Journal
REVIEWS IN ENDOCRINE & METABOLIC DISORDERS
Volume 14, Issue 1, Pages 59-68Publisher
SPRINGER
DOI: 10.1007/s11154-012-9235-3
Keywords
Pathways and mechanisms; Vascular dysfunction; Ceramide; Adiponectin; Nitric oxide; Reactive oxygen species; Insulin resistance; Obesity; Inflammation; Mitochondria; Endothelial dysfunction; Glucotoxicity; Diabetes
Categories
Funding
- National Institutes of Health (NIH) [2R15HL091493]
- American Diabetes Association (ADA) [1-12-BS-208, ADA 7-08-RA-164]
- University of Utah College of Health and School of Medicine
- NIH [R01 DK092065, R01HL108379, U01 HL087947]
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Cardiovascular complications are the leading causes of morbidity and mortality in individuals with obesity, type 2 diabetes mellitus (T2DM), and insulin resistance. Complications include pathologies specific to large (atherosclerosis, cardiomyopathy) and small (retinopathy, nephropathy, neuropathy) vessels. Common among all of these pathologies is an altered endothelial cell phenotype i.e., endothelial dysfunction. A crucial aspect of endothelial dysfunction is reduced nitric oxide (NO) bioavailability. Hyperglycemia, oxidative stress, activation of the renin-angiotensin system, and increased pro-inflammatory cytokines are systemic disturbances in individuals with obesity, T2DM, and insulin resistance and each of these contribute independently and synergistically to decreasing NO bioavailability. This review will examine the contribution from elevated circulating fatty acids in these subjects that lead to lipotoxicity. Particular focus will be placed on the fatty acid metabolite ceramide.
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