title: A dietary restriction influences the progression but not the initiation of MSG-Induced nonalcoholic steatohepatitis.
abstract: The metabolic syndrome is a major worldwide health care issue and a dominant risk factor for cardiovascular disease. The liver manifestations of this syndrome include nonalcoholic fatty liver disease (NAFLD) and its progressive variant nonalcoholic steatohepatitis (NASH). Although significant research has been performed, the basic pathogenesis of NAFLD/NASH remains controversial and effective treatments are still unavailable. We have previously reported on a murine model of NASH induced by the neonatal injection of monosodium glutamate (MSG), which includes the clinical manifestations of central obesity, diabetes, hyperlipidemia, and ultimately liver inflammation, fibrosis, and cancer. Although MSG is considered a safe food additive, its administration to pregnant rats increases the voracity and growth hormone levels in the offspring. To further understand the biology of this model, we have investigated the influence of the calorie intake on these clinical manifestations by feeding animals a restrictive diet. MSG-treated animals fed a restrictive diet continue to manifest obesity and early stage NASH but have improvements in serum lipid profiles. At 12 months of age, mice had manifestations of obesity, whether animals were fed a restricted or control diet, but animals fed a restrictive diet had a reduction in the progression of NASH. In conclusion, MSG appears to be a critical factor in the initiation of obesity, whereas calorie intake may modulate the progression of disease.
authors.affiliation: 1 Department of Diagnostic Pathology, University of Toyama , Toyama, Japan.
authors.forename: Makoto
authors.initials: M
authors.lastname: Fujimoto
authors.forename: Koichi
authors.initials: K
authors.lastname: Tsuneyama
authors.forename: Yuko
authors.initials: Y
authors.lastname: Nakanishi
authors.forename: Thucydides L
authors.initials: TL
authors.lastname: Salunga
authors.forename: Kazuhiro
authors.initials: K
authors.lastname: Nomoto
authors.forename: Yoshiyuki
authors.initials: Y
authors.lastname: Sasaki
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: Yutaka
authors.initials: Y
authors.lastname: Shimada
authors.forename: M Eric
authors.initials: ME
authors.lastname: Gershwin
authors.forename: Carlo
authors.initials: C
authors.lastname: Selmi
mesh_terms: D000818:Animals; D004038:Diet, Reducing; D018450:Disease Progression; D005234:Fatty Liver / Q000178:diet therapy / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D006801:Humans; D008297:Male; D008813:Mice, Inbred ICR; D065626:Non-alcoholic Fatty Liver Disease; D009765:Obesity / Q000150:complications / Q000178:diet therapy* / Q000378:metabolism; D012970:Sodium Glutamate / Q000009:adverse effects* / Q000378:metabolism
chemical_list: D012970:Sodium Glutamate