title: Monosodium glutamate (MSG): a villain and promoter of liver inflammation and dysplasia.
abstract: Chronic inflammation is a common theme in a variety of disease pathways, including autoimmune diseases. The pathways of chronic inflammation are well illustrated by nonalcoholic steatohepatitis (NASH), which is of a serious concern due to its increasing prevalence in the westernized world and its direct correlation with lifestyle factors, particularly diet. Importantly, NASH may ultimately lead to the development of hepatocellular carcinoma. We previously reported that injection of monosodium glutamate (MSG) in ICR mice leads to the development of significant inflammation, central obesity, and type 2 diabetes. To directly address the long-term consequences of MSG on inflammation, we have performed serial analysis of MSG-injected mice and focused in particular on liver pathology. By 6 and 12 months of age, all MSG-treated mice developed NAFLD and NASH-like histology, respectively. In particular, the murine steatohepatitis at 12 months was virtually undistinguishable from human NASH. Further, dysplastic nodular lesions were detected in some cases within the fibrotic liver parenchyma. We submit that MSG treatment of mice induces obesity and diabetes with steatosis and steatohepatitis resembling human NAFLD and NASH with pre-neoplastic lesions. These results take on considerable significance in light of the widespread usage of dietary MSG and we suggest that MSG should have its safety profile re-examined and be potentially withdrawn from the food chain.
authors.affiliation: Department of Diagnostic Pathology, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, Toyama, Japan.
authors.forename: Yuko
authors.initials: Y
authors.lastname: Nakanishi
authors.forename: Koichi
authors.initials: K
authors.lastname: Tsuneyama
authors.forename: Makoto
authors.initials: M
authors.lastname: Fujimoto
authors.forename: Thucydides L
authors.initials: TL
authors.lastname: Salunga
authors.forename: Kazuhiro
authors.initials: K
authors.lastname: Nomoto
authors.forename: Jun-Ling
authors.initials: JL
authors.lastname: An
authors.forename: Yasuo
authors.initials: Y
authors.lastname: Takano
authors.forename: Seiichi
authors.initials: S
authors.lastname: Iizuka
authors.forename: Mitsunobu
authors.initials: M
authors.lastname: Nagata
authors.forename: Wataru
authors.initials: W
authors.lastname: Suzuki
authors.forename: Tsutomu
authors.initials: T
authors.lastname: Shimada
authors.forename: Masaki
authors.initials: M
authors.lastname: Aburada
authors.forename: Masayuki
authors.initials: M
authors.lastname: Nakano
authors.forename: Carlo
authors.initials: C
authors.lastname: Selmi
authors.forename: M Eric
authors.initials: ME
authors.lastname: Gershwin
mesh_terms: D000818:Animals; D056486:Chemical and Drug Induced Liver Injury / Q000209:etiology / Q000473:pathology*; D003924:Diabetes Mellitus, Type 2 / Q000139:chemically induced / Q000276:immunology / Q000473:pathology*; D005234:Fatty Liver / Q000139:chemically induced / Q000276:immunology / Q000473:pathology*; D006801:Humans; D008099:Liver / Q000473:pathology*; D008103:Liver Cirrhosis / Q000473:pathology; D051379:Mice; D009765:Obesity / Q000139:chemically induced / Q000276:immunology; D012970:Sodium Glutamate / Q000008:administration & dosage / Q000633:toxicity*
chemical_list: D012970:Sodium Glutamate