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Abstract Title:

Monosodium glutamate neonatal intoxication associated with obesity in adult stage is characterized by chronic inflammation and increased mRNA expression of peroxisome proliferator-activated receptors in mice.

Abstract Source:

Basic Clin Pharmacol Toxicol. 2011 Jun;108(6):406-13. Epub 2011 Feb 9. PMID: 21205225

Abstract Author(s):

Ruben Roman-Ramos, Julio C Almanza-Perez, Rebeca Garcia-Macedo, Gerardo Blancas-Flores, Angeles Fortis-Barrera, Edgar I Jasso, Mario Garcia-Lorenzana, Alfonso E Campos-Sepulveda, Miguel Cruz, Francisco J Alarcon-Aguilar

Article Affiliation:

Department of Health Sciences, Division of Health and Biological Sciences, Metropolitan Autonomous University of Iztapalapa, DF, Mexico Hospital of Specialities, CMNSXXI, Mexican Institute of Social Security, DF, Mexico Department of Reproduction Biology, Division of Health and Biological Sciences, Metropolitan Autonomous University of Iztapalapa, DF, Mexico Department of Pharmacology, Faculty of Medicine, Autonomous National University of Mexico, DF, Mexico.

Abstract:

The monosodium glutamate (MSG) neonatal administration in mice provides a model of obesity with impaired glucose tolerance (IGT) and insulin resistance. However, the inflammatory profile of cytokines produced from fat tissue and its relationship to the metabolic dysfunction induced by MSG have not yet been revealed. The aim of this study was to establish the inflammatory profile attributed to MSG by measuring the expression of adipokines in visceral fat and serum of 19-week-old mice as well as the peroxisome proliferator-activated receptors alpha and gamma (PPARα and γ). Some metabolic and biochemical parameters were also quantified. The MSG increased mRNA expression of interleukin-6 (IL-6), tumour necrosis factor-alpha (TNFα), resistin and leptin, but adiponectin did not exhibit any changes. In addition, impaired glucose tolerance, increased levels ofinsulin, resistin and leptin were observed in serum. Both PPARα and PPARγ were activated in MSG-induced obese mice, which might explain its inflammatory profile. However, liver transaminases were severely depressed, indicating that MSG may also induce liver injury, contributing to inflammation. The MSG neonatal neuro-intoxication in mice may thus provide a model of obesity and inflammation characterized by the dual activation of PPARα and PPARγ, which might offer new insights into the mechanism of inflammatory diabetes in obesity leading to steatohepatitis, as well as a suitable model to study the role of new therapeutic agents to prevent or reduce insulin resistance, the inflammatory state and liver steatosis.

Study Type : Animal Study

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Sayer Ji
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