Please use this identifier to cite or link to this item:
https://hdl.handle.net/10316/108381
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Rodrigues, Tiago | - |
dc.contributor.author | Matafome, Paulo N. | - |
dc.contributor.author | Sereno, José | - |
dc.contributor.author | Almeida, José | - |
dc.contributor.author | Castelhano, João | - |
dc.contributor.author | Gamas, Luís | - |
dc.contributor.author | Neves, Christian | - |
dc.contributor.author | Gonçalves, Sónia | - |
dc.contributor.author | Carvalho, Catarina | - |
dc.contributor.author | Arslanagic, Amina | - |
dc.contributor.author | Wilcken, Elinor | - |
dc.contributor.author | Fonseca, Rita | - |
dc.contributor.author | Simões, Ilda | - |
dc.contributor.author | Conde, Silvia Vilares | - |
dc.contributor.author | Castelo-Branco, Miguel | - |
dc.contributor.author | Seiça, Raquel | - |
dc.date.accessioned | 2023-08-28T09:31:26Z | - |
dc.date.available | 2023-08-28T09:31:26Z | - |
dc.date.issued | 2017-05-10 | - |
dc.identifier.issn | 2045-2322 | pt |
dc.identifier.uri | https://hdl.handle.net/10316/108381 | - |
dc.description.abstract | Microvascular dysfunction has been suggested to trigger adipose tissue dysfunction in obesity. This study investigates the hypothesis that glycation impairs microvascular architecture and expandability with an impact on insulin signalling. Animal models supplemented with methylglyoxal (MG), maintained with a high-fat diet (HFD) or both (HFDMG) were studied for periepididymal adipose (pEAT) tissue hypoxia and local and systemic insulin resistance. Dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) was used to quantify blood flow in vivo, showing MG-induced reduction of pEAT blood flow. Increased adipocyte size and leptin secretion were observed only in rats feeding the high-fat diet, without the development of hypoxia. In turn, hypoxia was only observed when MG was combined (HFDMG group), being associated with impaired activation of the insulin receptor (Tyr1163), glucose intolerance and systemic and muscle insulin resistance. Accordingly, the adipose tissue angiogenic assay has shown decreased capillarization after dose-dependent MG exposure and glyoxalase-1 inhibition. Thus, glycation impairs adipose tissue capillarization and blood flow, hampering its expandability during a high-fat diet challenge and leading to hypoxia and insulin resistance. Such events have systemic repercussions in glucose metabolism and may lead to the onset of unhealthy obesity and progression to type 2 diabetes. | pt |
dc.language.iso | eng | pt |
dc.publisher | Springer Nature | pt |
dc.relation | UID/NEU/04539/2013 | pt |
dc.relation | QREN- COMPETE (project DoIT – Diamarker: a consortium for the discovery of novel biomarker in diabetes), POCI-01-0145-FEDER-007440 | pt |
dc.relation | Faculty of Medicine, University of Coimbra | pt |
dc.relation | SFRH/BD/101172/2014 | pt |
dc.relation | SFRH/BPD/104881/2014 | pt |
dc.relation | Portuguese Society of Diabetology (Portuguese National Prize of Diabetes) | pt |
dc.rights | openAccess | pt |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/ | pt |
dc.subject.mesh | Adipose Tissue | pt |
dc.subject.mesh | Animals | pt |
dc.subject.mesh | Diet, High-Fat | pt |
dc.subject.mesh | Fasting | pt |
dc.subject.mesh | Fibrosis | pt |
dc.subject.mesh | Glycated Hemoglobin | pt |
dc.subject.mesh | Glycoconjugates | pt |
dc.subject.mesh | Glycosylation | pt |
dc.subject.mesh | Hypoxia | pt |
dc.subject.mesh | Insulin | pt |
dc.subject.mesh | Male | pt |
dc.subject.mesh | Muscle, Skeletal | pt |
dc.subject.mesh | Neovascularization, Physiologic | pt |
dc.subject.mesh | Obesity | pt |
dc.subject.mesh | Organ Size | pt |
dc.subject.mesh | Pyruvaldehyde | pt |
dc.subject.mesh | Rats, Wistar | pt |
dc.subject.mesh | Regional Blood Flow | pt |
dc.subject.mesh | Signal Transduction | pt |
dc.subject.mesh | Triglycerides | pt |
dc.subject.mesh | Insulin Resistance | pt |
dc.title | Methylglyoxal-induced glycation changes adipose tissue vascular architecture, flow and expansion, leading to insulin resistance | pt |
dc.type | article | - |
degois.publication.firstPage | 1698 | pt |
degois.publication.issue | 1 | pt |
degois.publication.title | Scientific Reports | pt |
dc.peerreviewed | yes | pt |
dc.identifier.doi | 10.1038/s41598-017-01730-3 | pt |
degois.publication.volume | 7 | pt |
dc.date.embargo | 2017-05-10 | * |
uc.date.periodoEmbargo | 0 | pt |
item.openairetype | article | - |
item.cerifentitytype | Publications | - |
item.languageiso639-1 | en | - |
item.fulltext | Com Texto completo | - |
item.grantfulltext | open | - |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
crisitem.author.researchunit | ICBR Coimbra Institute for Clinical and Biomedical Research | - |
crisitem.author.researchunit | CNC - Center for Neuroscience and Cell Biology | - |
crisitem.author.researchunit | CNC - Center for Neuroscience and Cell Biology | - |
crisitem.author.researchunit | CNC - Center for Neuroscience and Cell Biology | - |
crisitem.author.researchunit | CNC - Center for Neuroscience and Cell Biology | - |
crisitem.author.researchunit | CIBIT - Coimbra Institute for Biomedical Imaging and Translational Research | - |
crisitem.author.parentresearchunit | Faculty of Medicine | - |
crisitem.author.orcid | 0000-0002-1255-9667 | - |
crisitem.author.orcid | 0000-0002-3422-290X | - |
crisitem.author.orcid | 0000-0002-8996-1515 | - |
crisitem.author.orcid | 0000-0001-7133-6386 | - |
crisitem.author.orcid | 0000-0003-4364-6373 | - |
crisitem.author.orcid | 0000-0002-8378-0895 | - |
Appears in Collections: | I&D IBILI - Artigos em Revistas Internacionais I&D ICNAS - Artigos em Revistas Internacionais FMUC Medicina - Artigos em Revistas Internacionais I&D CNC - Artigos em Revistas Internacionais |
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