Background/Aims: In type 1 diabetes (T1D), type 2 diabetes (T2D) and metabolic syndrome (MetS), the associated complex metabolomic changes in the involvement of carnitine metabolism in total carnitine ester level has already been documented; here we extended the investigations to the individual acylcarnitines. Methods: The fasting serum acylcarnitine concentrations were determined in 49 T1D, 38 T2D and 38 MetS patients and 40 controls by isotope dilution electrospray ionization tandem mass spectrometry. Results: The acylcarnitine profiles of the 3patient groups shared elements with the controls. Considerably higher levels of almost all short-chain acylcarnitines (p < 0.05) and lower levels of some long-chain acylcarnitines were detected in T2D and MetS patients. The amounts of C3 and C4 carnitine were higher and most of the medium-chain and long-chain acylcarnitine levels were lower (p < 0.05) in T1D and MetS patients than in the controls. In T1D and T2D, the levels of C3 and C4 acylcarnitines were markedly elevated and some long-chain acylcarnitines were lower than the controls (p < 0.05). Moreover, significantly lower concentrations of free- and total carnitine were observed in T1D patients (p < 0.05). Conclusions: Profound alterations were detected in acylcarnitine profiles in the 3 patient groups. Similarities in the patterns suggest different degrees of involvement of the same metabolic systems in a systems biology approach.

A simple method is described for the measurement of free brain glutamine by spectrophotometric means, without prior separation by either paper or column chromatography. Through the application of this method, it was also possible to obtain an approximate value for the combined concentrations of glutamic acid, 7-aminobutyric acid and glutathione in brain.

Abstract— In this work we have studied the effect of afferent electrical stimulation (AES) of the contralateral brachial plexus on the release of glutamine and glutamate from the cat's brain into the cerebral venous blood, at rest and during continuous infusion of L‐glutamine and sucrose solutions. (1) In the resting state, before stimulation, there was a net outflow of glutamine from the brain into the cerebral venous blood, but no release of glutamic acid. (2) AES caused release of glutamate and increased 3.5‐fold the release of glutamine. The increase in release of glutamine and glutamate was found to be reversed very shortly after stimulation. (3) Steady intravenous infusion of a 0.3 M‐gluta‐mine solution for 10 min changed the negative arterio‐venous difference in glutamine to a positive one and increased the content in brain by 15×20%. In this case AES caused a singificant drop, to zero of the glutamine arterio‐venous difference. (4) At the onset of pentamethylenetetrazole (PTZ) seizures, like AES, there was a significant reduction of the level of glutamine in the cats’cerebral cortex. This reduction vanished when the animals were infused with L‐glutamine solution but not with 0.3 M‐sucrose solution that was used as an inert electrolyte. (5) The kinetic behaviour of the glutamine transport is compatible with a carrier‐mediated process, but not with passive diffusion.

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