Detection and alterations of acetylcarnitine (AC) in human liver by 1H MRS at 3T after supplementation with l-carnitine

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Detection and alterations of acetylcarnitine (AC) in human liver by 1H MRS at 3T after supplementation with l-carnitine

Dragana Savic, Ferenc E. Mózes, Peregrine G. Green, Matthew K. Burrage, Mette Skalshøi Kjær, Leanne Hodson, Stefan Neubauer, Michael Pavlides, Ladislav Valkovič

Abstract

Purpose

Acetylcarnitine can be assessed in vivo using proton MRS (1H-MRS) with long TEs and this has been previously applied successfully in muscle. The aim of this study was to evaluate a 1H-MRS technique for liver acetylcarnitine quantification in healthy humans before and after l-carnitine supplementation.

Method

Baseline acetylcarnitine levels were quantified using a STEAM sequence with prolonged TE in 15 healthy adults. Using STEAM with four different TEs was evaluated in phantoms. To assess reproducibility of the measurements, five of the participants had repeated 1H-MRS without receiving l-carnitine supplementation. To determine if liver acetylcarnitine could be changed after l-carnitine supplementation, acetylcarnitine was quantified 2 h after intravenous l-carnitine supplementation (50 mg/kg body weight) in the other 10 participants. Hepatic lipids were also quantified from the 1H-MRS spectra.

Results

There was good separation between the acetylcarnitine and fat in the phantoms using TE = 100 ms. Hepatic acetylcarnitine levels were reproducible (coefficient of reproducibility = 0.049%) and there was a significant (p < 0.001) increase in the relative abundance after a single supplementation of l-carnitine. Hepatic allylic, methyl, and methylene peaks were not altered by l-carnitine supplementation in healthy volunteers.

Conclusion

Our results demonstrate that our 1H-MRS technique could be used to measure acetylcarnitine in the liver and detect changes following intravenous supplementation in healthy adults despite the presence of lipids. Our techniques should be explored further in the study of fatty liver disease, where acetylcarnitine is suggested to be altered due to hepatic inflexibilities.