ArticleJournal of lipid research2013
Diabetic atherosclerosis in APOE*4 mice: synergy between lipoprotein metabolism and vascular inflammation.
Article in Journal of lipid research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- Steady solution and its stability of a mathematical model of diabetic atherosclerosis.Journal of biological dynamics · 2023Article
- WELL-POSEDNESS OF A MATHEMATICAL MODEL OF DIABETIC ATHEROSCLEROSIS.Journal of mathematical analysis and applications · 2022Article
- WELL-POSEDNESS OF A MATHEMATICAL MODEL OF DIABETIC ATHEROSCLEROSIS WITH ADVANCED GLYCATION END-PRODUCTS.Applicable analysis · 2022Article
- Article
- ApoE and cerebral insulin: Trafficking, receptors, and resistance.Neurobiology of disease · 2020Review
- Apolipoprotein E4 mediates insulin resistance-associated cerebrovascular dysfunction and the post-prandial response.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2019Article
- Inflammation: Bridging Age, Menopause and APOEε4 Genotype to Alzheimer's Disease.Frontiers in aging neuroscience · 2018Review
- Cellular and Molecular Mechanisms of Diabetic Atherosclerosis: Herbal Medicines as a Potential Therapeutic Approach.Oxidative medicine and cellular longevity · 2017Review
- Animal models of diabetic macrovascular complications: key players in the development of new therapeutic approaches.Journal of diabetes research · 2015Review
- Apolipoprotein E-low density lipoprotein receptor interaction affects spatial memory retention and brain ApoE levels in an isoform-dependent manner.Neurobiology of disease · 2014Article
- 2013 Russell Ross memorial lecture in vascular biology: cellular and molecular mechanisms of diabetes mellitus-accelerated atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2014Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Diabetes is a major risk factor for cardiovascular disease. To examine how diabetes interacts with a mildly compromised lipid metabolism, we introduced the diabetogenic Ins2(C96Y/+) (Akita) mutation into mice expressing human apoE4 (E4) combined with either an overexpressing human LDL receptor gene (hLDLR) or the wild-type mouse gene. The hLDLR allele caused 2-fold reductions in plasma HDL-cholesterol, plasma apoA1, and hepatic triglyceride secretion. Diabetes increased plasma total cholesterol 1.3-fold and increased apoB48 secretion 3-fold, while reducing triglyceride secretion 2-fold. Consequently, diabetic E4 mice with hLDLR secrete increased numbers of small, cholesterol-enriched, apoB48-containing VLDL, although they have near normal plasma cholesterol (<120 mg/dl). Small foam cell lesions were present in the aortic roots of all diabetic E4 mice with hLDLR that we analyzed at six months of age. None were present in nondiabetic mice or in diabetic mice without hLDLR. Aortic expression of genes affecting leukocyte recruitment and adhesion was enhanced by diabetes. ApoA1 levels, but not diabetes, were strongly correlated with the ability of plasma to efflux cholesterol from macrophages. We conclude that the diabetes-induced proinflammatory changes in the vasculature and the hLDLR-mediated cholesterol accumulation in macrophages synergistically trigger atherosclerosis in mice with human apoE4, although neither alone is sufficient.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.