in fatty acid oxidation; however, it could play an alternative role in neuronal oxidative metabolism.
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Keywords {🔍}

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Topics {✒️}

brain-specific carnitine palmitoyl-transferase-1c long chain acyl-coa full size image fatty acid beta-oxidation carnitine palmitoyltransferase-1c gain short-term food deprivation article download pdf anti-rabbit horseradish peroxidase fatty acid biochemistry brain-specific carnitine palmitoyltransferase gamma-glutamyl redox cycle medium-chain acyl-coa gas chromatography/mass spectrometry regulate food intake regulates food intake malonyl-coa insensitive cpt2 fatty acid catabolism mouse monoclonal anti-hsc70 exhibited diet-induced obesity fatty acid oxidation central orexigenic drive metabolomic profiling reveals brain-expressed protein related fatty acid metabolism oxidative stress-induced apoptosis full access acyl chain back suppressing food intake identified stress-induced manner neurochemistry remains elusive neuronal oxidative metabolism elevated oxidative demands article lee suppressed food intake regulating food intake privacy choices/manage cookies redox biochemistry consistent steady-state biochemicals oxidize fatty acids redox homeostasis including tissue-specific manner related subjects facilitate acyl transfer authors’ original file facilitate beta-oxidation high fat diet high-fat diet [10] steady-state metabolites biochemical pathways altered wolfgang mj

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         headline:Metabolomic profiling reveals a role for CPT1c in neuronal oxidative metabolism
         description:Carnitine Palmitoyltransferase-1c (CPT1c) is a neuron specific homologue of the carnitine acyltransferase family of enzymes. CPT1 isoenzymes transfer long chain acyl groups to carnitine. This constitutes a rate setting step for mitochondrial fatty acid beta-oxidation by facilitating the initial step in acyl transfer to the mitochondrial matrix. In general, neurons do not heavily utilize fatty acids for bioenergetic needs and definitive enzymatic activity has been unable to be demonstrated for CPT1c. Although there are studies suggesting an enzymatic role of CPT1c, its role in neurochemistry remains elusive. In order to better understand how CPT1c functions in neural metabolism, we performed unbiased metabolomic profiling on wild-type (WT) and CPT1c knockout (KO) mouse brains. Consistent with the notion that CPT1c is not involved in fatty acid beta-oxidation, there were no changes in metabolites associated with fatty acid oxidation. Endocannabinoids were suppressed in the CPT1c KO, which may explain the suppression of food intake seen in CPT1c KO mice. Although products of beta-oxidation were unchanged, small changes in carnitine and carnitine metabolites were observed. Finally, we observed changes in redox homeostasis including a greater than 2-fold increase in oxidized glutathione. This indicates that CPT1c may play a role in neural oxidative metabolism. Steady-state metabolomic analysis of CPT1c WT and KO mouse brains identified a small number of metabolites that differed between CPT1c WT and KO mice. The subtle changes in a broad range of metabolites in vivo indicate that CPT1c does not play a significant or required role in fatty acid oxidation; however, it could play an alternative role in neuronal oxidative metabolism.
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      headline:Metabolomic profiling reveals a role for CPT1c in neuronal oxidative metabolism
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         Fatty Acid Oxidation
         Free Carnitine
         Regulate Food Intake
         Suppress Food Intake
         Biochemistry
         general
         Life Sciences
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