Alterations in glucose metabolism on cognition: A possible link between diabetes and dementia

The use of the carbohydrate glucose as an energetic source is essential for an adequate function of the human body. The complex regulation of this molecule involves the coordinated action of various organs such as pancreas, liver and brain. Any disruption of this physiological balance may result in...

Full description

Autores:
Tipo de recurso:
Fecha de publicación:
2016
Institución:
Universidad del Rosario
Repositorio:
Repositorio EdocUR - U. Rosario
Idioma:
eng
OAI Identifier:
oai:repository.urosario.edu.co:10336/26673
Acceso en línea:
https://doi.org/10.2174/1381612822666151209152013
https://repository.urosario.edu.co/handle/10336/26673
Palabra clave:
Diabetes
Alzheimer Disease
Dementia
Insulin resistance
Antidiabetic drugs
Rights
License
Restringido (Acceso a grupos específicos)
id EDOCUR2_745381f6c91426ea0c3d541af6529623
oai_identifier_str oai:repository.urosario.edu.co:10336/26673
network_acronym_str EDOCUR2
network_name_str Repositorio EdocUR - U. Rosario
repository_id_str
spelling 799427726007caa7b58-f3f2-44b1-8bd1-894c2ae24046-1c4e0e11b-1bf6-4831-a478-a2269f284892-1756df063-3b80-4568-a1b7-e90dcd52fcca-12020-08-19T14:40:01Z2020-08-19T14:40:01Z2016-02-01The use of the carbohydrate glucose as an energetic source is essential for an adequate function of the human body. The complex regulation of this molecule involves the coordinated action of various organs such as pancreas, liver and brain. Any disruption of this physiological balance may result in a dangerous compromise of general metabolic activities increasing the possibility of developing T1DM, T2DM and possibly AD. Astrocytes convert glucose into lactate and transfer it to neurons. This lactate is essential for neuronal metabolism and for various processes including the formation of synapses, dendrites and the expression of genes involved in memory. The brain is highly susceptible to variations in glucose blood levels, and both hypoglycemia and hyperglycemia can be dangerous. Pathological hyperglycemia induces changes in plasmatic osmotic pressure, mitochondrial production of free radicals, oxidative stress and activation of neuronal apoptosis, among others. Both AD and diabetes are chronic diseases having age as an important risk factor. As the brain ages, it seems to become much more susceptible to cellular damage induced by excess of circulating glucose and this could explain the appearance of cognitive changes observed in some patients with diabetes. Excessive circulation of pro-inflammatory agents has been observed in insulin resistance and is likely that some of these mediators may cross the bloodbrain barrier and induce abnormal neuroinflammation. GSK-3 is overexpressed in diabetes and also has been reported to regulate tau phosphorylation and production of A? peptides in the brain. Currently, diabetes (hyperglycemia) is considered as a risk factor for the development of AD. A novel therapeutic approach, using intranasal insulin and anti-diabetic medications in patients suffering from AD is being explored and is discussed in this review.application/pdfhttps://doi.org/10.2174/1381612822666151209152013ISSN: 1381-6128EISSN: 1873-4286https://repository.urosario.edu.co/handle/10336/26673engBentham Science818No. 7812Current Pharmaceutical DesignVol. 22Current Pharmaceutical Design, ISSN:1381-6128;EISSN:1873-4286, Vol.22, No.7 (2016); pp. 812 - 818https://benthamscience.com/journals/current-pharmaceutical-design/volume/22/issue/7/page/812/Restringido (Acceso a grupos específicos)http://purl.org/coar/access_right/c_16ecCurrent Pharmaceutical Designinstname:Universidad del Rosarioreponame:Repositorio Institucional EdocURDiabetesAlzheimer DiseaseDementiaInsulin resistanceAntidiabetic drugsAlterations in glucose metabolism on cognition: A possible link between diabetes and dementiaAlteraciones en el metabolismo de la glucosa en la cognición: un posible vínculo entre la diabetes y la demenciaarticleArtículohttp://purl.org/coar/version/c_970fb48d4fbd8a85http://purl.org/coar/resource_type/c_6501González Reyes, Rodrigo EstebanAliev, GjumrakchAvila-Rodrigues, MarcoBarreto, George E.10336/26673oai:repository.urosario.edu.co:10336/266732021-06-03 00:49:57.255https://repository.urosario.edu.coRepositorio institucional EdocURedocur@urosario.edu.co
dc.title.spa.fl_str_mv Alterations in glucose metabolism on cognition: A possible link between diabetes and dementia
dc.title.TranslatedTitle.spa.fl_str_mv Alteraciones en el metabolismo de la glucosa en la cognición: un posible vínculo entre la diabetes y la demencia
title Alterations in glucose metabolism on cognition: A possible link between diabetes and dementia
spellingShingle Alterations in glucose metabolism on cognition: A possible link between diabetes and dementia
Diabetes
Alzheimer Disease
Dementia
Insulin resistance
Antidiabetic drugs
title_short Alterations in glucose metabolism on cognition: A possible link between diabetes and dementia
title_full Alterations in glucose metabolism on cognition: A possible link between diabetes and dementia
title_fullStr Alterations in glucose metabolism on cognition: A possible link between diabetes and dementia
title_full_unstemmed Alterations in glucose metabolism on cognition: A possible link between diabetes and dementia
title_sort Alterations in glucose metabolism on cognition: A possible link between diabetes and dementia
dc.subject.keyword.spa.fl_str_mv Diabetes
Alzheimer Disease
Dementia
Insulin resistance
Antidiabetic drugs
topic Diabetes
Alzheimer Disease
Dementia
Insulin resistance
Antidiabetic drugs
description The use of the carbohydrate glucose as an energetic source is essential for an adequate function of the human body. The complex regulation of this molecule involves the coordinated action of various organs such as pancreas, liver and brain. Any disruption of this physiological balance may result in a dangerous compromise of general metabolic activities increasing the possibility of developing T1DM, T2DM and possibly AD. Astrocytes convert glucose into lactate and transfer it to neurons. This lactate is essential for neuronal metabolism and for various processes including the formation of synapses, dendrites and the expression of genes involved in memory. The brain is highly susceptible to variations in glucose blood levels, and both hypoglycemia and hyperglycemia can be dangerous. Pathological hyperglycemia induces changes in plasmatic osmotic pressure, mitochondrial production of free radicals, oxidative stress and activation of neuronal apoptosis, among others. Both AD and diabetes are chronic diseases having age as an important risk factor. As the brain ages, it seems to become much more susceptible to cellular damage induced by excess of circulating glucose and this could explain the appearance of cognitive changes observed in some patients with diabetes. Excessive circulation of pro-inflammatory agents has been observed in insulin resistance and is likely that some of these mediators may cross the bloodbrain barrier and induce abnormal neuroinflammation. GSK-3 is overexpressed in diabetes and also has been reported to regulate tau phosphorylation and production of A? peptides in the brain. Currently, diabetes (hyperglycemia) is considered as a risk factor for the development of AD. A novel therapeutic approach, using intranasal insulin and anti-diabetic medications in patients suffering from AD is being explored and is discussed in this review.
publishDate 2016
dc.date.created.spa.fl_str_mv 2016-02-01
dc.date.accessioned.none.fl_str_mv 2020-08-19T14:40:01Z
dc.date.available.none.fl_str_mv 2020-08-19T14:40:01Z
dc.type.eng.fl_str_mv article
dc.type.coarversion.fl_str_mv http://purl.org/coar/version/c_970fb48d4fbd8a85
dc.type.coar.fl_str_mv http://purl.org/coar/resource_type/c_6501
dc.type.spa.spa.fl_str_mv Artículo
dc.identifier.doi.none.fl_str_mv https://doi.org/10.2174/1381612822666151209152013
dc.identifier.issn.none.fl_str_mv ISSN: 1381-6128
EISSN: 1873-4286
dc.identifier.uri.none.fl_str_mv https://repository.urosario.edu.co/handle/10336/26673
url https://doi.org/10.2174/1381612822666151209152013
https://repository.urosario.edu.co/handle/10336/26673
identifier_str_mv ISSN: 1381-6128
EISSN: 1873-4286
dc.language.iso.spa.fl_str_mv eng
language eng
dc.relation.citationEndPage.none.fl_str_mv 818
dc.relation.citationIssue.none.fl_str_mv No. 7
dc.relation.citationStartPage.none.fl_str_mv 812
dc.relation.citationTitle.none.fl_str_mv Current Pharmaceutical Design
dc.relation.citationVolume.none.fl_str_mv Vol. 22
dc.relation.ispartof.spa.fl_str_mv Current Pharmaceutical Design, ISSN:1381-6128;EISSN:1873-4286, Vol.22, No.7 (2016); pp. 812 - 818
dc.relation.uri.spa.fl_str_mv https://benthamscience.com/journals/current-pharmaceutical-design/volume/22/issue/7/page/812/
dc.rights.coar.fl_str_mv http://purl.org/coar/access_right/c_16ec
dc.rights.acceso.spa.fl_str_mv Restringido (Acceso a grupos específicos)
rights_invalid_str_mv Restringido (Acceso a grupos específicos)
http://purl.org/coar/access_right/c_16ec
dc.format.mimetype.none.fl_str_mv application/pdf
dc.publisher.spa.fl_str_mv Bentham Science
dc.source.spa.fl_str_mv Current Pharmaceutical Design
institution Universidad del Rosario
dc.source.instname.none.fl_str_mv instname:Universidad del Rosario
dc.source.reponame.none.fl_str_mv reponame:Repositorio Institucional EdocUR
repository.name.fl_str_mv Repositorio institucional EdocUR
repository.mail.fl_str_mv edocur@urosario.edu.co
_version_ 1814167713436663808