Effects of the nitric oxide donor, sodium nitroprusside, on resting leg glucose uptake in patients with type 2 diabetes

Henstridge, Darren C.; Kingwell, Bronwyn A.; Formosa, Melissa F.; Drew, Brian G.; McConell, Glenn K.; Duffy, Stephen J.

doi:10.1007/s00125-005-0018-1

Cited by 25 publications

(23 citation statements)

References 50 publications

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“…NF-B activation also may induce insulin resistance via endothelial dysfunction that arises from altered fatty acid flux, elevated concentrations of asymmetric dimethylarginine, and impaired nitric oxide synthase (NOS) regulation (36 -38). Treatment studies in humans show that antioxidant therapy with vitamin C significantly improves endothelial dysfunction associated with insulin resistance (39) and that NOSmediated endothelial dysfunction in skeletal muscle is associated with impaired nutritive flow redistribution and diminished insulin-mediated and insulinindependent glucose uptake (40,41). We and others have recently shown that biomarkers of endothelial dysfunction are precursors of incident diabetes independent of obesity, inflammation, and other diabetes risk factors (42)(43)(44).…”

Section: Discussionmentioning

confidence: 99%

Association of Oxidative Stress, Insulin Resistance, and Diabetes Risk Phenotypes

et al. 2007

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OBJECTIVE -Systemic oxidative stress causes insulin resistance in rodents. We tested the hypothesis that oxidative stress and insulin resistance are associated in humans.RESEARCH DESIGN AND METHODS -We used cross-sectional data from 2,002 nondiabetic subjects of the community-based Framingham Offspring Study. We measured insulin resistance with the homeostasis model and defined categorical insulin resistance as homeostasis model assessment of insulin resistance (HOMA-IR) Ͼ75th percentile. We measured oxidative stress using the ratio of urine 8-epi-prostaglandin F 2␣ (8-epi-PGF 2␣ ) to creatinine and used age-and sex-adjusted regression models to test the association of oxidative stress with insulin resistance in individuals without diabetes and among subgroups at elevated risk of diabetes.RESULTS -Across 8-epi-PGF 2␣ /creatinine tertiles, the prevalence of insulin resistance increased (18.0, 27.5, and 29.4% for the first, second, and third tertiles, respectively; P Ͻ 0.0001), as did mean levels of HOMA-IR (3.28, 3.83, and 4.06 units; P Ͻ 0.0001). The insulin resistanceoxidative stress association was attenuated by additional adjustment for BMI (P ϭ 0.06 across tertiles for insulin resistance prevalence; P ϭ 0.004 for mean HOMA-IR). Twenty-six percent of participants were obese (BMI Ն30 kg/m 2 ), 39% had metabolic syndrome (according to the Adult Treatment Panel III definition), and 37% had impaired fasting glucose (IFG) (fasting glucose 5.6 -6.9 mmol/l). Among 528 obese participants, respectively, insulin resistance prevalence was 41.3, 60.6, and 54.2% across 8-epi-PGF 2␣ /creatinine tertiles (P ϭ 0.005); among 781 subjects with metabolic syndrome, insulin resistance prevalence was 41.3, 56.7, and 51.7% (P ϭ 0.0025); and among 749 subjects with IFG, insulin resistance prevalence was 39.6, 47.2, and 51.6% (P ϭ 0.04).CONCLUSIONS -Systemic oxidative stress is associated with insulin resistance in individuals at average or elevated risk of diabetes even after accounting for BMI.

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Section: Discussionmentioning

confidence: 99%

Association of Oxidative Stress, Insulin Resistance, and Diabetes Risk Phenotypes

et al. 2007

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“…Previous work has shown a robust increase in peripheral glucose uptake after administration of the NO donor sodium nitroprusside [22]. Based on this work and pilot work, we estimated …”

Section: Statistical Analysesmentioning

confidence: 99%

“…Indeed, it has been shown that infusion of the NO donor sodium nitroprusside improves leg glucose uptake in resting conditions in individuals with and without type 2 diabetes [22,26]. This finding has been attributed to NO-mediated increments in capillary recruitment and nutritive blood flow [22,26].…”

Section: Accepted M Manuscriptmentioning

confidence: 99%

A single dose of sodium nitrate does not improve oral glucose tolerance in patients with type 2 diabetes mellitus

et al. 2015

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A single dose of sodium nitrate does not improve oral glucose tolerance in patients with type 2 diabetes mellitus, Nutrition Research (2015Research ( ), doi: 10.1016Research ( /j.nutres.2015 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. A C C E P T E DM A N U S C R I P T A C C E P T E D M A N U S C R I P T ACCEPTED MANUSCRIPT

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“…Nitric Oxide (NO) plays a critical role in skeletal muscle (SkM) physiology [1–3] and has been implicated in glucose uptake during exercise [4–9] and in response to insulin [8, 10, 11]. However, the regulatory mechanisms controlling endogenous NO production by nitric oxide synthases (NOSs) in SkM are not fully understood.…”

Section: Introductionmentioning

confidence: 99%

Neuronal nitric oxide synthase mediates insulin- and oxidative stress-induced glucose uptake in skeletal muscle myotubes

Kellogg

McCammon

Hinchee-Rodriguez

et al. 2017

Free Radical Biology and Medicine

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Previously published studies strongly suggested that insulin- and exercise-induced skeletal muscle glucose uptake require nitric oxide (NO) production. However, the signal transduction mechanisms by which insulin and contraction regulated NO production and subsequent glucose transport are not known. In the present study, we utilized the myotube cell lines treated with insulin or hydrogen peroxide, the latter to mimic contraction-induced oxidative stress, to characterize these mechanisms. We found that insulin stimulation of neuronal nitric oxide synthase (nNOS) phosphorylation, NO production, and GLUT4 translocation were all significantly reduced by inhibition of either nNOS or Akt2. Moreover, in muscle strips from mice with a complete knock out of nNOS, insulin was not capable of stimulating glucose uptake. Hydrogen peroxide (H2O2) induced phosphorylation of nNOS at the same residue as did insulin, and also stimulated NO production and GLUT4 translocation. nNOS inhibition prevented H2O2-induced GLUT4 translocation. AMP activated protein kinase (AMPK) inhibition prevented H2O2 activation and phosphorylation of nNOS, leading to reduced NO production and significantly attenuated GLUT4 translocation. We conclude that nNOS phosphorylation and subsequently increased NO production are required for both insulin- and H2O2-stimulated glucose transport. Although the two stimuli result in phosphorylation of the same residue on nNOS, they do so through distinct protein kinases. Thus, insulin and H2O2-activated signaling pathways converge on nNOS, which is a common mediator of glucose uptake in both pathways. However, the fact that different kinases are utilized provides a basis for the use of exercise to activate glucose transport in the face of insulin resistance.

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Effects of the nitric oxide donor, sodium nitroprusside, on resting leg glucose uptake in patients with type 2 diabetes

Cited by 25 publications

References 50 publications

Association of Oxidative Stress, Insulin Resistance, and Diabetes Risk Phenotypes

Association of Oxidative Stress, Insulin Resistance, and Diabetes Risk Phenotypes

A single dose of sodium nitrate does not improve oral glucose tolerance in patients with type 2 diabetes mellitus

Neuronal nitric oxide synthase mediates insulin- and oxidative stress-induced glucose uptake in skeletal muscle myotubes

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