Lipids versus glucose in inflammation and the pathogenesis of macrovascular disease in diabetes.
Type 1 and type 2 diabetes both accelerate cardiovascular disease, yet the triggers are likely different for the two types of diabetes. Results from large-scale clinical trials suggest that intense blood glucose control can reduce cardiovascular events many years later in patients with type 1 diabetes. In type 2 diabetes, mechanisms related to insulin resistance and obesity may be more prominent in promoting atherosclerosis. In this article, we discuss the potential effects of hyperglycemia and diabetes-induced lipid abnormalities on atherosclerosis, particularly focusing on advanced stages of atherosclerosis and evidence from mouse models. In addition, we discuss new research findings in monocyte/macrophage biology that may present intriguing new areas of research related to diabetes and atherosclerosis.
Averill
Michelle M
MM
Department of Pathology and Diabetes and Obesity Center of Excellence, University of Washington School of Medicine, 815 Mercer Street, Seattle, WA 98109, USA.
Bornfeldt
Karin E
KE
D000273:Adipose Tissue / Q000473:pathology / Q000503:physiopathology*; D050197:Atherosclerosis / Q000097:blood* / Q000473:pathology / Q000503:physiopathology; D003922:Diabetes Mellitus, Type 1 / Q000097:blood / Q000150:complications / Q000503:physiopathology; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000150:complications / Q000503:physiopathology; D003925:Diabetic Angiopathies / Q000097:blood* / Q000473:pathology / Q000503:physiopathology*; D006801:Humans; D006943:Hyperglycemia / Q000097:blood / Q000503:physiopathology*; D007249:Inflammation / Q000097:blood / Q000503:physiopathology*; D008055:Lipids / Q000097:blood*; D008264:Macrophages / Q000473:pathology / Q000502:physiology; D009000:Monocytes / Q000473:pathology / Q000502:physiology
D008055:Lipids