Radish Seed Exerts Anti-Diabetic and Obesity-Reducing Effects in Mice by Promoting the Activation of Uncoupling Protein 1 and Peroxisome Proliferator-Activated Receptor-γ Coactivator 1-α

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Obesity is primarily due to excessive energy intake and lipid accumulation, leading to type 2 diabetes. Studies showed radish seed extract (RSE) can impede weight gain in mice, but the mechanism was unclear. We hypothesized that RSE inhibits obesity by stimulating adipocyte browning. Radish seeds were water-extracted, yielding a sulforaphene (SE) concentration of 1.381 ± 0.005 mg/g RSE. In 3T3-L1 adipocyte differentiation experiments, RSE and SE increased the expression of beige adipocyte markers uncoupling protein 1 (UCP1) and peroxisome proliferator-activated receptor-γ coactivator 1-α (PGC1α). In C57BL/6 mice, RSE and SE mitigated weight increase, averted fatty liver, and diminished fat accumulation. In the adipose tissue, we also noted the enhanced browning of white adipocytes through elevated expression of UCP1 and PGC1α. Increased mitochondrial numbers in treated adipocytes supported this effect. Additionally, RSE and SE improved glucose homeostasis and insulin sensitivity in high-fat diet-fed mice, indicating RSE's potential to prevent obesity and diabetes by enhancing adipocyte thermogenesis.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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