Key result
Peanut sprout extract suppresses lipid accumulation in animal models but yields no systemic metabolic benefit.
Why the study?
The influence of extraction conditions on the anti-adipogenic activity and cross-species relevance of peanut sprout extract remained unclear.
Peanut sprout extract suppresses adipogenic lipid accumulation in vitro through AMPK-related mitochondrial responses, though in vivo systemic metabolic benefits were not observed.
PSE extraction optimization may inform functional food research; leaves open efficacy in human metabolic disorders.
We previously reported that peanut sprout extract (PSE) possesses metabolic regulatory potential; however, the influence of extraction conditions on its anti-adipogenic activity and cross-species relevance remains unclear. In this study, PSE was prepared under multiple extraction conditions using electrodialysis-processed lava seawater to identify a selected extract with enhanced lipid-regulatory activity. Among the tested preparations, extraction at 60 °C with electrodialysis water (60 °C EDW) was selected based on its chemical profile and lipid-lowering efficacy. The selected PSE significantly reduced lipid accumulation during both early and late stages of adipogenesis in 3 T3-L1 adipocytes and increased glucose uptake. Although systemic metabolic abnormalities were not significantly improved after 8 weeks of PSE administration in high-fat diet–fed mice (100 or 400 mg/kg) or in a small pre–post trial of obese companion dogs given 5% PSE-supplemented drinking water, adipose tissue–derived stem cells isolated from murine and canine adipose tissues (mAT MSCs and cAT MSCs, respectively) showed consistent lipid-lowering responses during adipogenic differentiation. In both mAT MSCs and cAT MSCs, PSE suppressed lipid accumulation, and in canine cells it significantly increased maximal mitochondrial oxygen consumption rate, indicating enhanced mitochondrial respiratory capacity. PSE induced AMP-activated protein kinase (AMPK) phosphorylation across adipocyte models. Pharmacological inhibition of AMPK with Compound C abolished the reduction in sterol regulatory element-binding protein-1c and the increase in mitochondrial respiration, whereas suppression of fatty acid synthase remained unaffected. These findings suggest that EDW-derived PSE suppresses adipogenic lipid accumulation and is associated with AMPK-related mitochondrial responses in murine and canine adipose-derived models.
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Choi et al. (2026) studied Obesity and adipogenesis. Peanut sprout extract (PSE) was evaluated on Lipid accumulation and systemic metabolic abnormalities. Peanut sprout extract (100 or 400 mg/kg) suppressed adipogenic lipid accumulation and enhanced AMPK-related mitochondrial responses in murine and canine adipose models, without systemic improvement.
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