The relationship between insulin resistance and polymorphisms of the endothelial nitric oxide synthase gene in patients with coronary artery disease
Open accessAbstract
Nitric oxide (NO) regulates endothelial function and is believed to prevent atherogenesis. In endothelial cells, endothelial nitric oxide synthase (eNOS) is expressed constitutively, and regulates NO synthesis. A mutation of the eNOS gene has been associated with the development of coronary artery disease (CAD). The development of CAD is also influenced by insulin resistance, and recent studies suggest that NO might affect cellular insulin activity. We investigated the association between eNOS polymorphisms and insulin resistance in patients with CAD. We screened 45 patients with a history of myocardial infarction (MI), angina pectoris (AP), or coronary spasm. Genotypes were determined by polymerase chain reaction-restriction fragment-length polymorphism analysis. We examined two polymorphisms of the eNOS gene (The T(-786)-->C variant and the missense Glu298Asp variant). Insulin resistance was measured by determining the plasma immunoreactive insulin concentration at the 120 min time point (IRI 120) of a 75 g oral glucose tolerance test. The IRI 120 of the T(-786)-->C variant group was higher than that for the control group (p<0.05). This finding demonstrates that the T(-786)-->C mutation in the eNOS gene decreases insulin sensitivity.
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Several studies have associated a T(−786)C variant of the NOS3 gene with insulin resistance.
“Most notably, several studies have associated a T(−786)C variant of the NOS3 gene with insulin resistance [318-320].”
From Regulation of obesity and insulin resistance by nitric oxide (2014) · cites this paper as [319]
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- Authors
- Yoshimura, T., Hisatomi, A., Kajihara, S., Yasutake, T., Ogawa, Y., Mizuta, T., Ozaki, I., Utsunomiya, T., & Yamamoto, K.
- Affiliations
- Saga University (JP)
- Saga Medical School Hospital (JP)
- Venue
- Journal of Atherosclerosis and Thrombosis
- Publisher
- Japan Atherosclerosis Society
- Published
- 2003
- Volume
- 10
- Issue
- 1
- Pages
- 43-47
- ISSN
- 1340-3478 (ISSN-L)
- 1880-3873
- OpenAlex
- W2075942862
- Cited by
- 25
- References
- 28
- Citations by year
- 2024: 1 · 2020: 2 · 2019: 2 · 2017: 1 · 2015: 1 · 2014: 3 · 2013: 2 · 2012: 1
- FWCI
- 1.15
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by-nc-sa
- Locations
- Journal of Atherosclerosis and Thrombosis (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- Institutional Repositories DataBase (IRDB) (submittedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Keywords
- insulin resistance, endothelial nitric oxide synthase, eNOS gene polymorphism, coronary artery disease, nitric oxide, insulin sensitivity, myocardial infarction, angina pectoris, coronary vasospasm
- MeSH terms
- Coronary Disease, Endothelium, Vascular, Female, Gene Frequency, Genotype, Humans, Insulin Resistance, Male, Middle Aged, Polymorphism, Genetic, Genetic Variation, Polymerase Chain Reaction, Nitric Oxide Synthase, Mutation, Missense, Nitric Oxide Synthase Type III
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