Effect of S-adenosylmethionine (SAMe) on Blood Levels of Homocysteine
The purpose of this study is to investigate whether S-adenosylmethionine (SAMe), a natural substance available as a nutritional supplement, can influence blood levels of homocysteine (Hcy). More specifically, we will determine if chronic oral SAMe administration affects homocysteine metabolism in patients with vascular disease who have mild to moderate hyperhomocysteinemia.
The purpose of this study is to investigate whether S-adenosylmethionine (SAMe), a natural substance available as a nutritional supplement, can influence blood levels of homocysteine (Hcy). More specifically, we will determine if chronic oral SAMe administration effects homocysteine metabolism in patients with vascular disease who have mild to moderate hyperhomocysteinemia through the following specific aims:
Specific Aim 1 - To determine the effect of oral SAMe (1200 mg/day) on plasma total homocysteine levels in subjects with mild to moderate hyperhomocysteinemia.
Specific Aim 2 - To determine the effect of oral SAMe (1200 mg/day) with and without supplementation of folate, vitamin B12 and B6, on plasma homocysteine levels in patients with mild to moderate hyperhomocysteinemia.
Specific Aim 3 - To determine the effect of oral SAMe (1200 mg/day) on plasma levels pf asymmetric dimethylarginine (ADMA) in subjects with mild to moderate hyperhomocysteinemia.
Allocation: Randomized, Endpoint Classification: Safety Study, Intervention Model: Parallel Assignment, Masking: Double Blind (Subject, Investigator), Primary Purpose: Basic Science
Baylor University Medical Center
Baylor Research Institute
Results (where available)
- Source: http://clinicaltrials.gov/show/NCT00473200
- Information obtained from ClinicalTrials.gov on March 06, 2013
Medical and Biotech [MESH] Definitions
Condition in which the plasma levels of homocysteine and related metabolites are elevated (>13.9 μmol/l). Hyperhomocysteinemia can be familial or acquired. Development of the acquired hyperhomocysteinemia is mostly associated with vitamins B and/or folate deficiency (e.g., PERNICIOUS ANEMIA, vitamin malabsorption). Familial hyperhomocysteinemia often results in a more severe elevation of total homocysteine and excretion into the urine, resulting in HOMOCYSTINURIA. Hyperhomocysteinemia is a risk factor for cardiovascular and neurodegenerative diseases, osteoporotic fractures and complications during pregnancy.
A multifunctional pyridoxal phosphate enzyme. In the second stage of cysteine biosynthesis it catalyzes the reaction of homocysteine with serine to form cystathionine with the elimination of water. Deficiency of this enzyme leads to HYPERHOMOCYSTEINEMIA and HOMOCYSTINURIA. EC 188.8.131.52.
5'-S-(3-Amino-3-carboxypropyl)-5'-thioadenosine. Formed from S-adenosylmethionine after transmethylation reactions.
Antineoplastic agent effective against myelogenous leukemia in experimental animals. Also acts as an inhibitor of animal S-adenosylmethionine decarboxylase.
An enzyme that catalyzes the synthesis of S-adenosylmethionine from methionine and ATP. EC 184.108.40.206.
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