Homocysteine: An aetiological contributor to peripheral vascular arterial disease

Magno

Journal of Vascular Surgery

et al. 2008

104

Improved nutrition is associated with a reduced prevalence of PAD in the US population. Higher consumption of specific nutrients, including antioxidants (vitamin A, C, and E), vitamin B(6), fiber, folate, and omega-3 fatty acids have a significant protective effect, irrespective of traditional cardiovascular risk factors. These findings suggest specific dietary supplementation may afford additional protection, above traditional risk factor modification, for the prevention of PAD.

Section: Discussionmentioning

confidence: 99%

Nutrition impacts the prevalence of peripheral arterial disease in the United States

Magno

Journal of Vascular Surgery

et al. 2008

104

“…Elevated Hcy levels increases the risk of developing peripheral vascular disease [38]. Hcy levels have been shown to be elevated in patients with peripheral vascular disease and chronic, non-healing lower-extremity ulcers [39-40].…”

Section: Pathophysiology Of Dpnmentioning

confidence: 99%

Metabolic Correction in the Management of Diabetic Peripheral Neuropathy: Improving Clinical Results Beyond Symptom Control

Miranda-Massari

González²,

Jiménez³

et al. 2011

CCP

Current Clinical Management Guidelines of Diabetic Peripheral Neuropathy (DPN) are based on adequate glucose control and symptomatic pain relief. However, meticulous glycemic control could delay the onset or slow the progression of diabetic neuropathy in patients with DM type 2, but it does not completely prevent the progression of the disease. Complications of DPN as it continues its natural course, produce increasing pain and discomfort, loss of sensation, ulcers, infections, amputations and even death. In addition to the increased suffering, disability and loss of productivity, there is a very significant economic impact related to the treatment of DPN and its complications. In USA alone, it has been estimated that there are more than 5,000,000 patients suffering from DPN and the total annual cost of treating the disease and its complications is over $10,000 million dollars. In order to be able to reduce complications of DPN, it is crucial to improve or correct the metabolic conditions that lead to the pathology present in this condition. Pathophysiologic mechanisms implicated in diabetic neuropathy include: increased polyol pathway with accumulation of sorbitol and reduced Na + /K + -ATPase activity, microvascular damage and hypoxia due to nitric oxide deficit and increased oxygen free radical activity. Moreover, there is a decrease in glutathione and increase in homocysteine. Clinical trials in the last two decades have demonstrated that the use of specific nutrients can correct some of these metabolic derangements, improving symptom control and providing further benefits such as improved sensorium, blood flow and nerve regeneration. We will discuss the evidence on lipoic acid, acetyi-L-carnitine, benfotiamine and the combination of active B vitamins L-methylfolate, methylcobalamin and piridoxal-6-phosphate. In addition, we discuss the role of metforrnin, an © 2011 Bentham Science Publishers * Address correspondence to this author at the Room 420, School of Pharmacy Medical Sciences Campus-University of Puerto Rico, PO Box 365067, San Juan, Puerto Rico; Tel: (787) important drug in the management of diabetes, and the presence of specific polymorphic genes, in the risk of developing DPN and how metabolic correction can reduce these risks.

“…Homocysteine is a thiol‐containing amino acid that is formed when methionine is converted to cysteine 1 . Recent epidemiological and experimental studies have demonstrated that homocysteine acts as an independent risk factor for ischaemic heart disease, 2 cerebrovascular disease 3 and peripheral arterial disease 4 . Previous studies have shown that homocysteine accelerates the progression of cardiovascular diseases by inducing endothelial dysfunction and endothelial cell apoptosis, 5,6 oxidative stress, 7 proliferation of vascular smooth muscle cells 8 and platelet function injury 9 .…”

Section: Introductionmentioning

confidence: 99%

Effects of Taurine and Homocysteine on Calcium Homeostasis and Hydrogen Peroxide and Superoxide Anions in Rat Myocardial Mitochondria

Chang

Zhao

et al. 2004

Clin Exp Pharma Physio

1. Taurine and homocysteine are metabolites of methionine. Hyperhomocysteinaemia is one of the risk factors for cardiovascular disease. Although taurine may be a cardiovascular cytoprotective substance, we hypothesized that it may antagonize the effects of homocysteine on myocardial mitochondrial function. 2. We studied the effects of taurine and homocysteine on [(45)Ca] uptake, Ca(2+)-ATPase activity and generation of hydrogen peroxide and superoxide anions in vitro in rat isolated myocardial mitochondria. 3. Results showed that the inhibition of mitochondrial [(45)Ca] uptake by homocysteine (0.1, 0.5 and 1.0 mmol/L) was concentration dependent. Taurine (5, 10 and 20 mmol/L) promoted [(45)Ca] uptake in a concentration-dependent manner, as well as concentration dependently reducing the homocysteine (0.5 mmol/L)-induced inhibition of mitochondrial [(45)Ca] uptake. 4. Homocysteine significantly inhibited mitochondrial Ca(2+)-ATPase activity, whereas taurine had a diphasic action on this activity. Taurine, at 5 and 10 mmol/L, increased Ca(2+)-ATPase activity (P < 0.01), but 20 mmol/L taurine inhibited Ca(2+)-ATPase activity (P < 0.05). Taurine attenuated the inhibitory effect of homocysteine on Ca(2+)-ATPase activity. 5. Homocysteine stimulated the generation of hydrogen peroxide and superoxide anions. Taurine had no effect on the generation of the anions, but inhibited their homocysteine-stimulated generation. 6. These results indicate that taurine and homocysteine have opposite effects in myocardial mitochondria with regard to [(45)Ca] uptake, Ca(2+)-ATPase activity and the generation of hydrogen peroxide and superoxide anions. Our results may show an important mechanism for the cardiovascular protective effects of taurine.