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[PMID]:29257861
[Au] Autor:Freitag S; Verrall SR; Pont SDA; McRae D; Sungurtas JA; Palau R; Hawes C; Alexander CJ; Allwood JW; Foito A; Stewart D; Shepherd LVT
[Ad] Endereço:Environmental and Biochemical Sciences, The James Hutton Institute , Invergowrie, Dundee DD2 5DA, UK.
[Ti] Título:Impact of Conventional and Integrated Management Systems on the Water-Soluble Vitamin Content in Potatoes, Field Beans, and Cereals.
[So] Source:J Agric Food Chem;66(4):831-841, 2018 Jan 31.
[Is] ISSN:1520-5118
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The reduction of the environmental footprint of crop production without compromising crop yield and their nutritional value is a key goal for improving the sustainability of agriculture. In 2009, the Balruddery Farm Platform was established at The James Hutton Institute as a long-term experimental platform for cross-disciplinary research of crops using two agricultural ecosystems. Crops representative of UK agriculture were grown under conventional and integrated management systems and analyzed for their water-soluble vitamin content. Integrated management, when compared with the conventional system, had only minor effects on water-soluble vitamin content, where significantly higher differences were seen for the conventional management practice on the levels of thiamine in field beans (p < 0.01), Spring barley (p < 0.05), and Winter wheat (p < 0.05), and for nicotinic acid in Spring barley (p < 0.05). However, for all crops, variety and year differences were of greater importance. These results indicate that the integrated management system described in this study does not significantly affect the water-soluble vitamin content of the crops analyzed here.
[Mh] Termos MeSH primário: Agricultura/métodos
Produtos Agrícolas/química
Grãos Comestíveis/química
Solanum tuberosum/química
Vicia faba/química
Vitaminas/análise
[Mh] Termos MeSH secundário: Ácido Ascórbico/análise
Hordeum/química
Niacina/análise
Valor Nutritivo
Estações do Ano
Tiamina/análise
Triticum/química
Reino Unido
Complexo Vitamínico B/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Vitamins); 12001-76-2 (Vitamin B Complex); 2679MF687A (Niacin); PQ6CK8PD0R (Ascorbic Acid); X66NSO3N35 (Thiamine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171220
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jafc.7b03509


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[PMID]:27771381
[Au] Autor:Montserrat-de la Paz S; Naranjo MC; Lopez S; Abia R; Muriana FJG; Bermudez B
[Ad] Endereço:Laboratory of Cellular and Molecular Nutrition, Instituto de la Grasa, CSIC, Seville, Spain.
[Ti] Título:Niacin and its metabolites as master regulators of macrophage activation.
[So] Source:J Nutr Biochem;39:40-47, 2017 Jan.
[Is] ISSN:1873-4847
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Niacin is a broad-spectrum lipid-regulating drug used for clinical therapy of chronic high-grade inflammatory diseases. However, the mechanisms by which either niacin or the byproducts of its catabolism ameliorate these inflammatory diseases are not clear yet. Human circulating monocytes and mature macrophages were used to analyze the effects of niacin and its metabolites (NAM, NUA and 2-Pyr) on oxidative stress, plasticity and inflammatory response by using biochemical, flow cytometry, quantitative real-time PCR and Western blot technologies. Niacin, NAM and 2-Pyr significantly decreased ROS, NO and NOS2 expression in LPS-treated human mature macrophages. Niacin and NAM skewed macrophage polarization toward antiinflammatory M2 macrophage whereas a trend toward proinflammatory M1 macrophage was noted following treatment with NUA. Niacin and NAM also reduced the inflammatory competence of LPS-treated human mature macrophages and promoted bias toward antiinflammatory CD14 CD16 nonclassical human primary monocytes. This study reveals for the first time that niacin and its metabolites possess antioxidant, reprogramming and antiinflammatory properties on human primary monocytes and monocyte-derived macrophages. Our findings imply a new understanding of the mechanisms by which niacin and its metabolites favor a continuous and gradual plasticity process in the human monocyte/macrophage system.
[Mh] Termos MeSH primário: Ativação de Macrófagos/efeitos dos fármacos
Niacina/farmacologia
Niacinamida/farmacologia
Ácidos Nicotínicos/farmacologia
Piridonas/farmacologia
[Mh] Termos MeSH secundário: Anti-Inflamatórios/farmacologia
Antioxidantes/farmacologia
Diferenciação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Seres Humanos
Monócitos/efeitos dos fármacos
Óxido Nítrico Sintase Tipo II/genética
Óxido Nítrico Sintase Tipo II/metabolismo
Estresse Oxidativo
Espécies Reativas de Oxigênio/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Antioxidants); 0 (N-methyl-2-pyridone-5-carboxamide); 0 (Nicotinic Acids); 0 (Pyridones); 0 (Reactive Oxygen Species); 25X51I8RD4 (Niacinamide); 2679MF687A (Niacin); 77V5315PIU (nicotinuric acid); EC 1.14.13.39 (NOS2 protein, human); EC 1.14.13.39 (Nitric Oxide Synthase Type II)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180117
[Lr] Data última revisão:
180117
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


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[PMID]:29176657
[Au] Autor:Agrawal S; Zaritsky JJ; Fornoni A; Smoyer WE
[Ad] Endereço:Center for Clinical and Translational Research, The Research Institute at Nationwide Children's Hospital, and Department of Pediatrics, The Ohio State University, 700 Children's Drive, W303, Columbus, Ohio 43205, USA.
[Ti] Título:Dyslipidaemia in nephrotic syndrome: mechanisms and treatment.
[So] Source:Nat Rev Nephrol;14(1):57-70, 2018 Jan.
[Is] ISSN:1759-507X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Nephrotic syndrome is a highly prevalent disease that is associated with high morbidity despite notable advances in its treatment. Many of the complications of nephrotic syndrome, including the increased risk of atherosclerosis and thromboembolism, can be linked to dysregulated lipid metabolism and dyslipidaemia. These abnormalities include elevated plasma levels of cholesterol, triglycerides and the apolipoprotein B-containing lipoproteins VLDL and IDL; decreased lipoprotein lipase activity in the endothelium, muscle and adipose tissues; decreased hepatic lipase activity; and increased levels of the enzyme PCSK9. In addition, there is an increase in the plasma levels of immature HDL particles and reduced cholesterol efflux. Studies from the past few years have markedly improved our understanding of the molecular pathogenesis of nephrotic syndrome-associated dyslipidaemia, and also heightened our awareness of the associated exacerbated risks of cardiovascular complications, progressive kidney disease and thromboembolism. Despite the absence of clear guidelines regarding treatment, various strategies are being increasingly utilized, including statins, bile acid sequestrants, fibrates, nicotinic acid and ezetimibe, as well as lipid apheresis, which seem to also induce partial or complete clinical remission of nephrotic syndrome in a substantial percentage of patients. Future potential treatments will likely also include inhibition of PCSK9 using recently-developed anti-PCSK9 monoclonal antibodies and small inhibitory RNAs, as well as targeting newly identified molecular regulators of lipid metabolism that are dysregulated in nephrotic syndrome.
[Mh] Termos MeSH primário: Anticolesterolemiantes/uso terapêutico
Dislipidemias/tratamento farmacológico
Ácidos Fíbricos/uso terapêutico
Inibidores de Hidroximetilglutaril-CoA Redutases/uso terapêutico
Síndrome Nefrótica/metabolismo
[Mh] Termos MeSH secundário: Colesterol/metabolismo
HDL-Colesterol/metabolismo
VLDL-Colesterol/metabolismo
Dislipidemias/complicações
Dislipidemias/metabolismo
Ezetimiba/uso terapêutico
Seres Humanos
Hipolipemiantes/uso terapêutico
Lipase/metabolismo
Lipase Lipoproteica/metabolismo
Lipoproteínas/metabolismo
Síndrome Nefrótica/complicações
Niacina/uso terapêutico
Pró-Proteína Convertase 9/metabolismo
Triglicerídeos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anticholesteremic Agents); 0 (Cholesterol, HDL); 0 (Cholesterol, VLDL); 0 (Fibric Acids); 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors); 0 (Hypolipidemic Agents); 0 (Lipoproteins); 0 (Triglycerides); 0 (lipoprotein cholesterol); 2679MF687A (Niacin); 97C5T2UQ7J (Cholesterol); EC 3.1.1.3 (Lipase); EC 3.1.1.3 (hepatic lipase, human); EC 3.1.1.34 (Lipoprotein Lipase); EC 3.4.21.- (PCSK9 protein, human); EC 3.4.21.- (Proprotein Convertase 9); EOR26LQQ24 (Ezetimibe)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180117
[Lr] Data última revisão:
180117
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1038/nrneph.2017.155


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[PMID]:29245288
[Au] Autor:Han JY; Kim HJ; Shin S; Park J; Lee IG
[Ad] Endereço:aDepartment of PediatricsbDepartment of RadiologycDepartment of Laboratory Medicine, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.
[Ti] Título:Elevated serum lipoprotein(a) as a risk factor for combined intracranial and extracranial artery stenosis in a child with arterial ischemic stroke: A case report.
[So] Source:Medicine (Baltimore);96(49):e9025, 2017 Dec.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Stroke is an uncommon disease in childhood with an estimated incidence of 1 to 6 per 100,000 and stenoocclusive arteriopathy is the main risk factor of recurrent pediatric arterial ischemic stroke (AIS). Dyslipidemia may influence strongly before puberty and in late adolescence when plasma levels are naturally highest. PATIENT CONCERNS: An 11-year-old male presented with acute onset seizure, a drowsy mentality, and right hemiplegia. DIAGNOSES: Magnetic resonance (MR) angiogram demonstrated occlusion of distal basilar artery and left vertebral arteries. Serum Lp(a) was significantly increased as 269 nmol/L (normal<75 nmol/L) only. Thus, he was diagnosed as pediatric AIS. INTERVENTIONS: He was started on aspirin (100 mg/day) for secondary stroke prevention and received nicotinic acid (2 g/day) as a Lp(a)-lowering agent. OUTCOMES: Consciousness gradually improved and the patient regained a normal orientation after 2 weeks. The Lp(a) level was reduced to 48 nmol/L after nicotinic acid administration. LESSONS: High Lp(a) level may be considered in the risk profile assessment of pediatric AIS. Niacin and certain inhibitors of cholesteryl ester transfer protein can be considered to reduce Lp(a).
[Mh] Termos MeSH primário: Dislipidemias/complicações
Arteriosclerose Intracraniana/complicações
Lipoproteína(a)/sangue
Acidente Vascular Cerebral/complicações
[Mh] Termos MeSH secundário: Criança
Dislipidemias/tratamento farmacológico
Seres Humanos
Masculino
Niacina/uso terapêutico
Fatores de Risco
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Lipoprotein(a)); 2679MF687A (Niacin)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180105
[Lr] Data última revisão:
180105
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171217
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009025


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[PMID]:27777319
[Au] Autor:Russo L; Ghadieh HE; Ghanem SS; Al-Share QY; Smiley ZN; Gatto-Weis C; Esakov EL; McInerney MF; Heinrich G; Tong X; Yin L; Najjar SM
[Ad] Endereço:Center for Diabetes and Endocrine Research, University of Toledo, Toledo, OH 43614.
[Ti] Título:Role for hepatic CEACAM1 in regulating fatty acid metabolism along the adipocyte-hepatocyte axis.
[So] Source:J Lipid Res;57(12):2163-2175, 2016 12.
[Is] ISSN:1539-7262
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) regulates insulin sensitivity by promoting hepatic insulin clearance and mediating suppression of fatty acid synthase activity. Feeding C57BL/6J male mice with a high-fat (HF) diet for 3-4 weeks triggered a >60% decrease in hepatic CEACAM1 levels to subsequently impair insulin clearance and cause systemic insulin resistance and hepatic steatosis. This study aimed at investigating whether lipolysis drives reduction in hepatic CEACAM1 and whether this constitutes a key mechanism leading to diet-induced metabolic abnormalities. Blocking lipolysis with a daily intraperitoneal injection of nicotinic acid in the last two days of a 30-day HF feeding regimen demonstrated that white adipose tissue (WAT)-derived fatty acids repressed hepatic CEACAM1-dependent regulation of insulin and lipid metabolism in 3-month-old male C57BL/6J mice. Adenoviral-mediated CEACAM1 redelivery countered the adverse metabolic effect of the HF diet on insulin resistance, hepatic steatosis, visceral obesity, and energy expenditure. It also reversed the effect of HF diet on inflammation and fibrosis in WAT and liver. This assigns a causative role for lipolysis-driven decrease in hepatic CEACAM1 level and its regulation of insulin and lipid metabolism in sustaining systemic insulin resistance, hepatic steatosis, and other abnormalities associated with excessive energy supply.
[Mh] Termos MeSH primário: Adipócitos/metabolismo
Antígeno Carcinoembrionário/fisiologia
Ácidos Graxos/metabolismo
Hepatócitos/metabolismo
[Mh] Termos MeSH secundário: Tecido Adiposo Branco/efeitos dos fármacos
Tecido Adiposo Branco/metabolismo
Tecido Adiposo Branco/patologia
Animais
Células Cultivadas
Dieta Hiperlipídica/efeitos adversos
Metabolismo Energético
Fibrose
Resistência à Insulina
Metabolismo dos Lipídeos
Masculino
Camundongos Endogâmicos C57BL
Niacina/farmacologia
Obesidade/etiologia
Obesidade/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Carcinoembryonic Antigen); 0 (Ceacam1 protein, mouse); 0 (Fatty Acids); 2679MF687A (Niacin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171201
[Lr] Data última revisão:
171201
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE


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[PMID]:28792876
[Au] Autor:Shi H; Enriquez A; Rapadas M; Martin EMMA; Wang R; Moreau J; Lim CK; Szot JO; Ip E; Hughes JN; Sugimoto K; Humphreys DT; McInerney-Leo AM; Leo PJ; Maghzal GJ; Halliday J; Smith J; Colley A; Mark PR; Collins F; Sillence DO; Winlaw DS; Ho JWK; Guillemin GJ; Brown MA; Kikuchi K; Thomas PQ; Stocker R; Giannoulatou E; Chapman G; Duncan EL; Sparrow DB; Dunwoodie SL
[Ad] Endereço:From the Divisions of Developmental and Stem Cell Biology (H.S., A.E., M.R., E.M.M.A.M., R.W., J.M., J.O.S., E.I., K.S., J.H., K.K., G.C., D.B.S., S.L.D.), Vascular Biology (G.J.M., R.S.), and Molecular, Structural, and Computational Biology (D.T.H., J.W.K.H., E.G.), Victor Chang Cardiac Research In
[Ti] Título:NAD Deficiency, Congenital Malformations, and Niacin Supplementation.
[So] Source:N Engl J Med;377(6):544-552, 2017 08 10.
[Is] ISSN:1533-4406
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Congenital malformations can be manifested as combinations of phenotypes that co-occur more often than expected by chance. In many such cases, it has proved difficult to identify a genetic cause. We sought the genetic cause of cardiac, vertebral, and renal defects, among others, in unrelated patients. METHODS: We used genomic sequencing to identify potentially pathogenic gene variants in families in which a person had multiple congenital malformations. We tested the function of the variant by using assays of in vitro enzyme activity and by quantifying metabolites in patient plasma. We engineered mouse models with similar variants using the CRISPR (clustered regularly interspaced short palindromic repeats)-Cas9 system. RESULTS: Variants were identified in two genes that encode enzymes of the kynurenine pathway, 3-hydroxyanthranilic acid 3,4-dioxygenase (HAAO) and kynureninase (KYNU). Three patients carried homozygous variants predicting loss-of-function changes in the HAAO or KYNU proteins (HAAO p.D162*, HAAO p.W186*, or KYNU p.V57Efs*21). Another patient carried heterozygous KYNU variants (p.Y156* and p.F349Kfs*4). The mutant enzymes had greatly reduced activity in vitro. Nicotinamide adenine dinucleotide (NAD) is synthesized de novo from tryptophan through the kynurenine pathway. The patients had reduced levels of circulating NAD. Defects similar to those in the patients developed in the embryos of Haao-null or Kynu-null mice owing to NAD deficiency. In null mice, the prevention of NAD deficiency during gestation averted defects. CONCLUSIONS: Disruption of NAD synthesis caused a deficiency of NAD and congenital malformations in humans and mice. Niacin supplementation during gestation prevented the malformations in mice. (Funded by the National Health and Medical Research Council of Australia and others.).
[Mh] Termos MeSH primário: 3-Hidroxiantranilato 3,4-Dioxigenase/genética
Anormalidades Congênitas/genética
Suplementos Nutricionais
Hidrolases/genética
NAD/deficiência
Niacina/uso terapêutico
[Mh] Termos MeSH secundário: 3-Hidroxiantranilato 3,4-Dioxigenase/metabolismo
Canal Anal/anormalidades
Animais
Anormalidades Congênitas/prevenção & controle
Modelos Animais de Doenças
Esôfago/anormalidades
Feminino
Cardiopatias Congênitas/genética
Cardiopatias Congênitas/prevenção & controle
Seres Humanos
Hidrolases/metabolismo
Rim/anormalidades
Deformidades Congênitas dos Membros/genética
Deformidades Congênitas dos Membros/prevenção & controle
Masculino
Camundongos
Camundongos Knockout
Mutação
NAD/biossíntese
NAD/genética
Análise de Sequência de DNA
Coluna Vertebral/anormalidades
Traqueia/anormalidades
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0U46U6E8UK (NAD); 2679MF687A (Niacin); EC 1.13.11.6 (3-Hydroxyanthranilate 3,4-Dioxygenase); EC 3.- (Hydrolases); EC 3.7.1.3 (kynureninase)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170822
[Lr] Data última revisão:
170822
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170810
[St] Status:MEDLINE
[do] DOI:10.1056/NEJMoa1616361


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[PMID]:28768650
[Au] Autor:Qin B; Xun P; Jacobs DR; Zhu N; Daviglus ML; Reis JP; Steffen LM; Van Horn L; Sidney S; He K
[Ad] Endereço:Department of Population Science, Rutgers Cancer Institute of New Jersey, New Brunswick, NJ.
[Ti] Título:Intake of niacin, folate, vitamin B-6, and vitamin B-12 through young adulthood and cognitive function in midlife: the Coronary Artery Risk Development in Young Adults (CARDIA) study.
[So] Source:Am J Clin Nutr;106(4):1032-1040, 2017 Oct.
[Is] ISSN:1938-3207
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Epidemiologic evidence regarding niacin, folate, vitamin B-6, and vitamin B-12 intake in relation to cognitive function is limited, especially in midlife. We hypothesize that higher intake of these B vitamins in young adulthood is associated with better cognition later in life. This study comprised a community-based multicenter cohort of black and white men and women aged 18-30 y in 1985-1986 (year 0, i.e., baseline) from the Coronary Artery Risk Development in Young Adults (CARDIA) study ( = 3136). We examined participants' CARDIA diet history at years 0, 7, and 20 to assess nutrient intake, including dietary and supplemental B vitamins. We measured cognitive function at year 25 (mean ± SD age: 50 ± 4 y) through the use of the Rey Auditory Verbal Learning Test (RAVLT) for verbal memory, the Digit Symbol Substitution Test (DSST) for psychomotor speed, and a modified Stroop interference test for executive function. Higher RAVLT and DSST scores and a lower Stroop score indicated better cognitive function. We used multivariable-adjusted linear regressions to estimate mean differences in cognitive scores and 95% CIs. Comparing the highest quintile with the lowest (quintile 5 compared with quintile 1), cumulative total intake of niacin was significantly associated with 3.92 more digits on the DSST (95% CI: 2.28, 5.55; -trend < 0.01) and 1.89 points lower interference score on the Stroop test (95% CI: -3.10, -0.68; -trend = 0.05). Total folate was associated with 2.56 more digits on the DSST (95% CI: 0.82, 4.31; -trend = 0.01). We also found that higher intakes of vitamin B-6 (quartile 5 compared with quartile 1: 2.62; 95% CI: 0.97, 4.28; -trend = 0.02) and vitamin B-12 (quartile 5 compared with quartile 1: 2.08; 95% CI: 0.52, 3.65; -trend = 0.02) resulted in better psychomotor speed measured by DSST scores. Higher intake of B vitamins throughout young adulthood was associated with better cognitive function in midlife.
[Mh] Termos MeSH primário: Transtornos Cognitivos/prevenção & controle
Cognição/efeitos dos fármacos
Ácido Fólico/administração & dosagem
Niacina/administração & dosagem
Vitamina B 12/administração & dosagem
Vitamina B 6/administração & dosagem
Complexo Vitamínico B/administração & dosagem
[Mh] Termos MeSH secundário: Adulto
Fatores Etários
Doença de Alzheimer/etiologia
Doença de Alzheimer/prevenção & controle
Transtornos Cognitivos/etiologia
Estudos de Coortes
Dieta
Suplementos Nutricionais
Função Executiva
Feminino
Ácido Fólico/farmacologia
Seres Humanos
Estudos Longitudinais
Masculino
Memória
Meia-Idade
Niacina/farmacologia
Desempenho Psicomotor
Aprendizagem Verbal
Vitamina B 12/farmacologia
Vitamina B 6/farmacologia
Complexo Vitamínico B/farmacologia
Deficiência de Vitaminas do Complexo B/etiologia
Deficiência de Vitaminas do Complexo B/prevenção & controle
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
12001-76-2 (Vitamin B Complex); 2679MF687A (Niacin); 8059-24-3 (Vitamin B 6); 935E97BOY8 (Folic Acid); P6YC3EG204 (Vitamin B 12)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170804
[St] Status:MEDLINE
[do] DOI:10.3945/ajcn.117.157834


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[PMID]:28624351
[Au] Autor:Abdullah KM; Qais FA; Ahmad I; Naseem I
[Ad] Endereço:Department of Biochemistry, Faculty of Life Sciences, Aligarh Muslim University, Aligarh, 202002, India.
[Ti] Título:Inhibitory effect of vitamin B against glycation and reactive oxygen species production in HSA: An in vitro approach.
[So] Source:Arch Biochem Biophys;627:21-29, 2017 Aug 01.
[Is] ISSN:1096-0384
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hyperglycaemia is a key factor for the formation of advanced glycated endproducts (AGEs). Inhibition of glycation may play key role in minimizing the diabetes related complications. We have tried to explore the glucose and methyl glyoxal mediated glycation and antiglycation activity of niacin using human serum albumin as model protein. Protein was incubated with glucose for 28 days at physiological temperature to achieve glycation. Antiglycation activity was evaluated by assessing free lysine, carbonyl content, AGE specific fluorescence. Molecular docking and isothermal titration calorimetry was deployed to study the interaction of niacin with HSA and get a detailed insight of binding site and thermodynamics of interaction. Niacin reduced the glycation significantly which was evident from the estimation of free lysine and carbonyl content. Niacin binds with HSA in a spontaneous manner with the binding constant in the range of 10 M . Niacin also prevented the loss in secondary structure induced by glycation. Reactive oxygen species were also effectively quenched by niacin leading to protection from DNA damage. Niacin was found to be located at Sudlow's site I with binding energy of 5.3 kcal/mol. These results clearly highlight the antiglycation activity of niacin and its potential in preventing disease progression in diabetes.
[Mh] Termos MeSH primário: Produtos Finais de Glicação Avançada/antagonistas & inibidores
Niacina/farmacologia
Niacinamida/farmacologia
Aldeído Pirúvico/metabolismo
Espécies Reativas de Oxigênio/antagonistas & inibidores
Albumina Sérica/metabolismo
Complexo Vitamínico B/farmacologia
[Mh] Termos MeSH secundário: Glucose/metabolismo
Produtos Finais de Glicação Avançada/metabolismo
Glicosilação/efeitos dos fármacos
Seres Humanos
Hiperglicemia/tratamento farmacológico
Hiperglicemia/metabolismo
Simulação de Acoplamento Molecular
Estrutura Secundária de Proteína/efeitos dos fármacos
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glycation End Products, Advanced); 0 (Reactive Oxygen Species); 0 (Serum Albumin); 12001-76-2 (Vitamin B Complex); 25X51I8RD4 (Niacinamide); 2679MF687A (Niacin); 722KLD7415 (Pyruvaldehyde); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170619
[St] Status:MEDLINE


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[PMID]:28616955
[Au] Autor:Schandelmaier S; Briel M; Saccilotto R; Olu KK; Arpagaus A; Hemkens LG; Nordmann AJ
[Ad] Endereço:Department of Health Research Methods, Evidence, and Impact, McMaster University, 1280 Main Street West, Hamilton, ON, Canada, L8S4L8.
[Ti] Título:Niacin for primary and secondary prevention of cardiovascular events.
[So] Source:Cochrane Database Syst Rev;6:CD009744, 2017 06 14.
[Is] ISSN:1469-493X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Nicotinic acid (niacin) is known to decrease LDL-cholesterol, and triglycerides, and increase HDL-cholesterol levels. The evidence of benefits with niacin monotherapy or add-on to statin-based therapy is controversial. OBJECTIVES: To assess the effectiveness of niacin therapy versus placebo, administered as monotherapy or add-on to statin-based therapy in people with or at risk of cardiovascular disease (CVD) in terms of mortality, CVD events, and side effects. SEARCH METHODS: Two reviewers independently and in duplicate screened records and potentially eligible full texts identified through electronic searches of CENTRAL, MEDLINE, Embase, Web of Science, two trial registries, and reference lists of relevant articles (latest search in August 2016). SELECTION CRITERIA: We included all randomised controlled trials (RCTs) that either compared niacin monotherapy to placebo/usual care or niacin in combination with other component versus other component alone. We considered RCTs that administered niacin for at least six months, reported a clinical outcome, and included adults with or without established CVD. DATA COLLECTION AND ANALYSIS: Two reviewers used pre-piloted forms to independently and in duplicate extract trials characteristics, risk of bias items, and outcomes data. Disagreements were resolved by consensus or third party arbitration. We conducted random-effects meta-analyses, sensitivity analyses based on risk of bias and different assumptions for missing data, and used meta-regression analyses to investigate potential relationships between treatment effects and duration of treatment, proportion of participants with established coronary heart disease and proportion of participants receiving background statin therapy. We used GRADE to assess the quality of evidence. MAIN RESULTS: We included 23 RCTs that were published between 1968 and 2015 and included 39,195 participants in total. The mean age ranged from 33 to 71 years. The median duration of treatment was 11.5 months, and the median dose of niacin was 2 g/day. The proportion of participants with prior myocardial infarction ranged from 0% (4 trials) to 100% (2 trials, median proportion 48%); the proportion of participants taking statin ranged from 0% (4 trials) to 100% (12 trials, median proportion 100%).Using available cases, niacin did not reduce overall mortality (risk ratio (RR) 1.05, 95% confidence interval (CI) 0.97 to 1.12; participants = 35,543; studies = 12; I = 0%; high-quality evidence), cardiovascular mortality (RR 1.02, 95% CI 0.93 to 1.12; participants = 32,966; studies = 5; I = 0%; moderate-quality evidence), non-cardiovascular mortality (RR 1.12, 95% CI 0.98 to 1.28; participants = 32,966; studies = 5; I = 0%; high-quality evidence), the number of fatal or non-fatal myocardial infarctions (RR 0.93, 95% CI 0.87 to 1.00; participants = 34,829; studies = 9; I = 0%; moderate-quality evidence), nor the number of fatal or non-fatal strokes (RR 0.95, 95% CI 0.74 to 1.22; participants = 33,661; studies = 7; I = 42%; low-quality evidence). Participants randomised to niacin were more likely to discontinue treatment due to side effects than participants randomised to control group (RR 2.17, 95% CI 1.70 to 2.77; participants = 33,539; studies = 17; I = 77%; moderate-quality evidence). The results were robust to sensitivity analyses using different assumptions for missing data. AUTHORS' CONCLUSIONS: Moderate- to high-quality evidence suggests that niacin does not reduce mortality, cardiovascular mortality, non-cardiovascular mortality, the number of fatal or non-fatal myocardial infarctions, nor the number of fatal or non-fatal strokes but is associated with side effects. Benefits from niacin therapy in the prevention of cardiovascular disease events are unlikely.
[Mh] Termos MeSH primário: Doenças Cardiovasculares/prevenção & controle
Niacina/administração & dosagem
Prevenção Primária
Prevenção Secundária
Vasodilatadores/administração & dosagem
[Mh] Termos MeSH secundário: Adulto
Idoso
Doenças Cardiovasculares/mortalidade
Seres Humanos
Meia-Idade
Infarto do Miocárdio/mortalidade
Infarto do Miocárdio/prevenção & controle
Niacina/efeitos adversos
Ensaios Clínicos Controlados Aleatórios como Assunto/estatística & dados numéricos
Acidente Vascular Cerebral/mortalidade
Acidente Vascular Cerebral/prevenção & controle
Vasodilatadores/efeitos adversos
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Vasodilator Agents); 2679MF687A (Niacin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170816
[Lr] Data última revisão:
170816
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170616
[St] Status:MEDLINE
[do] DOI:10.1002/14651858.CD009744.pub2


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[PMID]:28424880
[Au] Autor:Isbister KM; Lamb EG; Stewart KJ
[Ad] Endereço:Department of Plant Sciences, University of Saskatchewan, 51 Campus Drive, Saskatoon, S7N 5A8, SK, Canada.
[Ti] Título:Herbicide Toxicity Testing with Non-Target Boreal Plants: The Sensitivity of Achillea millefolium L. and Chamerion angustifolium L. to Triclopyr and Imazapyr.
[So] Source:Environ Manage;60(1):136-156, 2017 Jul.
[Is] ISSN:1432-1009
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Terrestrial plant toxicity tests were conducted to determine the sensitivity of two boreal plants, yarrow (Achillea millefolium L.) and fireweed (Chamerion angustifolium L.), to the herbicides imazapyr and triclopyr. Both plants are common non-target species on northern powerline rights-of-way where the impacts of proposed herbicide applications are of concern. In the vegetative vigour test, triclopyr foliar spray caused extensive damage to A. millefolium at <50% of the maximum field application rate (inhibition concentration (IC) = 1443.8 g a.i. ha ) and was lethal to C. angustifolium at the lowest dose tested (1210.9 g a.i. ha ). Both species demonstrated extremely high sensitivity to imazapyr foliar spray: IC = 8.29 g a.i. ha and 4.82 g a.i. ha (<1.5% of the maximum field rate). The seedling emergence and seedling growth tests were conducted in the organic horizon of five boreal soils. Few differences in herbicide bioavailability between soils were detected. Triclopyr limited growth of A. millefolium, C. angustifolium and standard test species Calamagrostis canadensis at low levels (most IC estimates between 2-20 µg g ). For imazapyr, IC estimates could not be calculated as there was >75% inhibition of endpoints at the lowest doses of ~2 µg g . A foliar application of triclopyr or imazapyr for woody species control would likely cause significant damage to boreal non-target plants. The high sensitivity of both species to herbicide residues in soil indicates long term impacts are dependent on herbicide degradation rates in northern conditions. A. millefolium performed well and is recommended for use in toxicity testing relevant to boreal regions.
[Mh] Termos MeSH primário: Achillea/efeitos dos fármacos
Glicolatos/toxicidade
Herbicidas/toxicidade
Imidazóis/toxicidade
Niacina/análogos & derivados
Onagraceae/efeitos dos fármacos
Poluentes do Solo/toxicidade
[Mh] Termos MeSH secundário: Achillea/crescimento & desenvolvimento
Clima Frio
Niacina/toxicidade
Onagraceae/crescimento & desenvolvimento
Projetos Piloto
Plântulas/efeitos dos fármacos
Plântulas/crescimento & desenvolvimento
Solo/química
Especificidade da Espécie
Testes de Toxicidade
Yukon
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glycolates); 0 (Herbicides); 0 (Imidazoles); 0 (Soil); 0 (Soil Pollutants); 2679MF687A (Niacin); 787MX0M5A6 (imazapyr); MV06PHJ6I0 (triclopyr)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170421
[St] Status:MEDLINE
[do] DOI:10.1007/s00267-017-0867-7



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