China 
Africa 
Explore chapters and articles related to this topic
Epilepsy/Seizures
Published in Charles Theisler, Adjuvant Medical Care, 2023
Dimethylglycine (DMG), sometimes called vitamin B15, is a normal body constituent formed in the metabolism of homocysteine to methionine. It is commercially available without a prescription and may be helpful in selected patients with seizures.17 One patient had a dramatic reduction in his seizure frequency after starting DMG 90 mg bid. Doses as high as 600–1,000 mg/day have been reported.18
Other Drugs Used to Treat Seizures
Published in Stanley R. Resor, Henn Kutt, The Medical Treatment of Epilepsy, 2020
Unfortunately, the report that a patient with a refractory mixed seizure disorder experienced an improvement in his seizure frequency on taking N,N-dimethylglycine (25) could not be confirmed in either of two controlled trials (26,27). Its beneficial effect in the initial case may therefore have been due to a unique and unrecognized metabolic dependency on N,N-dimethylglycine or a placebo effect (28).
Dimethylglycine
Published in Linda M. Castell, Samantha J. Stear (Nottingham), Louise M. Burke, Nutritional Supplements in Sport, Exercise and Health, 2015
Dimethylglycine (N,N-Dimethylglycine, DMG) is a dimethylated derivative of the amino acid glycine. Found naturally in animal and plant cells, it is an intermediate in glycine synthesis from the degradation of choline. Indirectly it is involved in a wide range of metabolic pathways through transmethylation. DMG is also an active ingredient in pangamic acid (see section on pangamic acid). It is proposed that DMG may enhance metabolic variables of aerobic performance in humans, and historically, supplementation has been used by Soviet athletes (Graber et al., 1981) and American Football players (Bishop et al., 1987).
Noninvasive biomarkers to guide intervention: toward personalized patient management in prostate cancer
Published in Expert Review of Precision Medicine and Drug Development, 2020
Maria Frantzi, Enrique Gomez-Gomez, Harald Mischak
To investigate the potential of lipids as biomarkers in urinary exosomes, a pilot lipidomics study was performed using high-throughput mass spectrometry to analyze urinary exosomes [76]. The 36 most abundant lipid molecules in urinary exosomes were quantified in 15 PCa patients and 13 healthy individuals. The highest significance was shown for phosphatidylserine (PS) 18:1/18:1 and lactosylceramide (LacSer) (d18:1/16:0). The combination of PS and LacSer distinguished the two groups with 93% sensitivity and 100% specificity. Although this was the first time that lipidomics markers were reported as promising candidates, this was a small pilot study and further validation studies must be performed before drawing any conclusions [76]. Additionally, urinary metabolomic profiling using 1H nuclear magnetic resonance (1H-NMR) was performed in 64 PCa and 51 BPH patients. 108 metabolic features were assessed and integrated using orthogonal partial least squares discriminant analysis (OPLS-DA). Subsequently, a model consisting of 40 metabolic variables was developed to discriminate PCa patients from individuals with BPH. The model included among others increased concentrations of branched-chain amino acids (BCAA), glutamate and pseudouridine, and decreased concentrations of glycine, dimethylglycine, fumarate, 4-imidazole-acetate, and one unknown metabolite (U1) associated with PCa (p ≤ 0.01; permutation test of 100 repeats) [77]. Yet, validation in an independent cohort to demonstrate potential value should be performed.
Oxysterol concentrations are associated with cholesterol concentrations and anemia in pediatric patients with sickle cell disease
Published in Scandinavian Journal of Clinical and Laboratory Investigation, 2019
Ahmet Yalcinkaya, Afshin Samadi, Incilay Lay, Selma Unal, Suna Sabuncuoglu, Yesim Oztas
Quantification of 7-KC and C-triol were performed with a modified version of the LC-MS/MS method developed by Jiang et al. [8]. Plasma samples (50 μl) were used for detection. Sample preparation included derivatization with N,N-dimethylglycine (DMG), and a cleaning phase via LC. Internal standards were 3ß,5α,6ß-trihydroxycholestane D7 (Toronto Research Chemicals) and 3ß-hydroxy-5-cholestenoate D7 (Avanti Polar Lipids). Plasma quality control samples were prepared via addition of known amounts of 7-KC and C-triol to yield a concentration of 40 and 150 ng/mL for both oxysterols. Quantification was performed with an eight-point calibration curve (3.12–400 ng/mL). LC was performed with a Symmetry C18 column (100 mm × 2.1 mm, 5 µm) (Thermo Fisher Scientific, Waltham, MA). Mobile phase was a linear gradient of water and acetonitrile (1 mM ammonium formate, pH = 3). Mass spectrometry analysis was performed in the positive ionization mode using electrospray ionization. The multiple reaction monitoring transitions used for the detection of oxysterols were as follows: M/z of 7-KC and C-triol in M+H+ were 486.0 and 591.5, while the m/z of 7-KC-D7 and C-triol-D7 in M+H+ were 493.0 and 598.5, respectively [9].
Plasma choline, homocysteine and vitamin status in healthy adults supplemented with krill oil: a pilot study
Published in Scandinavian Journal of Clinical and Laboratory Investigation, 2018
Bodil Bjørndal, Inge Bruheim, Vegard Lysne, Marie S. Ramsvik, Per M. Ueland, Jan E. Nordrehaug, Ottar K. Nygård, Rolf K. Berge
Elevated plasma total homocysteine (tHcy) is related to increased risk of atherosclerosis and cardiovascular disase (CVD) [1], but lowering of tHcy with B-vitamins has not improved prognosis among CVD patients [2]. Hcy may be remethylated back to methionine (Met) through the B12-dependent methionine synthase, using 5′-methyltetrahydrofolate (mTHF) as the methyl donor. In the liver and kidney, Hcy may also be remethylated by betaine-homocysteine methyltransferase (BHMT), using betaine as the methyl donor. This couples the Hcy metabolism to the choline oxidation pathway, and the reaction yields dimethylglycine (DMG). Recently, it has been found that higher plasma concentration of DMG is associated with increased CVD risk [3,4]. Irreversible catabolism of Hcy takes place through the B6-dependent transsulfuration pathway (Figure 1).