Purpose To determine whether neurochemical concentrations obtained at two MRI sites using clinical 3T scanners can be pooled when a highly optimized, nonvendor short‐echo, single‐voxel proton MRS pulse sequence is used in conjunction with identical calibration and quantification procedures. Methods A modified semi‐LASER sequence (T_E = 28 ms) was used to acquire spectra from two brain regions (cerebellar vermis and pons) on two Siemens 3T scanners using the same B₀ and B₁ calibration protocols from two different cohorts of healthy volunteers (N = 24–33 per site) matched for age and body mass index. Spectra were quantified with LCModel using water scaling. Results The spectral quality was very consistent between the two sites and allowed reliable quantification of at least 13 metabolites in the vermis and pons compared with 3–5 metabolites in prior multisite magnetic resonance spectroscopy trials using vendor‐provided sequences. The neurochemical profiles were nearly identical at the two sites and showed the feasibility to detect interindividual differences in the healthy brain. Conclusion Highly reproducible neurochemical profiles can be obtained on different clinical 3T scanners at different sites, provided that the same, optimized acquisition and analysis techniques are used. This will allow pooling of multisite data in clinical studies, which is particularly critical for rare neurological diseases. Magn Reson Med 73:1718–1725, 2015.

Acetate, a glial‐specific substrate, is an attractive alternative to glucose for the study of neuronal‐glial interactions. The present study investigates the kinetics of acetate uptake and utilization in the rat brainin vivoduring infusion of [2‐¹³C]acetate using NMR spectroscopy. When plasma acetate concentration was increased, the rate of brain acetate utilization (CMR_ace) increased progressively and reached close to saturation for plasma acetate concentration > 2–3 mM, whereas brain acetate concentration continued to increase. The Michaelis–Menten constant for brain acetate utilization ( = 0.01 ± 0.14 mM) was much smaller than for acetate transport through the blood–brain barrier (BBB) ( = 4.18 ± 0.83 mM). The maximum transport capacity of acetate through the BBB ( = 0.96 ± 0.18 μmol/g/min) was nearly twofold higher than the maximum rate of brain acetate utilization ( = 0.50 ± 0.08 μmol/g/min). We conclude that, under our experimental conditions, brain acetate utilization is saturated when plasma acetate concentrations increase above 2–3 mM. At such high plasma acetate concentration, the rate‐limiting step for glial acetate metabolism is not the BBB, but occurs after entry of acetate into the brain.