Nitric oxide and vascular insulin resistance

@article{Wu2009NitricOA,
  title={Nitric oxide and vascular insulin resistance},
  author={Guoyao Wu and Cynthia J. Meininger},
  journal={BioFactors},
  year={2009},
  volume={35}
}
Obesity and type‐II diabetes are growing major health issues worldwide. They are the leading risk factors for vascular insulin resistance, which plays an important role in the pathogenesis of cardiovascular disease, the leading cause of death in developed nations. Recent studies have shown that reduced synthesis of nitric oxide (NO; a major vasodilator) from L‐arginine in endothelial cells is a major factor contributing to the impaired action of insulin in the vasculature of obese and diabetic… Expand

Paper Mentions

l-Leucine and NO-mediated cardiovascular function
TLDR
It is proposed that reducing circulating levels of l-leucine or endothelial GFAT activity may provide a potentially novel strategy for preventing and/or treating cardiovascular disease in obese and diabetic subjects. Expand
Uric acid induces endothelial dysfunction by vascular insulin resistance associated with the impairment of nitric oxide synthesis
TLDR
Taking together, uric acid induced endothelial dysfunction by contributing to vascular insulin resistance in terms of insulin‐induced NO production, potentially leading to the development of hypertension. Expand
Regulation of carbohydrate metabolism by nitric oxide and hydrogen sulfide: Implications in diabetes.
TLDR
The aim of this review is to provide a better understanding of the individual and the interactive roles of NO and H2S in carbohydrate metabolism, especially in diabetes. Expand
Association between insulin resistance and the development of cardiovascular disease
TLDR
It can be concluded that insulin resistance in the myocardium generates damage by at least three different mechanisms: (1) signal transduction alteration, (2) impaired regulation of substrate metabolism, and (3) altered delivery of substrates to theMyocardium. Expand
Nitric oxide and energy metabolism in mammals
TLDR
Modulation of NO‐mediated pathways through dietary supplementation with L‐arginine or its precursor L‐citrulline may provide an effective, practical strategy to prevent and treat metabolic syndrome, including obesity, diabetes, and dyslipidemia in mammals, including humans. Expand
Anti-obesity and anti-diabetic effects of nitrate and nitrite.
TLDR
Based on current data, it could be suggested that amplifying the nitrate-nitrite-nitric oxide pathway is a diet-based strategy for increasing nitric oxide bioavailability and the management of these two interlinked conditions. Expand
Renal endothelial dysfunction in diabetic nephropathy.
TLDR
Both pharmacological approaches and potential regenerative therapies hold promise for restoration of impaired endothelial cells in diabetic nephropathy. Expand
Regulation of nitric oxide production in health and disease
TLDR
Future research is needed to expand the understanding of the regulation and adequate measurement of nitric oxide production at the organ level and by the different Nitric oxide synthase isoforms, also in relation to clinical nutrition. Expand
The nitrate-nitrite-nitric oxide pathway: Its role in human exercise physiology
TLDR
There is evidence that the muscle ATP turnover at a fixed work rate is reduced and the mitochondrial P/O ratio is increased following NO3 − supplementation, which offers important insights into the physiological bases for the reduced during exercise. Expand
A Mitochondrial Approach to Cardiovascular Risk and Disease.
TLDR
Regular physical activity has been shown to improve mitochondrial parameters and myocardial tolerance to ischemia-reperfusion (IR) and several approaches that act by improving mitochondrial function in the heart, contributing to decrease some of the risk factors associated to CVDs. Expand
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 52 REFERENCES
Arginine nutrition and cardiovascular function.
TLDR
Dietary Arg supplementation may represent a potentially novel nutritional strategy for preventing and treating cardiovascular disease. Expand
Effect of Endothelium-Specific Insulin Resistance on Endothelial Function In Vivo
TLDR
Selective endothelial insulin resistance is sufficient to induce a reduction in NO bioavailability and endothelial dysfunction that is secondary to increased generation of reactive oxygen species, independent of a significant metabolic phenotype. Expand
Cardiovascular actions of insulin.
TLDR
Molecular mechanisms underlying cardiovascular actions of insulin, the reciprocal relationships between insulin resistance and endothelial dysfunction, and implications for developing beneficial therapeutic strategies that simultaneously target metabolic and cardiovascular diseases are discussed. Expand
Impaired arginine metabolism and NO synthesis in coronary endothelial cells of the spontaneously diabetic BB rat.
Arginine metabolism via nitric oxide (NO) synthase and other pathways was studied in coronary endothelial cells (EC) from the spontaneously diabetic BB rat, an animal model of human type I diabetesExpand
Vascular function, insulin resistance and fatty acids
TLDR
Raised non-esterified fatty acids impair insulin's effect on glucose uptake in skeletal muscle and the vascular endothelium and thus could have detrimental effects on the vasculature, leading to premature cardiovascular disease. Expand
Regulatory role for the arginine-nitric oxide pathway in metabolism of energy substrates.
TLDR
Modulation of the arginine-NO pathway through dietary supplementation with L-arginine or L-citrulline may aid in the prevention and treatment of the metabolic syndrome in obese humans and companion animals, and in reducing unfavorable fat mass in animals of agricultural importance. Expand
Regulation of nitric oxide synthesis by dietary factors.
TLDR
The discovery of NO synthesis has unified traditionally diverse research areas in nutrition, physiology, immunology, pathology, and neuroscience, and it is necessary to investigate the interactions of dietary factors on NO synthesis and to define the underlying molecular mechanisms. Expand
Impaired nitric oxide production in coronary endothelial cells of the spontaneously diabetic BB rat is due to tetrahydrobiopterin deficiency.
TLDR
Endothelial cells from diabetic BioBreeding rats have an impaired ability to produce NO because of a deficiency in tetrahydrobiopterin (BH(4), a cofactor necessary for enzyme activity in de novo biosynthesis of GTP-cyclohydrolase I, and increasing BH( 4) levels with sepiapterin increased NO production. Expand
Tetrahydrobiopterin increases insulin sensitivity in patients with type 2 diabetes and coronary heart disease.
TLDR
BH(4) significantly increases insulin sensitivity in type 2 diabetic patients without any discernible improvement in endothelial function and does not affect the relative changes in brachial artery diameter from baseline FMD. Expand
Tetrahydrobiopterin-dependent preservation of nitric oxide-mediated endothelial function in diabetes by targeted transgenic GTP-cyclohydrolase I overexpression.
TLDR
Findings indicate that BH4 is an important mediator of eNOS regulation in diabetes and is a rational therapeutic target to restore NO-mediated endothelium-dependent vasodilatation in Diabetes and other vascular disease states. Expand
...
1
2
3
4
5
...