Carnitine (3-hydroxy-4-trimethylaminobutyrate) is required for the transport of long chain fatty acids into the mitochondria for oxidation. Carnitine palmitoyltransferase (CPT) catalyses the removal of coenzyme A from the activated fatty acids and replaces it with carnitine. Carnitine then shuttles the fatty acid through the mitochondrial membrane, where it is then re-activated with coenzyme A. Malonyl-CoA inhibits CPT and this prevents the oxidation of newly synthesised fatty acids. Therefore in the anabolic state, CPT is inhibited and fatty acid synthesis occurs, but in the catabolic state the inhibition of CPT is removed and fatty acid oxidation and ketone production proceeds. Increased fatty acid turnover and non-alcoholic fatty liver disease (NAFLD) are associated with increased hepatic concentrations of carnitine in animals. In humans, obesity is characterised by increased fatty acid turnover and NAFLD and also appears to be associated with increased hepatic carnitine accumulation.
For example, researchers1 have investigated the carnitine concentration in the liver, abdominal muscle and blood of 14 morbidly obese women. The results showed that the liver and abdominal muscle tissue concentrations of carnitine were significantly higher in the obese women compared to normal-weight controls (around 60% higher). In addition, the authors reported an association between the liver and abdominal muscle carnitine concentrations. The majority of subjects had physiological changes to their livers that may have signified the development of NAFLD, supporting evidence from animal studies that show high liver carnitine with fatty liver. Other studies have shown that hepatocytes from obese individuals are roughly twice the size of non-obese subjects because of fat infiltration. Obesity therefore appears to increase liver carnitine in humans just as animal models suggest. However, the cause is not known but may signify metabolic dysfunction due to the development of fatty liver disease.
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