Mitigating Dexamethasone-Induced Muscle Wasting and Mitochondrial Impairment in Mice on a High-Fat and High-Sucrose Diet With Peanut Sprout Extract.

Prolonged high-fat and high-sucrose diets (HFHS) diet accelerates skeletal muscle atrophy and impairs muscle function. Combined HFHS diet and dexamethasone (Dex), a synthetic glucocorticoid which involves the induction of protein degradation, will promote atrophy of skeletal muscle. Although we previously demonstrated that peanut sprout extract (PSE) inhibits adipogenesis, its impact on HFHS+Dex-induced muscle atrophy remained unknown. To investigate, we treated C57BL/6 male mice with a control or HFHS diet, with or without PSE (10 mg/kg BW), over 10 weeks, introducing Dex (10 mg/kg BW) once daily for six consecutive days to induce muscle atrophy. PSE treatment reduced skeletal muscle triglyceride accumulation, restored muscle strength (grip and hanging capacity), and mitigated muscle atrophy expression. While systemic interleukin (IL)-1β levels were unaffected, PSE reduced inflammatory gene expression and inhibited nuclear factor-κB (NF-κB) protein expression in skeletal muscle, enhanced mitochondrial function (increased mitochondrial transcription factor A (TFAM), oxidative phosphorylation (OXPHOS) complex IV/V protein expression, but no differences in peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α)). Consistent with these results, PSE protected against muscle atrophy in Dex-treated C2C12 cells by modulating atrophic and inflammatory expression. This study highlights PSE's efficacy in attenuating skeletal muscle atrophy and mitigating inflammation with partial enhancement of mitochondrial function.