Park Kyungeun, Jung Sunyoon, Ha Jung-Heun, Jeong Yoonhwa
Department of Food Science and Nutrition, Dankook University, Cheonan 31116, Republic of Korea.
Research Center for Industrialization of Natural Neutralization, Dankook University, Yongin 16890, Republic of Korea.
Nutrients. 2025 Jan 8;17(2):213. doi: 10.3390/nu17020213.
BACKGROUND/OBJECTIVES: Obesity is a key factor in metabolic syndrome (MetS) development. Consumption of a high-fat diet (HFD) accelerates the onset of obesity and associated metabolic complications. (PB) has been traditionally utilized in Korean medicine for its antioxidant, anti-diabetic, anticancer, and hepatoprotective effects. However, specific effects of PB hydrolysate on skeletal muscles have not been fully elucidated. Therefore, this study sought to assess the influence of PB on HFD-induced MetS, focusing on the lipid metabolism and inflammatory responses mediated by AMP-activated protein kinase activation.
To induce obesity, 6-week-old C57BL/6J mice were maintained on an HFD for 8 weeks, after which PB hydrolysate was orally administered for 16 weeks while the HFD regimen was sustained. A glucose tolerance test was conducted orally to evaluate glucose regulation, and forelimb grip strength was assessed upon completion of the experimental period. Histological assessments, serum biochemical analysis, lipid extraction, Western blot analysis, and quantitative reverse-transcription polymerase chain reaction (qRT-PCR) were performed following euthanasia.
PB significantly reduced ectopic lipid deposition in skeletal muscles, enhanced muscle strength, and improved insulin sensitivity by increasing fatty acid oxidation via AMP-activated protein kinase/carnitine palmitoyltransferase 1 activation and inhibiting lipogenesis via stearoyl-CoA desaturase 1 gene downregulation. Furthermore, PB alleviated HFD-induced low-grade chronic inflammation by decreasing systemic monocyte chemoattractant protein 1 levels, thereby reducing ectopic fat deposition.
This study highlights the potential of PB as a nutraceutical to mitigate MetS in HFD-fed mice.
背景/目的：肥胖是代谢综合征（MetS）发生发展的关键因素。高脂饮食（HFD）的摄入会加速肥胖及相关代谢并发症的发生。传统上，葛根（PB）在韩医学中因其抗氧化、抗糖尿病、抗癌和保肝作用而被使用。然而，葛根水解产物对骨骼肌的具体作用尚未完全阐明。因此，本研究旨在评估葛根对高脂饮食诱导的代谢综合征的影响，重点关注由AMP激活的蛋白激酶激活介导的脂质代谢和炎症反应。
为诱导肥胖，将6周龄的C57BL/6J小鼠喂饲高脂饮食8周，之后在持续高脂饮食方案的同时口服给予葛根水解产物16周。口服进行葡萄糖耐量试验以评估葡萄糖调节情况，并在实验期结束时评估前肢握力。安乐死后进行组织学评估、血清生化分析、脂质提取、蛋白质印迹分析和定量逆转录聚合酶链反应（qRT-PCR）。
葛根通过激活AMP激活的蛋白激酶/肉碱棕榈酰转移酶1增加脂肪酸氧化，并通过下调硬脂酰辅酶A去饱和酶1基因抑制脂肪生成，从而显著减少骨骼肌中的异位脂质沉积，增强肌肉力量并改善胰岛素敏感性。此外，葛根通过降低全身单核细胞趋化蛋白1水平减轻高脂饮食诱导的低度慢性炎症，从而减少异位脂肪沉积。
本研究强调了葛根作为一种营养保健品减轻高脂饮食喂养小鼠代谢综合征的潜力。
