摘要：The aim of this study was to determine how 3-guanidinopropionic acid (?-GPA) treatment, that reduces body mass, alters obese skeletal muscle mass and regulatory mechanisms controlling muscle mass. Lean (L) and ob/ ob (O) mice were fed either a control (C) or a ?-GPA-containing (F) diet for 8 weeks. Body mass decreased in both ?-GPA treated groups. Despite a lower plantar flexor-complex muscle mass, both ?-GPA treated groups achieved the same muscle mass. Raptor-mammalian Target of Rapamycin protein association was lower in OC muscle (vs. LC) and was not altered with ?-GPA, despite reductions in S6K1 activation (OF only). 4E-BP1 phosphorylation increased in the ?-GPA treated groups, but only the OF mice displayed an increase in eIF4E phosphorylation that corresponded with a trending increase in eIF4G-eIF4E association. Thus, long-term ?-GPA treatment augments obesity-induced dysregulation of mechanisms controlling skeletal muscle mass to that of the lean, while reducing body mass.
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