PMID- 17982895
OWN - NLM
STAT- MEDLINE
DCOM- 20071210
LR  - 20220409
IS  - 0303-6995 (Print)
IS  - 0303-6995 (Linking)
IP  - 72
DP  - 2007
TI  - Long-term abnormalities in brain glucose/energy metabolism after inhibition of 
      the neuronal insulin receptor: implication of tau-protein.
PG  - 195-202
AB  - The triplicate intracerebroventricular (icv) application of the diabetogenic 
      compound streptozotocin (STZ) in low dosage was used in 1-year-old male Wistar 
      rats to induce a damage of the neuronal insulin signal transduction (IST) system 
      and to investigate the activities of hexokinase (HK), phosphofructokinase (PFK), 
      glyceraldehyde-3-phosphate dehydrogenase (GDH), pyruvate kinase (PK), lactate 
      dehydrogenase (LDH) and alpha-ketoglutarate dehydrogenase (alpha-KGDH) in 
      frontoparietotemporal brain cortex (ct) and hippocampus (h) 9 weeks after damage. 
      In parallel, the concentrations of adenosine triphosphate (ATP), adenosine 
      diphosphate (ADP), guanosine triphosphate (GTP) and creatine phosphate (CrP) were 
      determined. We found reductions of HK to 53% (ct) and 60% (h) of control, PFK to 
      63/64% (ct/h); GDH to 56/61% (ct/h), PFK to 57/59% (ct/h), alpha-KGDH to 37/35% 
      (ct/h) and an increase of LDH to 300/240% (ct/h). ATP decreased to 82/87% (ct/h) 
      of control, GTP to 69/81% (ct/h), CrP to 82/81% (ct/h), approximately P to 82/82% 
      (ct/h), whereas ADP increased to 189/154% (ct/h). The fall of the activities of 
      the glycolytic enzymes HK, PFK, GDH and PK was found to be more marked after 9 
      weeks of damage when compared with 3- and 6-week damage whereas the diminution in 
      the concentration of energy rich compound was stably reduced by between 20 and 
      10% relative to control. The abnormalities in glucose/energy metabolism were 
      discussed in relation to tau-protein mismetabolism of experimental animals, and 
      of sporadic AD.
FAU - Hoyer, S
AU  - Hoyer S
AD  - Institute of Pathology, University of Heidelberg, Heidelberg, Germany. 
      siegfried_hoyer@med.uni-heidelberg.de
FAU - Lannert, H
AU  - Lannert H
LA  - eng
PT  - Journal Article
PL  - Austria
TA  - J Neural Transm Suppl
JT  - Journal of neural transmission. Supplementum
JID - 0425126
RN  - 0 (Blood Glucose)
RN  - 020IUV4N33 (Phosphocreatine)
RN  - 5W494URQ81 (Streptozocin)
RN  - 61D2G4IYVH (Adenosine Diphosphate)
RN  - 86-01-1 (Guanosine Triphosphate)
RN  - 8L70Q75FXE (Adenosine Triphosphate)
RN  - EC 1.1.1.27 (L-Lactate Dehydrogenase)
RN  - EC 1.2.1.9 (Glyceraldehyde 3-Phosphate Dehydrogenase (NADP+))
RN  - EC 1.2.4.2 (Ketoglutarate Dehydrogenase Complex)
RN  - EC 2.7.1 - (Phosphofructokinases)
RN  - EC 2.7.1.1 (Hexokinase)
RN  - EC 2.7.1.40 (Pyruvate Kinase)
RN  - EC 2.7.10.1 (Receptor, Insulin)
SB  - IM
MH  - Adenosine Diphosphate/metabolism
MH  - Adenosine Triphosphate/metabolism
MH  - Animals
MH  - Blood Glucose/*metabolism
MH  - Brain/*drug effects/enzymology
MH  - Cerebral Cortex/drug effects/enzymology
MH  - Energy Metabolism/*drug effects
MH  - Glyceraldehyde 3-Phosphate Dehydrogenase (NADP+)/metabolism
MH  - Guanosine Triphosphate/metabolism
MH  - Hexokinase/metabolism
MH  - Hippocampus/drug effects/enzymology
MH  - Ketoglutarate Dehydrogenase Complex/metabolism
MH  - L-Lactate Dehydrogenase/metabolism
MH  - Male
MH  - Neurons/drug effects
MH  - Phosphocreatine/metabolism
MH  - Phosphofructokinases/metabolism
MH  - Pyruvate Kinase/metabolism
MH  - Rats
MH  - Rats, Wistar
MH  - Receptor, Insulin/*antagonists & inhibitors
MH  - Signal Transduction/*drug effects
MH  - Streptozocin/*pharmacology
MH  - Time Factors
EDAT- 2007/11/07 09:00
MHDA- 2007/12/11 09:00
CRDT- 2007/11/07 09:00
PHST- 2007/11/07 09:00 [pubmed]
PHST- 2007/12/11 09:00 [medline]
PHST- 2007/11/07 09:00 [entrez]
AID - 10.1007/978-3-211-73574-9_25 [doi]
PST - ppublish
SO  - J Neural Transm Suppl. 2007;(72):195-202. doi: 10.1007/978-3-211-73574-9_25.