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dc.contributor.authorMorris, G
dc.contributor.authorMaes, M
dc.contributor.authorBerk, M
dc.contributor.authorCarvalho, AF
dc.contributor.authorPuri, BK
dc.date.accessioned2020-11-26T22:48:11Z
dc.date.available2020-11-26T22:48:11Z
dc.date.issued2020-01-01
dc.identifierpii: S0924933819000130
dc.identifier.citationMorris, G., Maes, M., Berk, M., Carvalho, A. F. & Puri, B. K. (2020). Nutritional ketosis as an intervention to relieve astrogliosis: Possible therapeutic applications in the treatment of neurodegenerative and neuroprogressive disorders. EUROPEAN PSYCHIATRY, 63 (1), https://doi.org/10.1192/j.eurpsy.2019.13.
dc.identifier.issn0924-9338
dc.identifier.urihttp://hdl.handle.net/11343/251996
dc.description.abstractNutritional ketosis, induced via either the classical ketogenic diet or the use of emulsified medium-chain triglycerides, is an established treatment for pharmaceutical resistant epilepsy in children and more recently in adults. In addition, the use of oral ketogenic compounds, fractionated coconut oil, very low carbohydrate intake, or ketone monoester supplementation has been reported to be potentially helpful in mild cognitive impairment, Parkinson's disease, schizophrenia, bipolar disorder, and autistic spectrum disorder. In these and other neurodegenerative and neuroprogressive disorders, there are detrimental effects of oxidative stress, mitochondrial dysfunction, and neuroinflammation on neuronal function. However, they also adversely impact on neurone-glia interactions, disrupting the role of microglia and astrocytes in central nervous system (CNS) homeostasis. Astrocytes are the main site of CNS fatty acid oxidation; the resulting ketone bodies constitute an important source of oxidative fuel for neurones in an environment of glucose restriction. Importantly, the lactate shuttle between astrocytes and neurones is dependent on glycogenolysis and glycolysis, resulting from the fact that the astrocytic filopodia responsible for lactate release are too narrow to accommodate mitochondria. The entry into the CNS of ketone bodies and fatty acids, as a result of nutritional ketosis, has effects on the astrocytic glutamate-glutamine cycle, glutamate synthase activity, and on the function of vesicular glutamate transporters, EAAT, Na+, K+-ATPase, Kir4.1, aquaporin-4, Cx34 and KATP channels, as well as on astrogliosis. These mechanisms are detailed and it is suggested that they would tend to mitigate the changes seen in many neurodegenerative and neuroprogressive disorders. Hence, it is hypothesized that nutritional ketosis may have therapeutic applications in such disorders.
dc.languageEnglish
dc.publisherCAMBRIDGE UNIV PRESS
dc.rights.urihttps://creativecommons.org/licenses/by/4.0
dc.titleNutritional ketosis as an intervention to relieve astrogliosis: Possible therapeutic applications in the treatment of neurodegenerative and neuroprogressive disorders
dc.typeJournal Article
dc.identifier.doi10.1192/j.eurpsy.2019.13
melbourne.affiliation.departmentPsychiatry
melbourne.source.titleEuropean Psychiatry
melbourne.source.volume63
melbourne.source.issue1
dc.rights.licensecc-by
melbourne.elementsid1439006
melbourne.contributor.authorBerk, Michael
dc.identifier.eissn1778-3585
melbourne.accessrightsOpen Access


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