ArticleCardiovascular diabetology2011
Left ventricular dysfunction with reduced functional cardiac reserve in diabetic and non-diabetic LDL-receptor deficient apolipoprotein B100-only mice.
Article in Cardiovascular diabetology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- In vivo inhibition of nuclear factor of activated T-cells leads to atherosclerotic plaque regression in IGF-II/LDLRDiabetes & vascular disease research · 2018Article
- Arterial Calcification in Diabetes Mellitus: Preclinical Models and Translational Implications.Arteriosclerosis, thrombosis, and vascular biology · 2017Review
- Type 2 diabetes enhances arterial uptake of choline in atherosclerotic mice: an imaging study with positron emission tomography tracer ¹⁸F-fluoromethylcholine.Cardiovascular diabetology · 2016Article
- Animal models of diabetic macrovascular complications: key players in the development of new therapeutic approaches.Journal of diabetes research · 2015Review
- Glibenclamide attenuates myocardial injury by lipopolysaccharides in streptozotocin-induced diabetic mice.Cardiovascular diabetology · 2014Article
- Promoting blood vessel growth in ischemic diseases: challenges in translating preclinical potential into clinical success.Disease models & mechanisms · 2013Review
- LDLR-/-ApoB100/100 mice with insulin-like growth factor II overexpression reveal a novel form of retinopathy with photoreceptor atrophy and altered morphology of the retina.Molecular vision · 2013Article
- The innovative medicines initiative: a public private partnership model to foster drug discovery.Computational and structural biotechnology journal · 2013Article
- Hyperglycemia in apolipoprotein E-deficient mouse strains with different atherosclerosis susceptibility.Cardiovascular diabetology · 2011Article
- Increased Calcific Aortic Valve Disease in response to a diabetogenic, procalcific diet in the LDLrCardiovascular pathology : the official journal of the Society for Cardiovascular PathologyArticle
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLack of suitable mouse models has hindered the studying of diabetic macrovascular complications. We examined the effects of type 2 diabetes on coronary artery disease and cardiac function in hypercholesterolemic low-density lipoprotein receptor-deficient apolipoprotein B100-only mice (LDLR-/-ApoB100/100). METHODS AND
results18-month-old LDLR-/-ApoB100/100 (n = 12), diabetic LDLR-/-ApoB100/100 mice overexpressing insulin-like growth factor-II (IGF-II) in pancreatic beta cells (IGF-II/LDLR-/-ApoB100/100, n = 14) and age-matched C57Bl/6 mice (n = 15) were studied after three months of high-fat Western diet. Compared to LDLR-/-ApoB100/100 mice, diabetic IGF-II/LDLR-/-ApoB100/100 mice demonstrated more calcified atherosclerotic lesions in aorta. However, compensatory vascular enlargement was similar in both diabetic and non-diabetic mice with equal atherosclerosis (cross-sectional lesion area ~60%) and consequently the lumen area was preserved. In coronary arteries, both hypercholesterolemic models showed significant stenosis (~80%) despite positive remodeling. Echocardiography revealed severe left ventricular systolic dysfunction and anteroapical akinesia in both LDLR-/-ApoB100/100 and IGF-II/LDLR-/-ApoB100/100 mice. Myocardial scarring was not detected, cardiac reserve after dobutamine challenge was preserved and ultrasructural changes revealed ischemic yet viable myocardium, which together with coronary artery stenosis and slightly impaired myocardial perfusion suggest myocardial hibernation resulting from chronic hypoperfusion.
conclusionsLDLR-/-ApoB100/100 mice develop significant coronary atherosclerosis, severe left ventricular dysfunction with preserved but diminished cardiac reserve and signs of chronic myocardial hibernation. However, the cardiac outcome is not worsened by type 2 diabetes, despite more advanced aortic atherosclerosis in diabetic animals.
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