RESUMEN
PURPOSE: Glycine is the simplest and major amino acid in humans. It is mainly generated in the liver and kidney and is used to produce collagen, creatine, glucose and purine. It is also involved in immune function, anti-inflammatory processes and anti-oxidation reactions. Here, we reviewed the current evidence supporting the role of glycine in the development and treatment of metabolic syndrome components. METHODS: We searched Scopus, PubMed and EMBASE databases for papers concerning glycine and metabolic syndrome. RESULTS: Available evidence shows that the amount of glycine synthesized in vivo is insufficient to meet metabolic demands in these species. Plasma glycine levels are lower in subjects with metabolic syndrome than in healthy individuals. Interventions such as lifestyle modification, exercise, weight loss, or drugs that improve manifestations of metabolic syndrome remarkably increase circulating glycine concentrations. CONCLUSION: Glycine supplementation improves various components of metabolic syndrome including diabetes, obesity, hyperlipidemia and hypertension. In the future, the use of glycine may have a significant clinical impact on the treatment of patients with metabolic syndrome.
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Síndrome Metabólico , Ejercicio Físico , Glicina/metabolismo , Glicina/uso terapéutico , Humanos , Estilo de Vida , Síndrome Metabólico/tratamiento farmacológico , Obesidad/terapiaRESUMEN
INTRODUCTION: Organophosphate compounds, such as diazinon (DZN), are widely used in agriculture and can lead to formation of reactive oxygen species (ROS) in cardiovascular system. ROS are highly toxic since they can cause serious changes in proteins including ubiquitylation. Crocin (a carotenoid isolated from saffron), has protective effects against DZN cardiotoxicity. In this study level of total protein ubiquitylation as markers of oxidative stress and level of ubiquitin-HIF-1α and P53, known substrates of ubiquitylation, in rat hearts exposed to DZN and crocin were evaluated. METHODS: Rats were divided into 7 groups: corn oil (control), DZN (15 mg/kg/day, gavage), crocin (12.5, 25, 50 mg/kg/day, i. p.) plus DZN, vitamin E (200 IU/kg, i. p., 3 days a week) plus DZN and crocin (50 mg/kg/day, i. p.). Treatments were continued for 4 weeks. Total protein ubiquitylation, total HIF-1α and P53 were analyzed by western blotting. Total HIF-1α and P53 were purified by immunoprecipitation (IP) and ubiquitin- HIF-1α and P53 were analyzed by western blotting. RESULTS: Higher protein ubiquitylation levels were observed in DZN treated rats. Decrease in ubiquitin-HIF-1α was also shown, and leads to higher HIF-1α protein levels in DZN group. Crocin (50 mg/kg) and vit. E protected cells against DZN protein ubiquitylation. Significant differences were not observed between the ubiquitin - P53 and total P53 protein levels. CONCLUSION: Our results showed that ubiquitylation could be considered as a marker of oxidative stress in rats exposed to DZN. Increase in level of HIF-α may compensate adverse effect of DNZ in rat heart.
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Cardiotoxicidad/prevención & control , Carotenoides/farmacología , Diazinón/toxicidad , Estrés Oxidativo/efectos de los fármacos , Animales , Cardiotónicos/administración & dosificación , Cardiotónicos/aislamiento & purificación , Cardiotónicos/farmacología , Carotenoides/administración & dosificación , Carotenoides/aislamiento & purificación , Crocus/química , Relación Dosis-Respuesta a Droga , Subunidad alfa del Factor 1 Inducible por Hipoxia/metabolismo , Insecticidas/toxicidad , Masculino , Ratas , Ratas Wistar , Especies Reactivas de Oxígeno/metabolismo , Proteína p53 Supresora de Tumor/metabolismo , Ubiquitinación/efectos de los fármacos , Vitamina E/farmacologíaRESUMEN
The antinociceptive effect of cyanocobalamin (Vit B12) has been reported in animal models and human studies. Our previous study showed the effect of Vit B12 on morphine tolerance. The dependence and tolerance were induced in male mice using subcutaneous morphine injections, 3 times a day (50, 50 and 75 mg/kg/day) for 3 days. Mice also received Vit B12 (100, 250 and 500 µg/kg), clonidine, memantine and saline intraperitoneally before morphine administration. On fourth day mice received only 7 mg /kg morphine just before tail-flick test. To determine the expression of morphine dependence and tolerance, all compounds were injected once intraperitoneally on the day of experiment. The tolerance was evaluated by the tail-flick test. The effect of Vit B12 and other agents on dependence were evaluated by counting the number of jumps (induced by naloxone 5 mg/kg). Co-administration of Vit B12 (100-500 µg/kg) and morphine in 3 days reduced the development of tolerance to morphine analgesic effect (8.2±0.5 and 7.83±0.5 s. vs. normal saline, 3.57±0.3 s). Repeated administration of Vit B12, also, diminished the reduced naloxane withdrawal signs of naloxone withdrawal test (100-500 µg/kg: 5±1.9 and 1.2±0.8 jumps vs. normal saline 72.6±12.2). However, Vit B12 had no effect on the expression of morphine tolerance and physical dependence. It is concluded that co-administration of Vit B12 and morphine could reduce tolerance to analgesic effect of morphine chronic administration and also reduce its withdrawal symptoms.