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Type 1 diabetes increases retention of low-density lipoprotein in the atherosclerosis-prone area of the murine aorta.

Abstract：

BACKGROUND AND AIMS:Individuals with type 1 diabetes mellitus are at high risk of developing atherosclerotic cardiovascular disease, but the underlying mechanisms by which type 1 diabetes accelerates atherosclerosis remain unknown. Increased retention of low-density lipoprotein (LDL) in atherosclerosis-prone sites of the diabetic vascular wall has been suggested, but direct evidence is lacking. In the present study, we investigated whether retention of LDL is increased in atherosclerotic-prone areas using a murine model of type 1 diabetes. METHODS:Fluorescently-labeled human LDL from healthy non-diabetic individuals was injected into diabetic Ins2Akita mice and non-diabetic, wild-type littermates. The amount of retained LDL after 24 h was quantified by fluorescence microscopy of cryosections and by scans of en face preparations. Vascular gene expression in the inner curvature of the aortic arch was analyzed by microarray and quantitative polymerase chain reaction. RESULTS:LDL retention was readily detected in atherosclerosis-prone areas of the aortic arch being located in both intimal and medial layers. Quantitative microscopy revealed 8.1-fold more retained LDL in type 1 diabetic mice compared to wild-type mice. These findings were confirmed in independent experiments using near-infrared scanning of en face preparations of the aorta. Diabetic status did not affect arterial expression of genes known to be involved in LDL retention. CONCLUSIONS:Type 1 diabetes increases the ability of the vascular wall to retain LDL in mice. These changes could contribute to the increased atherosclerotic burden seen in type 1 diabetic patients.

journal_name

Atherosclerosis

journal_title

Atherosclerosis

authors

Hagensen MK,Mortensen MB,Kjolby M,Stillits NL,Steffensen LB,Bentzon JF

doi

10.1016/j.atherosclerosis.2017.05.019

subject

Has Abstract

pub_date

2017-08-01 00:00:00

pages

7-14

eissn

0021-9150

issn

1879-1484

pii

S0021-9150(17)30222-8

journal_volume

263

pub_type

杂志文章

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