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dc.contributor.author | Hagensen, Mette K | |
dc.contributor.author | Mortensen, Martin B | |
dc.contributor.author | Kjolby, Mads | |
dc.contributor.author | Palmfeldt, Johan | |
dc.contributor.author | Bentzon, Jacob F | |
dc.contributor.author | Gregersen, Soeren | |
dc.date.accessioned | 2020-05-07T10:49:13Z | |
dc.date.available | 2020-05-07T10:49:13Z | |
dc.date.issued | 2019-07 | |
dc.identifier.citation | Atherosclerosis. 2019; 286:156-162 | es_ES |
dc.identifier.issn | 0021-9150 | es_ES |
dc.identifier.uri | http://hdl.handle.net/20.500.12105/9946 | |
dc.description.abstract | BACKGROUND AND AIMS: Type 1 diabetes accelerates the development of atherosclerotic cardiovascular diseases. Retention of low-density lipoprotein (LDL) in the arterial wall is a causal step in atherogenesis, but it is unknown whether diabetes alters the propensity of LDL for retention. The present study investigated whether LDL from type 1 diabetic and healthy non-diabetic subjects differed in their ability to bind to the arterial wall in a type 1 diabetic mouse model. METHODS: Fluorescently-labeled LDL obtained from type 1 diabetic patients or healthy controls was injected into mice with type 1 diabetes. The amount of retained LDL in the atherosclerosis-prone inner curvature of the aortic arch was quantified by fluorescence microscopy. Healthy control LDL was in vitro glycated, analyzed for protein glycation by LC-MS/MS, and tested for retention propensity. RESULTS: Retention of LDL from type 1 diabetic patients was 4.35-fold higher compared to LDL from nondiabetic subjects. Nuclear magnetic resonance (NMR) spectroscopy analysis of LDL revealed no differences in the concentration of the atherogenic small dense LDL between type 1 diabetic and non-diabetic subjects. In vitro glycation of LDL from a non-diabetic subject increased retention compared to non-glycated LDL. LC-MS/MS revealed four new glycated spots in the protein sequence of ApoB of in vitro glycated LDL. CONCLUSIONS: LDL from type 1 diabetic patients showed increased retention at atherosclerosis-prone sites in the arterial wall of diabetic mice. Glycation of LDL is one modification that may increase retention, but other, yet unknown, mechanisms are also likely to contribute. | es_ES |
dc.description.sponsorship | This work was supported by The Arvid Nilssons Foundation, Fonden til Laegevidenskabens Fremme, Snedkermester Sophus Jacobsen & Hustru Astrid Jacobsens Fond, Laegeforeningen, The Novo Nordisk Foundation, John and Birthe Meyer Foundation, The Danish Council for Independent Research (10-093408) and Danish Diabetes Academy. AGRADECIENTOS: | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | Elsevier | es_ES |
dc.type.hasVersion | AM | es_ES |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/4.0/ | * |
dc.subject | Atherosclerosis | es_ES |
dc.subject | Low density lipoprotein | es_ES |
dc.subject | Retention | es_ES |
dc.subject | Type 1 diabetes | es_ES |
dc.title | Increased retention of LDL from type 1 diabetic patients in atherosclerosis-prone areas of the murine arterial wall | es_ES |
dc.type | journal article | es_ES |
dc.rights.license | Attribution-NonCommercial-NoDerivatives 4.0 Internacional | * |
dc.identifier.pubmedID | 30871723 | es_ES |
dc.format.volume | 286 | es_ES |
dc.format.page | 156-162 | es_ES |
dc.identifier.doi | 10.1016/j.atherosclerosis.2019.02.027 | es_ES |
dc.embargo.terms | 2020-07-01 | es_ES |
dc.identifier.e-issn | 1879-1484 | es_ES |
dc.relation.publisherversion | https://doi.org/10.1016/j.atherosclerosis.2019.02.027 | es_ES |
dc.identifier.journal | Atherosclerosis | es_ES |
dc.repisalud.orgCNIC | CNIC::Grupos de investigación::Patología Experimental de la Aterosclerosis | es_ES |
dc.repisalud.institucion | CNIC | es_ES |
dc.rights.accessRights | open access | es_ES |