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Tytuł:
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Nicotinamide reduces inflammation and oxidative stress via the cholinergic system in fructose-induced metabolic syndrome in rats.
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Autorzy:
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Villeda-González JD; Programa de Posgrado en Biología Experimental, Universidad Autónoma Metropolitana-Iztapalapa, San Rafael Atlixco 186, México City, México; Unidad de Investigación Médica en Bioquímica, Hospital de Especialidades 'Bernardo Sepúlveda Gutiérrez' Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Ciudad de México, México.
Gómez-Olivares JL; Laboratorio de Biomembranas, División de Ciencias Biológicas y de la Salud, Universidad Autónoma Metropolitana-Iztapalapa, San Rafael Atlixco 186, México City, México.
Baiza-Gutman LA; Laboratorio en Biología del Desarrollo, Unidad de Morfología y Función, Facultad de Estudios Superiores Iztacala, Universidad Nacional Autónoma de México, Estado de México, México.
Manuel-Apolinar L; Unidad de Investigación Médica en Enfermedades Endocrinas, Hospital de Especialidades 'Bernardo Sepúlveda Gutiérrez' Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Ciudad de México, México.
Damasio-Santana L; Unidad de Investigación Médica en Enfermedades Endocrinas, Hospital de Especialidades 'Bernardo Sepúlveda Gutiérrez' Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Ciudad de México, México.
Millán-Pacheco C; Facultad de Farmacia, Universidad Autónoma del Estado de Morelos, Cuernavaca, Morelos, México.
Ángeles-Mejía S; Laboratorio en Biología del Desarrollo, Unidad de Morfología y Función, Facultad de Estudios Superiores Iztacala, Universidad Nacional Autónoma de México, Estado de México, México.
Cortés-Ginez MC; Unidad de Investigación Médica en Bioquímica, Hospital de Especialidades 'Bernardo Sepúlveda Gutiérrez' Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Ciudad de México, México.
Cruz-López M; Unidad de Investigación Médica en Bioquímica, Hospital de Especialidades 'Bernardo Sepúlveda Gutiérrez' Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Ciudad de México, México.
Vidal-Moreno CJ; Departamento de Bioquímica y Biología Molecular-A, Universidad de Murcia, Regional Campus of International Excellence 'Campus Mare Nostrum', Murcia, Spain.
Díaz-Flores M; Unidad de Investigación Médica en Bioquímica, Hospital de Especialidades 'Bernardo Sepúlveda Gutiérrez' Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Ciudad de México, México. Electronic address: .
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Źródło:
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Life sciences [Life Sci] 2020 Jun 01; Vol. 250, pp. 117585. Date of Electronic Publication: 2020 Mar 31.
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Typ publikacji:
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Journal Article
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Język:
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English
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Imprint Name(s):
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Publication: <2008->: Amsterdam : Elsevier
Original Publication: Oxford; Elmsford, N. Y. [etc.] Pergamon Press.
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MeSH Terms:
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Oxidative Stress*
Inflammation/*metabolism
Metabolic Syndrome/*drug therapy
Niacinamide/*therapeutic use
Receptors, Cholinergic/*metabolism
Acetylcholinesterase/metabolism ; Animals ; Anthropometry ; Anti-Inflammatory Agents/therapeutic use ; Aryldialkylphosphatase/metabolism ; Butyrylcholinesterase/metabolism ; Cholinesterases/metabolism ; Fructose ; Gene Expression Regulation ; Glucose Tolerance Test ; Hemodynamics ; Humans ; Lipid Peroxidation ; Liver/enzymology ; Male ; Metabolic Syndrome/chemically induced ; Molecular Docking Simulation ; Rats ; Rats, Sprague-Dawley
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Contributed Indexing:
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Keywords: Acetylcholinesterase; Butyrylcholinesterase; Fructose; Metabolic syndrome; Nicotinamide
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Substance Nomenclature:
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0 (Anti-Inflammatory Agents)
0 (Receptors, Cholinergic)
25X51I8RD4 (Niacinamide)
30237-26-4 (Fructose)
EC 3.1.1.7 (Acetylcholinesterase)
EC 3.1.1.8 (Butyrylcholinesterase)
EC 3.1.1.8 (Cholinesterases)
EC 3.1.8.1 (Aryldialkylphosphatase)
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Entry Date(s):
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Date Created: 20200404 Date Completed: 20200505 Latest Revision: 20200505
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Update Code:
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20240105
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DOI:
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10.1016/j.lfs.2020.117585
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PMID:
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32243928
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Aims: Acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) have been associated with risk factors for metabolic syndrome (MetS). Our objective was to evaluate the effect of nicotinamide (NAM) on the activities, expression and protein content of cholinesterases in a MetS model.
Main Methods: MetS was induced in male rats administrating 40% fructose to the drinking water for 16 weeks. Additionally, from 5th week onward, the carbohydrate solution was replaced by NAM, at several concentrations for 5 h each morning for the next 12 weeks. In the 15th week, the glucose tolerance test was conducted, and blood pressure was measured. After the treatment period had concluded, the biochemical profile; oxidant stress; proinflammatory markers; and the activity, quantity and expression of cholinesterases were evaluated, and molecular docking analysis was performed.
Key Findings: The MetS group showed anthropometric, hemodynamic and biochemical alterations and increased cholinesterase activity, inflammation and stress markers. In the liver, cholinesterase activity and mRNA, free fatty acid, tumor necrosis factor-alpha (TNF-α), and thiobarbituric acid-reactive substance (TBARS) levels were increased, while reduced glutathione (GSH) levels were decreased. NAM partially or totally decreased risk factors for MetS, markers of stress and inflammation, and the activity (serum and liver) and expression (liver) of cholinesterases. Molecular docking analysis showed that NAM has a greater affinity for cholinesterases than acetylcholine (ACh), suggesting NAM as an inhibitor of cholinesterases.
Significance: Supplementation with 40% fructose induced MetS, which increased the activity and expression of cholinesterases, oxidative stress and the inflammation. NAM attenuated these MetS-induced alterations and changes in cholinesterases.
(Copyright © 2020 Elsevier Inc. All rights reserved.)
