Caffeine consumption attenuates neurochemical modifications in the hippocampus of streptozotocin-induced diabetic rats

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Caffeine consumption attenuates neurochemical modifications in the hippocampus of streptozotocin-induced diabetic rats. / Duarte, João M N; Carvalho, Rui A.; Cunha, Rodrigo A; Gruetter, Rolf.

In: Journal of Neurochemistry, Vol. 111, No. 2, 10.2009, p. 368-79.

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T1 - Caffeine consumption attenuates neurochemical modifications in the hippocampus of streptozotocin-induced diabetic rats

AU - Duarte,João M N

AU - Carvalho,Rui A.

AU - Cunha,Rodrigo A

AU - Gruetter,Rolf

PY - 2009/10

Y1 - 2009/10

N2 - 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.

AB - 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.

KW - Animals

KW - Blood Glucose

KW - Caffeine

KW - Central Nervous System Stimulants

KW - Chronic Disease

KW - Diabetes Mellitus, Experimental

KW - Gliosis

KW - Hippocampus

KW - Inositol

KW - Magnetic Resonance Spectroscopy

KW - Male

KW - Models, Biological

KW - Nerve Degeneration

KW - Rats

KW - Rats, Sprague-Dawley

KW - Synapses

KW - Taurine

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

U2 - 10.1111/j.1471-4159.2009.06349.x

DO - 10.1111/j.1471-4159.2009.06349.x

M3 - Article

VL - 111

SP - 368

EP - 379

JO - Journal of Neurochemistry

T2 - Journal of Neurochemistry

JF - Journal of Neurochemistry

SN - 1471-4159

IS - 2

ER -