dc.contributor.author | Renard, Catherine B. | en_US |
dc.contributor.author | Kramer, Farah | en_US |
dc.contributor.author | Johansson, Fredrik | en_US |
dc.contributor.author | Lamharzi, Najib | en_US |
dc.contributor.author | Tannock, Lisa R. | en_US |
dc.contributor.author | von Herrath, Matthias G. | en_US |
dc.contributor.author | Chair, Alan | en_US |
dc.contributor.author | Bornfeldt, Karin E. | en_US |
dc.date.accessioned | 2010-04-21T15:55:58Z | |
dc.date.available | 2010-04-21T15:55:58Z | |
dc.date.issued | 2004-09-01 | en_US |
dc.identifier.citation | Renard CB, Kramer F, Johansson F, et al. Diabetes and diabetes-associated lipid abnormalities have distinct effects on initiation and progression of atherosclerotic lesions. J Clin Invest. 2004;114(5):659-668. | en_US |
dc.identifier.other | 10.1172/JCI17867 | en_US |
dc.identifier.uri | http://www.jci.org/articles/view/17867 | en_US |
dc.identifier.uri | http://hdl.handle.net/1773/15774 | |
dc.description.abstract | Diabetes in humans accelerates cardiovascular disease caused by atherosclerosis. The relative contributions of hyperglycemia and dyslipidemia to atherosclerosis in patients with diabetes are not clear, largely because there is a lack of suitable animal models. We therefore have developed a transgenic mouse model that closely mimics atherosclerosis in humans with type 1 diabetes by breeding low-density lipoprotein receptor–deficient mice with transgenic mice in which type 1 diabetes can be induced at will. These mice express a viral protein under control of the insulin promoter and, when infected by the virus, develop an autoimmune attack on the insulin-producing β cells and subsequently develop type 1 diabetes. When these mice are fed a cholesterol-free diet, diabetes, in the absence of associated lipid abnormalities, causes both accelerated lesion initiation and increased arterial macrophage accumulation. When diabetic mice are fed cholesterol-rich diets, on the other hand, they develop severe hypertriglyceridemia and advanced lesions, characterized by extensive intralesional hemorrhage. This progression to advanced lesions is largely dependent on diabetes-induced dyslipidemia, because hyperlipidemic diabetic and nondiabetic mice with similar plasma cholesterol levels show a similar extent of atherosclerosis. Thus, diabetes and diabetes-associated lipid abnormalities have distinct effects on initiation and progression of atherosclerotic lesions. | en_US |
dc.description.sponsorship | NIH grants HL62887 and HL076719, and a grant from the Juvenile Diabetes Research Foundation (JDRF). | en_US |
dc.language.iso | en_US | en_US |
dc.title | Diabetes and diabetes-associated lipid abnormalities have distinct effects on initiation and progression of atherosclerotic lesions | en_US |