TY - JOUR
T1 - Monosodium glutamate (MSG)
T2 - A villain and promoter of liver inflammation and dysplasia
AU - Nakanishi, Yuko
AU - Tsuneyama, Koichi
AU - Fujimoto, Makoto
AU - Salunga, Thucydides L.
AU - Nomoto, Kazuhiro
AU - An, Jun Ling
AU - Takano, Yasuo
AU - Iizuka, Seiichi
AU - Nagata, Mitsunobu
AU - Suzuki, Wataru
AU - Shimada, Tsutomu
AU - Aburada, Masaki
AU - Nakano, Masayuki
AU - Selmi, Carlo
AU - Gershwin, M. Eric
N1 - Funding Information:
We would like to thank Mr. Tokimasa Kumada, Mr. Hideki Hatta, and Ms. Kanako Yasuyoshi for their excellent technical assistance and Ms. Yukari Inoue for her excellent support in the preparation of this manuscript. This work was supported in part by a Grant-in-Aid for Scientific Research (No. 18590324), a Grant-in-Aid for the 21st Century COE Program and ‘High-Tech Research Center’ Project for Private Universities: matching fund subsidy from MEXT (Ministry of Education Culture, Sports, Science and Technology) of Japan, and the Uehara Memorial Foundation.
PY - 2008/2
Y1 - 2008/2
N2 - 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widespread usage of dietary MSG and we suggest that MSG should have its safety profile re-examined and be potentially withdrawn from the food chain.
AB - 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.
KW - Diabetes mellitus
KW - Liver steatosis
KW - Nonalcoholic steatohepatitis
KW - Obesity
UR - http://www.scopus.com/inward/record.url?scp=38049028313&partnerID=8YFLogxK
U2 - 10.1016/j.jaut.2007.11.016
DO - 10.1016/j.jaut.2007.11.016
M3 - 学術論文
C2 - 18178378
AN - SCOPUS:38049028313
SN - 0896-8411
VL - 30
SP - 42
EP - 50
JO - Journal of Autoimmunity
JF - Journal of Autoimmunity
IS - 1-2
ER -