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Neonatal MSG reduces hypothalamic DA, beta-endorphin, and delays weight gain in genetically obese (A viable
F A Caputo1, S F Ali, G L Wolff
1Division of Neurotoxicology, National Center for Toxicological Research/USFDA, Jefferson, AR 72079, USA.
Abstract:
Neonatal treatment with monosodium glutamate (MSG) decreases proopiomelanocortin (POMC) peptides and results in obesity. The yellow mouse is a model of obesity induced by the viable yellow (Avy) gene at the agouti locus on Chromosome 2, which results in overproduction of a POMC receptor antagonist. Thus we hypothesized that MSG, when imposed on the genetically susceptible model, would alter the development of obesity. Both yellow obese (Avy) and black lean (alpha/alpha) males were injected on Postnatal Days 1, 3, 5, 7, and 9 with 2.0 mg/g body weight MSG or saline SC. Their food intake, growth parameters, and neurochemical status were examined. Paradoxically, MSG interacted with the yellow phenotype to delay the rapid rate of weight gain characteristic of this model (p < 0.05). Food intake was decreased (p < 0.05) in both phenotypes treated with MSG, as was hypothalamic content of dopamine (p < 0.05) and of the POMC peptide, beta-endorphin (p < 0.001). The yellow obese phenotype was more sensitive than the black lean phenotype to the neurochemical effect of early postnatal MSG administration. Recent reports suggest the agouti locus protein is an antagonist of the receptor for another POMC peptide, melanocyte-stimulating hormone (MSH). Therefore, the balance of functional activity between various POMC peptides appears to be an important factor in the development of both acquired and genetic obesity.
Insights
Neonatal monosodium glutamate (MSG) treatment paradoxically delayed weight gain in a genetic obesity model. MSG decreased food intake and altered neurochemicals, with yellow obese mice showing greater sensitivity.
Area of Science:
- Neuroendocrinology
- Obesity Research
- Developmental Biology
Background:
- Neonatal monosodium glutamate (MSG) administration is known to decrease proopiomelanocortin (POMC) peptides, leading to obesity.
- The viable yellow (Avy) mouse model exhibits obesity due to a genetic mutation affecting the agouti locus, resulting in POMC receptor antagonist overproduction.
Purpose of the Study:
- To investigate the hypothesis that MSG administration would alter obesity development in genetically susceptible yellow mice.
- To examine the effects of neonatal MSG on food intake, growth, and neurochemical status in both yellow obese and black lean mice.
Main Methods:
- Neonatal male mice (yellow obese Avy and black lean alpha/alpha) received daily subcutaneous injections of MSG (2.0 mg/g body weight) or saline from postnatal days 1-9.
- Evaluated food intake, growth parameters, and hypothalamic neurochemical status, including dopamine and beta-endorphin levels.
Main Results:
- MSG paradoxically delayed weight gain in the yellow obese phenotype (p < 0.05).
- Food intake was significantly reduced in both phenotypes treated with MSG (p < 0.05).
- Hypothalamic dopamine and beta-endorphin content decreased in MSG-treated mice (p < 0.05 and p < 0.001, respectively), with yellow mice showing higher sensitivity.
Conclusions:
- Early postnatal MSG administration interacts with genetic susceptibility to influence obesity development.
- The balance of POMC peptides is crucial for both acquired and genetic obesity, as suggested by the neurochemical alterations observed.
- The agouti locus protein's role as a melanocyte-stimulating hormone (MSH) receptor antagonist highlights the complex interplay of POMC peptides in metabolic regulation.