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Overexpression of Endothelial Nitric Oxide Synthase Prevents Diet-Induced Obesity and Regulates Adipocyte Phenotype
Open accessAbstract
RATIONALE: Endothelial dysfunction is a characteristic feature of diabetes and obesity in animal models and humans. Deficits in nitric oxide production by endothelial nitric oxide synthase (eNOS) are associated with insulin resistance, which is exacerbated by high-fat diet. Nevertheless, the metabolic effects of increasing eNOS levels have not been studied. OBJECTIVE: The current study was designed to test whether overexpression of eNOS would prevent diet-induced obesity and insulin resistance. METHODS AND RESULTS: In db/db mice and in high-fat diet-fed wild-type C57BL/6J mice, the abundance of eNOS protein in adipose tissue was decreased without significant changes in eNOS levels in skeletal muscle or aorta. Mice overexpressing eNOS (eNOS transgenic mice) were resistant to diet-induced obesity and hyperinsulinemia, although systemic glucose intolerance remained largely unaffected. In comparison with wild-type mice, high-fat diet-fed eNOS transgenic mice displayed a higher metabolic rate and attenuated hypertrophy of white adipocytes. Overexpression of eNOS did not affect food consumption or diet-induced changes in plasma cholesterol or leptin levels, yet plasma triglycerides and fatty acids were decreased. Metabolomic analysis of adipose tissue indicated that eNOS overexpression primarily affected amino acid and lipid metabolism; subpathway analysis suggested changes in fatty acid oxidation. In agreement with these findings, adipose tissue from eNOS transgenic mice showed higher levels of PPAR-α and PPAR-γ gene expression, elevated abundance of mitochondrial proteins, and a higher rate of oxygen consumption. CONCLUSIONS: These findings demonstrate that increased eNOS activity prevents the obesogenic effects of high-fat diet without affecting systemic insulin resistance, in part, by stimulating metabolic activity in adipose tissue.
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“lower NOS3 abundance is found in both adipose tissue and skeletal muscle of obese humans and rodents [120-124].”
From Regulation of obesity and insulin resistance by nitric oxide (2014) · cites this paper as [122]
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Metadata
- Authors
- Sansbury, B. E., Cummins, T. D., Tang, Y., Hellmann, J., Holden, C. R., Harbeson, M. A., Chen, Y., Patel, R. P., Spite, M., Bhatnagar, A., & Hill, B. G.
- Affiliations
- University of Alabama at Birmingham (US)
- ORCID
- Venue
- Circulation Research
- Published
- 2012-10-12
- Volume
- 111
- Issue
- 9
- Pages
- 1176-1189
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- PMC
- PMC3707504
- OpenAlex
- W2078821762
- Cited by
- 156
- References
- 79
- Citations by year
- 2026: 3 · 2025: 7 · 2024: 6 · 2023: 11 · 2022: 13 · 2021: 6 · 2020: 14 · 2019: 10 · 2018: 6 · 2017: 17 · 2016: 12 · 2015: 12 · 2014: 24 · 2013: 13 · 2012: 1
- FWCI
- 11.93
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Circulation Research (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Heart, Lung, and Blood Institute (HL-106173, HL 59378, R01HL059378, R01HL055477, HL55477, R01HL106173)
- National Institute of General Medical Sciences (P20GM103492)
- National Center for Research Resources (RR-024489, P20RR024489)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Keywords
- endothelial nitric oxide synthase, diet-induced obesity, insulin resistance, adipocyte hypertrophy, adipose tissue metabolism, fatty acid oxidation, PPARα, PPARγ, mitochondrial function, hyperinsulinemia, db/db mice, transgenic mice, nitric oxide
- MeSH terms
- Amino Acids, Animals, Disease Models, Animal, Hypertrophy, Insulin Resistance, Mice, Inbred C57BL, Mice, Transgenic, Obesity, Phenotype, Adipocytes, PPAR alpha, PPAR gamma, Lipid Metabolism, Mice, Nitric Oxide Synthase Type III, Diet, High-Fat
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