High-fructose intake as risk factor for neurodegeneration: Key role for carboxy methyllysine accumulation in mice hippocampal neurons
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- 作者：Raffaella Mastrocolaa ; raffaella.mastrocola@unito.it" class="auth_mail" title="E-mail the corresponding author ; Debora Nigroa ; Alessia S. Centoa ; Fausto Chiazzab ; Massimo Collinob ; Manuela Aragnoa
- 关键词：AGEs ; advanced glycation end products ; CML ; carboxy methyllysine ; DHE ; dihydroethidium ; GFAP ; glial fibrillary acidic protein ; Glo-1 ; glyoxalase-1 ; GLUT-5 ; fructose transporter-5 ; GSH ; reduced glutathione ; GSSG ; oxidized glutathione ; Keap1 ; Kelch-Like ECH-Associated Protein 1 ; KHK ; ketohesokinase ; MnSOD ; manganese superoxide dismutase ; NFkB ; nuclear factor-kappa B ; Nrf2 ; nuclear factor erythroid 2-related factor 2 ; RAGE ; receptor for AGE ; ROS ; reactive oxygen species
- 刊名：Neurobiology of Disease
- 出版年：2016
- 出版时间：May 2016
- 年：2016
- 卷：89
- 期：Complete
- 页码：65-75
- 全文大小：2089 K
文摘
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High-fructose intake induces early signs of neurodegeneration in hippocampus.
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Fructose intake generates CML accumulation in mouse hippocampal neurons.
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Fructose-derived CML is involved in mitochondrial impairment and oxidative stress.
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Oxidative stress impairs CML-detoxifying activity of Glo-1.
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Inhibition of CML by pyridoxamine prevents gliosis and neuronal alterations.