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| Research article summary (published 16 Aug 2009): |
Caffeine consumption attenuates neurochemical modifications in the hippocampus of streptozotocin-induced diabetic rats.
Full Abstract
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 vivo(1)H 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.
Author information
Author/s: Duarte, Joćo M N (JM); Carvalho, Rui A (RA); Cunha, Rodrigo A (RA); Gruetter, Rolf (R);
Affiliation: Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal. joao.duarte(-atsign-)epfl.ch
Journal and publication information
Publication Type: Journal Article; Research Support, Non-U.S. Gov't
Journal: Journal of neurochemistry (J Neurochem), published in England. (Language: eng)
Reference: 2009-Oct; vol 111 (issue 2) : pp 368-79
Dates: Created 2009/09/29; Completed 2009/10/22;
PMID: 19694901, status: MEDLINE (last retrieval date: 10/22/2009, IMS Date: )
Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.
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