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Biochim Biophys Acta Mol Basis Dis. 2018 Jan;1864(1):24-33. doi: 10.1016/j.bbadis.2017.10.012. Epub 2017 Oct 7.

Short-term fructose ingestion affects the brain independently from establishment of metabolic syndrome.

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Department of Integrative Biology & Physiology, UCLA, Los Angeles, USA.
Department of Integrative Biology & Physiology, UCLA, Los Angeles, USA; Department of Neurosurgery, UCLA Brain Injury Research Center, Los Angeles, USA. Electronic address:


Chronic fructose ingestion is linked to the global epidemic of metabolic syndrome (MetS), and poses a serious threat to brain function. We asked whether a short period (one week) of fructose ingestion potentially insufficient to establish peripheral metabolic disorder could impact brain function. We report that the fructose treatment had no effect on liver/body weight ratio, weight gain, glucose tolerance and insulin sensitivity, was sufficient to reduce several aspects of hippocampal plasticity. Fructose consumption reduced the levels of the neuronal nuclear protein NeuN, Myelin Basic Protein, and the axonal growth-associated protein 43, concomitant with a decline in hippocampal weight. A reduction in peroxisome proliferator-activated receptor gamma coactivator-1 alpha and Cytochrome c oxidase subunit II by fructose treatment is indicative of mitochondrial dysfunction. Furthermore, the GLUT5 fructose transporter was increased in the hippocampus after fructose ingestion suggesting that fructose may facilitate its own transport to brain. Fructose elevated levels of ketohexokinase in the liver but did not affect SIRT1 levels, suggesting that fructose is metabolized in the liver, without severely affecting liver function commensurable to an absence of metabolic syndrome condition. These results advocate that a short period of fructose can influence brain plasticity without a major peripheral metabolic dysfunction.


Energy homeostasis; Fructose; Hippocampus; Mitochondria; Neurons; Plasticity

[Available on 2019-01-01]
[Indexed for MEDLINE]

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