Showing papers by "Robin A. de Graaf published in 2009"
TL;DR: High-field B0 shimming of the brain, specifically within small rodents and humans is focused, and B0 field perturbations within the brain are particularly prominent near the air-tissue interfaces at the sinus and auditory cavities.
69 citations
TL;DR: When combined with pre‐FBMI infusion of 13C‐labeled substrates, like [1‐13C]‐glucose, the technique can generate maps of metabolic fluxes, like the tricarboxylic acid and glutamate‐glutamine neurotransmitter cycle fluxes at an unprecedented spatial resolution.
Abstract: The rapid elevation in rat brain temperature achieveable with focused beam microwave irradiation (FBMI) leads to a permanent inactivation of enzymes, thereby minimizing enzyme-dependent post-mortem metabolic changes. An additional characteristic of FBMI is that the NMR properties of the tissue are close to those of the in vivo condition and remain so for at least 12 h. These features create an opportunity to develop magnetic resonance spectroscopy and imaging on microwave-irradiated samples into a technique with a resolution, coverage and sensitivity superior to any experiment performed directly in vivo. Furthermore, when combined with pre-FBMI infusion of (13)C-labeled substrates, like [1-(13)C]-glucose, the technique can generate maps of metabolic fluxes, like the tricarboxylic acid and glutamate-glutamine neurotransmitter cycle fluxes at an unprecedented spatial resolution.
40 citations
TL;DR: It is suggested that after antecedent hypoglycemia, glucose utilization is increased at euglycemia and decreased after acute hypoglyCEmia, which was not the case in controls.
Abstract: OBJECTIVE The objective of this study was to characterize the changes in brain metabolism caused by antecedent recurrent hypoglycemia under euglycemic and hypoglycemic conditions in a rat model and to test the hypothesis that recurrent hypoglycemia changes the brain's capacity to utilize different energy substrates.
RESEARCH DESIGN AND METHODS Rats exposed to recurrent insulin-induced hypoglycemia for 3 days (3dRH rats) and untreated controls were subject to the following protocols: [2-13C]acetate infusion under euglycemic conditions ( n = 8), [1-13C]glucose and unlabeled acetate coinfusion under euglycemic conditions ( n = 8), and [2-13C]acetate infusion during a hyperinsulinemic-hypoglycemic clamp ( n = 8). In vivo nuclear magnetic resonance spectroscopy was used to monitor the rise of13C-labeling in brain metabolites for the calculation of brain metabolic fluxes using a neuron-astrocyte model.
RESULTS At euglycemia, antecedent recurrent hypoglycemia increased whole-brain glucose metabolism by 43 ± 4% ( P < 0.01 vs. controls), largely due to higher glucose utilization in neurons. Although acetate metabolism remained the same, control and 3dRH animals showed a distinctly different response to acute hypoglycemia: controls decreased pyruvate dehydrogenase (PDH) flux in astrocytes by 64 ± 20% ( P = 0.01), whereas it increased by 37 ± 3% in neurons ( P = 0.01). The 3dRH animals decreased PDH flux in both compartments (−75 ± 20% in astrocytes, P < 0.001, and −36 ± 4% in neurons, P = 0.005). Thus, acute hypoglycemia reduced total brain tricarboxylic acid cycle activity in 3dRH animals (−37 ± 4%, P = 0.001), but not in controls.
CONCLUSIONS Our findings suggest that after antecedent hypoglycemia, glucose utilization is increased at euglycemia and decreased after acute hypoglycemia, which was not the case in controls. These findings may help to identify better methods of preserving brain function and reducing injury during acute hypoglycemia.
40 citations