ArticleThe Biochemical journal2012
Identification of a novel malonyl-CoA IC(50) for CPT-I: implications for predicting in vivo fatty acid oxidation rates.
Article in The Biochemical journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 38 citations in OpenAlex.
- Skeletal muscle carnitine loading increases energy expenditure, modulates fuel metabolism gene networks and prevents body fat accumulation in humans.The Journal of physiology · 2013Trial
- Bioenergetic profiles and respiratory control in mitochondrial physiology: Precision analysis of oxidative phosphorylation.Experimental physiology · 2026Article
- Isotope Labeling and Biochemical Assessment of Liver-Triacylglycerol in Patients with Different Levels of Histologically-Graded Liver Disease.The Journal of nutrition · 2023Article
- Knockdown of carnitine palmitoyltransferase I (CPT1) reduces fat body lipid mobilization and resistance to starvation in the insect vectorFrontiers in physiology · 2023Article
- Insights into the development of insulin resistance: Unraveling the interaction of physical inactivity, lipid metabolism and mitochondrial biology.Frontiers in physiology · 2023Review
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- Acute insulin deprivation results in altered mitochondrial substrate sensitivity conducive to greater fatty acid transport.American journal of physiology. Endocrinology and metabolism · 2020Article
- Review
- Exercise Metabolism: Fuels for the Fire.Cold Spring Harbor perspectives in medicine · 2018Review
- Regulation of Muscle Glycogen Metabolism during Exercise: Implications for Endurance Performance and Training Adaptations.Nutrients · 2018Review
- Salsalate (Salicylate) Uncouples Mitochondria, Improves Glucose Homeostasis, and Reduces Liver Lipids Independent of AMPK-β1.Diabetes · 2016 · on this mapArticle
- Article
- Skeletal muscle ACC2 S212 phosphorylation is not required for the control of fatty acid oxidation during exercise.Physiological reports · 2015Article
- Impairments in mitochondrial palmitoyl-CoA respiratory kinetics that precede development of diabetic cardiomyopathy are prevented by resveratrol in ZDF rats.The Journal of physiology · 2014Article
- New insights into the interaction of carbohydrate and fat metabolism during exercise.Sports medicine (Auckland, N.Z.) · 2014Review
- Matrix revisited: mechanisms linking energy substrate metabolism to the function of the heart.Circulation research · 2014Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Published values regarding the sensitivity (IC(50)) of CPT-I (carnitine palmitoyltransferase I) to M-CoA (malonyl-CoA) inhibition in isolated mitochondria are inconsistent with predicted in vivo rates of fatty acid oxidation. Therefore we have re-examined M-CoA inhibition kinetics under various P-CoA (palmitoyl-CoA) concentrations in both isolated mitochondria and PMFs (permeabilized muscle fibres). PMFs have an 18-fold higher IC(50) (0.61 compared with 0.034 μM) in the presence of 25 μM P-CoA and a 13-fold higher IC(50) (6.3 compared with 0.49 μM) in the presence of 150 μM P-CoA compared with isolated mitochondria. M-CoA inhibition kinetics determined in PMFs predicts that CPT-I activity is inhibited by 33% in resting muscle compared with >95% in isolated mitochondria. Additionally, the ability of M-CoA to inhibit CPT-I appears to be dependent on P-CoA concentration, as the relative inhibitory capacity of M-CoA is decreased with increasing P-CoA concentrations. Altogether, the use of PMFs appears to provide an M-CoA IC(50) that better reflects the predicted in vivo rates of fatty acid oxidation. These findings also demonstrate that the ratio of [P-CoA]/[M-CoA] is critical for regulating CPT-I activity and may partially rectify the in vivo disconnect between M-CoA content and CPT-I flux within the context of exercise and Type 2 diabetes.
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