Aside from the de novo synthesis of PC, two other potential mechanisms could contribute to PC accumulation: a decrease in the further metabolism of PC via CCT and an increase in the breakdown of PtdCho.
We attribute this to a lack of NE reuptake that results in both elevated NE in plasma and urine and a decrease in the intraneuronal metabolism of NE to DHPG.
After 24 hours of incubation with different concentrations (IC50 and two higher concentrations) of AH.FC.09 and AH.FEr.09, there was a decrease in the glycolytic metabolism of HCT-15 cells.
Examination of this pathway reveals three sources that could be responsible for increased PC following 17-AAG treatment: an increase in the de novo synthesis of PC from extracellular choline, a decrease in the further metabolism of PC via CCT, or an increase in the breakdown of PtdCho.
A linear relationship was observed between decrease in the photocurrent (the metabolism response) and the concentration to less than 60 mM of glucose (r=0.990).
As these changes coincided with the decrease in oxidative metabolism, the increase in MyHCIIX/IIB mRNA and induction of MyHCIIB mRNA, this would appear to contradict previous studies linking MyoD and myogenin mRNA expression with fibre type transitions in rats.
In a rat model of type II diabetes induced by high-fat feeding and streptozotocin injection, cardiac GLUT4 protein was reduced, likely contributing to the decrease in glucose metabolism in the diabetic heart [ 29].
In both groups receiving AS, there was an increase in metabolism in the MTC and MCC, and a decrease in metabolism in the cerebellum, compared with the MG.
Hepatic enzyme inhibition usually occurs because of competition at the enzyme site and results in a decrease in the rate of metabolism of the affected drug [ 10, 11].
A recent study using micro Positron Emission Tomography supports these findings, in that chronic mild stress induced a significant decrease in glucose metabolism in the IC, but not in the superior colliculus (visual mesencephalon) [ 67].
