Caffeine consumption attenuates neurochemical modifications in the hippocampus of streptozotocin-induced diabetic rats
Version of Record online: 18 AUG 2009
© 2009 The Authors. Journal Compilation © 2009 International Society for Neurochemistry
Journal of Neurochemistry
Volume 111, Issue 2, pages 368–379, October 2009
How to Cite
Duarte, J. M. N., Carvalho, R. A., Cunha, R. A. and Gruetter, R. (2009), Caffeine consumption attenuates neurochemical modifications in the hippocampus of streptozotocin-induced diabetic rats. Journal of Neurochemistry, 111: 368–379. doi: 10.1111/j.1471-4159.2009.06349.x
- Issue online: 23 SEP 2009
- Version of Record online: 18 AUG 2009
- Received June 10, 2009; revised manuscript received July 16, 2009; accepted July 24, 2009.
Vol. 112, Issue 1, 319, Version of Record online: 29 OCT 2009
- nuclear magnetic resonance;
Type 1 diabetes can affect hippocampal function triggering cognitive impairment through unknown mechanisms. Caffeine consumption prevents hippocampal degeneration and memory dysfunction upon different insults and is also known to affect peripheral glucose metabolism. Thus we now characterized glucose transport and the neurochemical profile in the hippocampus of streptozotocin-induced diabetic rats using in vivo1H NMR spectroscopy and tested the effect of caffeine consumption thereupon. We found that hippocampal glucose content and transport were unaltered in diabetic rats, irrespective of caffeine consumption. However diabetic rats displayed alterations in their hippocampal neurochemical profile, which were normalized upon restoration of normoglycaemia, with the exception of myo-inositol that remained increased (36 ± 5%, p < 0.01 compared to controls) likely reflecting osmolarity deregulation. Compared to controls, caffeine-consuming diabetic rats displayed increased hippocampal levels of myo-inositol (15 ± 5%, p < 0.05) and taurine (23 ± 4%, p < 0.01), supporting the ability of caffeine to control osmoregulation. Compared to controls, the hippocampus of diabetic rats displayed a reduced density of synaptic proteins syntaxin, synaptophysin and synaptosome-associated protein of 25 kDa (in average 18 ± 1%, p < 0.05) as well increased glial fibrillary acidic protein (20 ± 5%, p < 0.05), suggesting synaptic degeneration and astrogliosis, which were prevented by caffeine consumption. In conclusion, neurochemical alterations in the hippocampus of diabetic rats are not related to defects of glucose transport but likely reflect osmoregulatory adaptations caused by hyperglycemia. Furthermore, caffeine consumption affected this neurochemical adaptation to high glucose levels, which may contribute to its potential neuroprotective effects, namely preventing synaptic degeneration and astrogliosis.