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Brain Lesions, Obesity, and Other Disturbances in Mice Treated with Monosodium Glutamate
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10
References
1969
Year
Brain DevelopmentMonosodium GlutamateObesityMetabolic SyndromeNueral CentersExperimental NeuropathologyNeuroendocrine MechanismAduls SyndromeHypothalamic PeptideOther DisturbancesBrain InjuryNeurologyNeuropathologyNeuroimmunologyNeurochemistryHealth SciencesEnergy HomeostasisNeuropharmacologyCerebral Blood FlowEndocrinologyPharmacologyNeurophysiologyPhysiologyMice TreatedNeuroscienceBiological PsychiatryMetabolismMedicine
The study postulates that the adult syndrome observed after monosodium glutamate exposure reflects a multifaceted neuroendocrine disturbance caused by disruption of developing neural centers that mediate endocrine function. Monosodium glutamate injection in newborn mice caused acute neuronal necrosis in multiple brain regions, and adults exhibited stunted growth, obesity, female sterility, and endocrine organ pathology, with obesity not attributable to increased food intake.
In newborn mice subcutaneous injectionis of monosodium glutamate induced acute neuronal necrosis in several regions of developing brain including the hypothanamus. As adults, treated animals showed stunted skeletal development, marked obesity, and female sterility. Pathological changes were also found in several organs associated with endocrine function. Studies of food consumption failed to demonstrate hyperphagia to explain the obesity. It is postulated that the aduls syndrome represents a multifacted nueroendocrine disturbance arising from the disruption of developing nueral centers concered in the mediation of endocrine function.
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