Brennen J. Dobberthien1, Anthony G. Tessier1,2, and Atiyah Yahya1,2
1Department of Oncology, University of Alberta, Edmonton, AB, Canada, 2Department of Medical Physics, Cross Cancer Institute, Edmonton, AB, Canada
Synopsis
Glutamate (Glu) incorporates 13C
label on its C4 carbon (13C4-Glu) following a 13C-labelled
glucose (Glc) infusion, resulting in a ≈2.51ppm proton “satellite” peak that provides
an indirect measure of 13C4-Glu. Quantification of the satellite peak is complicated
at short echo time (TE) due to overlap with the ≈2.49ppm N-acetylaspartate (NAA) peak. A PRESS, point resolved spectroscopy,
(TE1, TE2) combination of (20ms, 106ms) was found to be suitable
for resolving the ≈2.51ppm 13C4-Glu proton peak from that
of NAA at 9.4T by exploiting differences in J-coupling evolution. The efficacy
of the technique is verified on rat brain during a [U-13C6]-Glc
infusion.
Introduction
Indirect 13C magnetic
resonance spectroscopy (MRS) measures 13C signal through the coupled
protons, exploiting the higher 1H sensitivity. Following a 13C-labelled
glucose infusion, glutamate (Glu) incorporates 13C label on its C4
carbon (13C4-Glu), the time course of which provides a rate
for the tricarboxylic acid cycle.1 A 3T short echo time (TE) 1H
MRS point resolved spectroscopy (PRESS) sequence was used to measure 13C4-Glu
indirectly, without the need for a 13C channel.2 This was
achieved by measuring “satellite” peaks resulting from the ≈2.35
ppm 12C4-Glu proton resonance splitting into two
(separated by ≈127Hz) due to heteronuclear J-coupling. The technique employs
subtraction to eliminate overlapping signals. The field strength of 9.4T is
used for preclinical studies of animal models. At 9.4T, the 13C4-Glu
proton satellite peaks are at ≈2.19ppm and ≈2.51ppm. Their quantification is complex
at short TE due to the ≈2.49ppm N-acetylaspartate
(NAA) peak overlapping the ≈2.51ppm peak, and signals from the C3 Glu protons, N-acetylaspartylglutamate, 13C3-Glu,
13C2-GABA (γ-aminobutyric acid), and macromolecules
overlapping the ≈2.19ppm peak. In this work, we find, at 9.4T, an optimal PRESS
TE combination that retains sufficient ≈2.51ppm 13C4-Glu proton
signal while suppressing overlapping ≈2.49ppm NAA signal by exploiting
differences in J-coupling evolution. The ≈2.19ppm peak was not targeted for
optimization because it is obscured by more signals. The technique resolves the
≈2.51ppm resonance without the need for subtraction editing. The efficacy of
the optimized standard proton PRESS sequence is verified in vivo in rat brain during infusion of uniformly-labelled-13C-glucose
([U-13C6]-Glc).Methods
NAA, 13C4-Glu,
glutamine (Gln), and Glu proton response as a function of PRESS TE1
and TE2 (2:130 ms in steps of 2ms) were calculated numerically.3,4
Normalized peak areas were found by integrating the signal in the 2.45-2.55ppm
region and dividing it by the (TE1, TE2) of (2ms, 2ms)
value. An objective function was created by subtracting the normalized peak
area of NAA from that of 13C4-Glu.
Spectra were acquired with a 9.4T,
animal MRI scanner. A birdcage RF coil was used for phantoms while a surface
coil was employed for in vivo scans.
Phantom spectra were obtained from 50mM solutions of NAA, 99% enriched 13C4-Glu,
Gln, and Glu. In addition, spectra were acquired from a phantom containing NAA,
13C4-Glu, Gln, Glu, and GABA, with concentration ratios
found in vivo in rat brain.5
PRESS spectra were acquired with the determined optimal TE and with a short TE
of (12ms, 9ms). Peak areas in the 2.45-2.55ppm region were found by direct integration.
In vivo spectra were acquired in 256 averages with a repetition
time of 3 s from the brains of two Sprague-Dawley rats during an infusion of 99%
enriched [U-13C6]-Glc. Six spectra were obtained with the
determined long TE, one pre-infusion and others at time points indicated in
Figure 4 (times correspond to midpoint of acquisition). One (12ms, 9ms) short
TE spectrum was also acquired post infusion. In vivo spectra were fit with LCModel 6 with numerically
simulated basis sets.
Results
The optimal TE combination was
determined to be (20ms, 106ms), which yielded an objective function value of 0.811
(Figure 1) and simulated peak areas of 58.7% and -2% for 13C4-Glu
and NAA, respectively, relative to their corresponding (2ms, 2ms) values. Figure
2 demonstrates close agreement between calculated and experimentally acquired
spectra. Figure 3 shows significant contamination of the ≈2.51ppm 13C4-Glu
resonance from NAA and Gln in the short TE spectrum. The long TE spectrum shows
a simplified peak in the region. The short TE peak area of the mixed phantom in
the 2.45-2.55ppm spectral region was 176% higher than that of the phantom with
13C4-Glu alone. This value was reduced to 36% with the
determined long TE value (LCModel is relied upon to account for residual NAA
signal).
Figure 4 shows LCModel fitted brain
spectra from one of the rats during the 13C labelled glucose
infusion; a clear peak at ≈2.51ppm with the optimal TE is visible. Spectra
acquired throughout the experiment showed an increase in the 13C4-Glu
satellite peaks, along with a decrease in the ≈2.35ppm 12C-Glu peak.
Figure 5 shows short TE and optimal TE in
vivo spectra. The contamination of 13C4-Glu is
improved at the optimal TE, resulting in lower LCModel Cramér-Rao Lower Bounds
of 7% and 8% for the two rats (compared to 15% and 23% obtained at short TE).Conclusion
A PRESS (TE1, TE2)
combination of (20ms, 106ms) is suitable for resolving the ≈2.51ppm 13C4-Glu
proton peak from that of NAA at 9.4T. The technique can be used for quantifying
13C4-Glu in rat brain during a [U-13C6]-Glc
infusion.Acknowledgements
We gratefully acknowledge the Natural Sciences and Engineering Research Council of Canada (NSERC) for grant funding.References
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