Effect of fenofibrate on the level of asymmetric dimethylarginine in individuals with hypertriglyceridemia

@article{Yang2005EffectOF,
  title={Effect of fenofibrate on the level of asymmetric dimethylarginine in individuals with hypertriglyceridemia},
  author={Tian-lun Yang and Meifang Chen and Xin Xia and Bai-Lin Luo and Yuan‐jian Li},
  journal={European Journal of Clinical Pharmacology},
  year={2005},
  volume={62},
  pages={179-184}
}
ObjectiveTo test whether treatment with fenofibrate decreases asymmetric dimethylarginine (ADMA) level in hypertriglyceridemic individuals.MethodsIn the present study, 45 subjects with hypertriglyceridemia were recruited to receive treatment with fenofibrate (200 mg/d). Serum concentrations of ADMA, malondialdehyde (MDA), nitric oxide (NO) and tumor necrosis factor-α (TNF-α) were measured. Endothelial function assessed by flow-mediated dilation (FMD) of the brachial artery was performed… 
View on Springer
ncbi.nlm.nih.gov
20 Citations
Highly Influential Citations
1
Background Citations
9

20 Citations

Fenofibrate: a review of its use in dyslipidaemia.
TLDR
Subgroup analyses in the FIELD and ACCORD Lipid trials indicate that fenofibrate is of the greatest benefit in decreasing CV events in patients with atherogenic dyslipidaemia, and in patients without type 2 diabetes, it is a useful treatment option either alone or in combination with a statin.
Fenofibrate: a review of its lipid-modifying effects in dyslipidemia and its vascular effects in type 2 diabetes mellitus.
  • G. Keating
  • Medicine, Biology
    American journal of cardiovascular drugs : drugs, devices, and other interventions
  • 2011
TLDR
Monotherapy with fenofibrate remains a useful option in patients with dyslipidemia, particularly in atherogenic dyslipIDemia characterized by high TG and low HDL-C levels, and monotherapy with statin monotherapy had a beneficial effect on atherogensic dys Lipidemia in Patients with the metabolic syndrome or type 2 diabetes mellitus.
Ameliorative effect of combination of benfotiamine and fenofibrate in diabetes-induced vascular endothelial dysfunction and nephropathy in the rat
TLDR
It may be concluded that diabetes-induced oxidative stress, lipids alteration, and consequent development of VED may be responsible for the induction of nephropathy in diabetic rats.
Protective effect of HDL on endothelial NO production: the role of DDAH/ADMA pathway
TLDR
Investigation of the protective effect of high density lipoprotein (HDL) on endothelial NO production was investigated, and HDL significantly increased the attenuated endothelial cell NO production induced by ox-LDL, which was attributed to its effect on DDAH/ADMA pathway.
Reduction of NO- and EDHF-Mediated Vasodilatation in Hypertension: Role of Asymmetric Dimethylarginine
TLDR
The present study suggests that the inhibitory effect of ADMA on endothelial function not only involves NO-mediated endothelium-dependent vasodilatation but also the EDHF-mediated pathways in hypertensive animals and humans, and that ADMA can down-regulate the expression of SK3 channels in endothelial cells.
Down-regulation of endogenous nitric oxide synthase inhibitors on endothelial SK3 expression.
Asymmetric Dimethylarginine: Clinical Significance and Novel Therapeutic Approaches.
TLDR
Novel therapeutic approaches targeting selectively ADMA are encouraging, but have only been tested in vitro or in animal studies and further research is needed in order to conclude on how therapeutic strategies modulating ADMA actions can affect atherosclerosis progression and cardiovascular diseases.
Asymmetric Dimethylarginine and Hepatic Encephalopathy: Cause, Effect or Association?
TLDR
The contribution of AD MA to the regulation of the NO-cGMP pathway in the brain, correlation of ADMA level with CBF and cognitive alterations observed during HE progression in patients and/or animal models of HE are discussed.
The relationship between L-arginine/ADMA ratio and coronary collateral development in patients with low glomerular filtration rate.
TLDR
These results showed that CCD was poor in patients with GFR < 60 mL/min, presumably because of the adverse effect of decreased L-arginine/ADMA ratio on endothelial cells and angiogenesis.
Pathogenesis and prevention of cardiovascular disease in patients with chronic kidney disease
TLDR
It has been shown that plasma homocysteine is strongly related to renal function and that virtually all ESRD patients have elevated homocy steine levels, probably due to decreased metabolic clearance, and that, in renal patients, the association of plasma ADMA carotid intima-media thickness, cardiovascular events and overall mortality is independent of homocy Steine, indicating that the negative vascular effects of ADMA and homocySteine have a different etiology.
...
...

References

SHOWING 1-10 OF 41 REFERENCES
Effect of fenofibrate on LDL-induced endothelial dysfunction in rats
TLDR
The results suggest that the protective effect of fenofibrate on endothelial cells in rats treated with LDL may be related to the reduction of ADMA concentration.
Increased levels of asymmetric dimethylarginine in populations at risk for atherosclerotic disease. Effects of pravastatin.
Fenofibrate increases the L-arginine:ADMA ratio by increase of L-arginine concentration but has no effect on ADMA concentration.
Endothelial Dysfunction Induced by Hyperhomocyst(e)inemia: Role of Asymmetric Dimethylarginine
TLDR
It is suggested that experimental hyperhomocyst(e)inemia leads to accumulation of the endogenous NO synthase inhibitor ADMA, accompanied by varying degrees of endothelial dysfunction according to the preexisting state of cardiovascular health.
[Pleiotropic effects of micronized fenofibrate in patients with combined hyperlipidemia].
TLDR
Evaluating the effect of fenofibrate on the plasma levels of Plasminogen Activator Inhibitor type 1 (PAI-1) and fibrinogen in patients with combined dyslipidemia revealed a significant decrease of triglycerides and total cholesterol and may confirm new pathways of fibrates action.
ADMA and oxidative stress are responsible for endothelial dysfunction in hyperhomocyst(e)inemia: effects of L-arginine and B vitamins.
Novel mechanism for endothelial dysfunction: dysregulation of dimethylarginine dimethylaminohydrolase.
TLDR
The results suggest that the endothelial vasodilator dysfunction observed in hypercholesterolemia may be due to reduced degradation of ADMA, the endogenous inhibitor of NOS.
Impact of vitamin E on plasma asymmetric dimethylarginine (ADMA) in chronic kidney disease (CKD): a pilot study.
  • R. SaranJames E. Novak S. Rajagopalan
  • Medicine
    Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association
  • 2003
TLDR
Antioxidant therapy with vitamin E has the potential to lower ADMA levels in CKD patients, implying increased NO.
The effect of fenofibrate treatment on endothelium-dependent relaxation induced by oxidative modified low density lipoprotein from hyperlipidemic patients
TLDR
The results suggest that while the reduced lysophosphatidylcholine levels may contribute to the attenuated impairment of the endothelium-dependent relaxation of the aortic ring, other unidentified factors impacted by fenofibrate are likely to contribute toThe attenuated effects.
Mild-to-moderate hypertriglyceridemia in young men is associated with endothelial dysfunction and increased plasma concentrations of asymmetric dimethylarginine.
...
...