MSG intake linked to obesity and metabolic syndrome
An international team of researchers investigating the links between monosodium glutamate (MSG) and obesity and metabolic syndrome in mice have suggested that the food additive may be 'a critical factor' in the initiation of obesity and metabolic syndrome.
Writing in the Journal of Medicinal Food, the team detailed findings from research in mice which they may suggest that MSG plays a role in the onset of obesity and non-alcoholic fatty liver disease (referred to as NASH) by decreasing metabolism rates "and that the calorie intake is capable of influencing its progression without affecting the degree of obesity in our animal model."
"MSG appears to be a critical factor in the initiation of obesity, whereas calorie intake may modulate the progression of disease," wrote the team - led by Makoto Fujimoto from the University of Toyama in Japan.
Commenting on the research, Sampath Parthasarathy, co-editor-in-chief of the journal said the findings "may have far reaching implications" - noting that although MSG has been deemed a safe food additive, its dosage, interaction with other drugs, effects on vulnerable populations, and effects on chronic inflammatory diseases and neurological diseases "are unknown."
Research details
Fujimoto and colleagues used a mouse model to investigate whether a light dietary restriction has an effect on the previously observed suggestion that MSG intake may be related to obesity.
Mice were fed MSG at birth before being split to receive either a estricted (75% of a full stomach) or ad libitum diet starting at three months of age. These mice were compared to restricted diet mice who had not been fed MSG.
The team found that by six months of age MSG mice on a restricted diet manifested the same degree of obesity, serum ALT, and liver histology changes compared to their unrestricted diet counterpart - and opposite of control mice on a restricted diet without MSG.
"These findings suggest that MSG induces metabolic changes by decreasing metabolism rates, rather than by increasing energy intake, as a moderate diet restriction is not sufficient to halt the fatty liver development," noted the research team.
By 12 months, the MSG-fed mice had developed obesity with visceral fat deposition regardless of the dietary regimen, said Fujimoto and colleagues.
"Both MSG-treated groups did not show significant lower body weight regardless of diet restriction at both evaluation points," the team wrote. "This result is congruent with the other reports using MSG-treated animal models."
However, the authors conceded that the fact that they did not include an MSG-free control that was fed ad libitum is a limitation of the present study.
"This group could have helped to get more solid conclusions on the effects of dietary effects," wrote the team. "Furthermore, since MSG was not administered orally in this study, we cannot infer strict advices on an acceptable intake of MSG for humans based on our data."
"Nonetheless, we believe that our results and the fact that MSG administered orally may pass through the placenta should be considered in future assessments," the team concluded.
Source: Journal of Medicinal Food
Volume 13, Number 3, Pages 374-383. doi:10.1089/jmf.2012.0029.
"A Dietary Restriction Influences the Progression But Not the Initiation of MSG-Induced Nonalcoholic Steatohepatitis"
Authors: Fujimoto Makoto, Tsuneyama Koichi, et al
