Authors: Shelton, J.¹; Wang, D.¹; Gupta, H.¹; Wyss, J. M.²; Oparil, S.¹; White, C. R.¹

Source: Diabetes, Obesity and Metabolism, Volume 5, Number 6, November 2003 , pp. 415-423(9)

Publisher: Wiley-Blackwell

Abstract:

Background: 

Restenosis after revascularization procedures is accelerated in persons with type 2 diabetes. Aim: 

The current study tested the hypothesis that the neointimal response to endovascular injury is enhanced in female obese Zucker (OZ) rats, a model of type 2 diabetes. Methods: 

Animals were randomized to receive either a standard diet (SD) or a diabetogenic diet (DD) for 6 weeks. Four weeks later, balloon injury of the right common carotid artery was induced. All rats were euthanized 2 weeks after injury. Lean Zucker (LZ) rats served as controls. Results: 

At the time of death, plasma glucose was elevated in OZ rats fed a SD (208 ± 13 mg/dl) and a DD (288 ± 21 mg/dl) compared to corresponding LZ rats (SD: 153 ± 8; DD: 132 ± 7 mg/dl). The ratio of high-density lipoprotein cholesterol (HDLc) to total cholesterol (Totc), an index of atherogenicity, was reduced in OZ rats on both diets (SD: 0.77 ± 0.06; DD: 0.80 ± 0.09) compared to LZ controls (SD: 1.11 ± 0.02; DD: 1.20 ± 0.05). Histomorphometric analysis of injured arteries showed that the intima to media (I : M) ratio was significantly increased in OZ (1.37 ± 0.07) compared to LZ (0.79 ± 0.08) rats. Elevations in plasma glucose and triglycerides (Tg) correlated positively and decreases in HDLc negatively with an increased I : M ratio. Administration of the DD did not further enhance the I : M ratio in LZ (0.87 ± 0.06) or OZ (1.29 ± 0.09) rats. Conclusions: 

These results suggest that neointima formation following endoluminal injury of the carotid artery is enhanced at an early stage in the development of diabetes mellitus.

Keywords: balloon injury; carotid artery; diabetes; hyperglycaemia; obesity; proliferation

Document Type: Research article

DOI: http://dx.doi.org/10.1046/j.1463-1326.2003.00296.x

Affiliations: 1: Departments of Medicine, Vascular Biology & Hypertension Program of the Division of Cardiovascular Disease, University of Alabama at Birmingham, Birmingham, AL, USA 2: Department of Cell Biology, University of Alabama at Birmingham, Birmingham, AL, USA

Publication date: 2003-11-01

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