Lipotoxicity contributes to endothelial dysfunction: a focus on the contribution from ceramide

J David Symons; E Dale Abel

doi:10.1007/s11154-012-9235-3

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Lipotoxicity contributes to endothelial dysfunction: a focus on the contribution from ceramide

Journal article

Open access

Peer reviewed

Lipotoxicity contributes to endothelial dysfunction: a focus on the contribution from ceramide

J David Symons and E Dale Abel

Reviews in endocrine & metabolic disorders, Vol.14(1), pp.59-68

03/2013

DOI: 10.1007/s11154-012-9235-3

PMCID: PMC4180664

PMID: 23292334

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http://doi.org/10.1007/s11154-012-9235-3View

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Abstract

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.

Inflammation - pathology

Inflammation - metabolism

Animals

Ceramides - metabolism

Endothelium, Vascular - metabolism

Insulin Resistance - physiology

Humans

Endothelium, Vascular - pathology

Nitric Oxide - metabolism

Obesity - metabolism

Details

Title: Subtitle: Lipotoxicity contributes to endothelial dysfunction: a focus on the contribution from ceramide
Creators: J David Symons - College of Health, University of Utah, School of Medicine, Salt Lake City, UT, USA. j.david.symons@hsc.utah.edu
E Dale Abel
Resource Type: Journal article
Publication Details: Reviews in endocrine & metabolic disorders, Vol.14(1), pp.59-68
DOI: 10.1007/s11154-012-9235-3
PMID: 23292334
PMCID: PMC4180664
NLM abbreviation: Rev Endocr Metab Disord
ISSN: 1389-9155
eISSN: 1573-2606
Publisher: Germany
Grant note: R15 HL091493 / NHLBI NIH HHS R01 HL108379 / NHLBI NIH HHS R01 DK092065 / NIDDK NIH HHS U01HL087947 / NHLBI NIH HHS U01 HL087947 / NHLBI NIH HHS 2R15HL091493 / NHLBI NIH HHS R01HL108379 / NHLBI NIH HHS
Language: English
Date published: 03/2013
Academic Unit: Roy J. Carver Department of Biomedical Engineering; Fraternal Order of Eagles Diabetes Research Center; Biochemistry and Molecular Biology; Endocrinology and Metabolism; Internal Medicine
Record Identifier: 9984025273502771

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