Obesity, insulin resistance, and skeletal muscle nitric oxide synthase
Open accessAbstract
The molecular mechanisms responsible for impaired insulin action have yet to be fully identified. Rodent models demonstrate a strong relationship between insulin resistance and an elevation in skeletal muscle inducible nitric oxide synthase (iNOS) expression; the purpose of this investigation was to explore this potential relationship in humans. Sedentary men and women were recruited to participate (means ± SE: nonobese, body mass index = 25.5 ± 0.3 kg/m(2), n = 13; obese, body mass index = 36.6 ± 0.4 kg/m(2), n = 14). Insulin sensitivity was measured using an intravenous glucose tolerance test with the subsequent modeling of an insulin sensitivity index (S(I)). Skeletal muscle was obtained from the vastus lateralis, and iNOS, endothelial nitric oxide synthase (eNOS), and neuronal nitric oxide synthase (nNOS) content were determined by Western blot. S(I) was significantly lower in the obese compared with the nonobese group (~43%; P < 0.05), yet skeletal muscle iNOS protein expression was not different between nonobese and obese groups. Skeletal muscle eNOS protein was significantly higher in the nonobese than the obese group, and skeletal muscle nNOS protein tended to be higher (P = 0.054) in the obese compared with the nonobese group. Alternative analysis based on S(I) (high and low tertile) indicated that the most insulin-resistant group did not have significantly more skeletal muscle iNOS protein than the most insulin-sensitive group. In conclusion, human insulin resistance does not appear to be associated with an elevation in skeletal muscle iNOS protein in middle-aged individuals under fasting conditions.
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Lower NOS3 abundance is found in both adipose tissue and skeletal muscle of obese humans and rodents.
“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 [124]
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“and skeletal muscle of obese humans and rodents [120–124].”
BackgroundIntramyocellular lipid and impaired myofiber contraction in normal weight and obese older adults
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- Authors
- Kraus, R. M., Houmard, J. A., Kraus, W. E., Tanner, C. J., Pierce, J. R., Choi, M. D., & Hickner, R. C.
- Affiliations
- East Carolina University (US)
- Duke University (US)
- Corresponding author
- Hickner, Robert C.
- Venue
- Journal of Applied Physiology
- Publisher
- American Physiological Society
- Published
- 2012-09-01
- Volume
- 113
- Issue
- 5
- Pages
- 758-765
- ISSN
- 0161-7567 (ISSN-L)
- 8750-7587
- 1522-1601
- PMC
- PMC3472472
- OpenAlex
- W2035176469
- Cited by
- 28
- References
- 58
- Citations by year
- 2025: 3 · 2024: 1 · 2022: 1 · 2020: 2 · 2019: 2 · 2018: 2 · 2017: 2 · 2016: 2 · 2015: 5 · 2014: 6 · 2013: 1 · 2012: 1
- FWCI
- 2.79
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Applied Physiology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute on Aging (R21AG019209, R21 AG-19209-02, P30AG028716)
- National Heart, Lung, and Blood Institute (R01 HL 57354, R01HL057354)
- Topics
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- obesity, insulin resistance, skeletal muscle, inducible nitric oxide synthase, endothelial nitric oxide synthase, neuronal nitric oxide synthase, insulin sensitivity, vastus lateralis, sedentary adults, middle-aged adults
- MeSH terms
- Adult, Aged, Blood Glucose, Exercise Test, Female, Humans, Insulin Resistance, Male, Middle Aged, Obesity, Cohort Studies, Muscle, Skeletal, Nitric Oxide Synthase, Nitric Oxide Synthase Type II, Nitric Oxide Synthase Type I, Nitric Oxide Synthase Type III
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