Alterations in brain glucose utilization accompanying elevations in blood ethanol and acetate concentrations in the rat.

@article{Pawlosky2010AlterationsIB,
  title={Alterations in brain glucose utilization accompanying elevations in blood ethanol and acetate concentrations in the rat.},
  author={Robert J. Pawlosky and Yoshihiro Kashiwaya and Shireesh Srivastava and Michael Todd King and Calvin Crutchfield and N. D. Volkow and George Kunos and T K Li and Richard L. Veech},
  journal={Alcoholism, clinical and experimental research},
  year={2010},
  volume={34 2},
  pages={375-81}
}
BACKGROUND Previous studies in humans have shown that alcohol consumption decreased the rate of brain glucose utilization. We investigated whether the major metabolite of ethanol, acetate, could account for this observation by providing an alternate to glucose as an energy substrate for brain and the metabolic consequences of that shift. METHODS Rats were infused with solutions of sodium acetate, ethanol, or saline containing (13)C-2-glucose as a tracer elevating the blood ethanol (BEC) and… CONTINUE READING

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The co - ordinate decrease in free cytosolic NAD , oxidation of mitochondrial NAD and Q couples and the decrease in DeltaG ' of ATP was similar to administration of uncoupling agents indicating that the metabolism of acetate in brain caused the mitochondrial voltage dependent pore to form .
The co - ordinate decrease in free cytosolic NAD , oxidation of mitochondrial NAD and Q couples and the decrease in DeltaG ' of ATP was similar to administration of uncoupling agents indicating that the metabolism of acetate in brain caused the mitochondrial voltage dependent pore to form .
The co - ordinate decrease in free cytosolic NAD , oxidation of mitochondrial NAD and Q couples and the decrease in DeltaG ' of ATP was similar to administration of uncoupling agents indicating that the metabolism of acetate in brain caused the mitochondrial voltage dependent pore to form .
The co - ordinate decrease in free cytosolic NAD , oxidation of mitochondrial NAD and Q couples and the decrease in DeltaG ' of ATP was similar to administration of uncoupling agents indicating that the metabolism of acetate in brain caused the mitochondrial voltage dependent pore to form .
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