title: Oral supplementation with glycine reduces oxidative stress in patients with metabolic syndrome, improving their systolic blood pressure.
abstract: Reactive oxygen species derived from abdominal fat and uncontrolled glucose metabolism are contributing factors to both oxidative stress and the development of metabolic syndrome (MetS). This study was designed to evaluate the effects of daily administration of an oral glycine supplement on antioxidant enzymes and lipid peroxidation in MetS patients. The study included 60 volunteers: 30 individuals that were supplemented with glycine (15 g/day) and 30 that were given a placebo for 3 months. We analysed thiobarbituric acid reactive substances (TBARS) and S-nitrosohemoglobin (SNO-Hb) in plasma; the enzymatic activities of glucose-6-phosphate dehydrogenase (G6PD), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPX) in erythrocytes; and the expression of CAT, GPX, and SOD2 in leukocytes. Individuals treated with glycine showed a 25% decrease in TBARS compared with the placebo-treated group. Furthermore, there was a 20% reduction in SOD-specific activity in the glycine-treated group, which correlated with SOD2 expression. G6PD activity and SNO-Hb levels increased in the glycine-treated male group. Systolic blood pressure (SBP) also showed a significant decrease in the glycine-treated men (p = 0.043). Glycine plays an important role in balancing the redox reactions in the human body, thus protecting against oxidative damage in MetS patients.
authors.affiliation: a Unidad de Investigación Médica en Bioquímica, Hospital de Especialidades (1er. Piso), CMN Siglo XXI, IMSS, Avenida Cuauhtémoc 330, C.P. 06725, D.F. México.
authors.forename: Margarita
authors.initials: M
authors.lastname: Díaz-Flores
authors.forename: Miguel
authors.initials: M
authors.lastname: Cruz
authors.forename: Genoveva
authors.initials: G
authors.lastname: Duran-Reyes
authors.forename: Catarina
authors.initials: C
authors.lastname: Munguia-Miranda
authors.forename: Hilda
authors.initials: H
authors.lastname: Loza-Rodríguez
authors.forename: Evelyn
authors.initials: E
authors.lastname: Pulido-Casas
authors.forename: Nayeli
authors.initials: N
authors.lastname: Torres-Ramírez
authors.forename: Olga
authors.initials: O
authors.lastname: Gaja-Rodriguez
authors.forename: Jesus
authors.initials: J
authors.lastname: Kumate
authors.forename: Luis Arturo
authors.initials: LA
authors.lastname: Baiza-Gutman
authors.forename: Daniel
authors.initials: D
authors.lastname: Hernández-Saavedra
mesh_terms: D000284:Administration, Oral; D000328:Adult; D000975:Antioxidants / Q000008:administration & dosage*; D015415:Biomarkers / Q000097:blood; D001794:Blood Pressure / Q000187:drug effects*; D002374:Catalase / Q000097:blood; D019587:Dietary Supplements; D004311:Double-Blind Method; D005260:Female; D005954:Glucosephosphate Dehydrogenase / Q000097:blood; D005979:Glutathione Peroxidase / Q000097:blood; D005998:Glycine / Q000008:administration & dosage*; D006454:Hemoglobins / Q000378:metabolism; D006801:Humans; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D024821:Metabolic Syndrome / Q000097:blood / Q000175:diagnosis / Q000188:drug therapy* / Q000503:physiopathology; D008800:Mexico; D008875:Middle Aged; D018384:Oxidative Stress / Q000187:drug effects*; D013482:Superoxide Dismutase / Q000097:blood; D013599:Systole; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D013997:Time Factors; D016896:Treatment Outcome; D000099156:Superoxide Dismutase 2
chemical_list: D000975:Antioxidants; D015415:Biomarkers; D002374:Catalase; D005954:Glucosephosphate Dehydrogenase; D005979:Glutathione Peroxidase; D005998:Glycine; D006454:Hemoglobins; D013482:Superoxide Dismutase; D017392:Thiobarbituric Acid Reactive Substances; D000099156:Superoxide Dismutase 2; C103574:S-nitrosohemoglobin