Laboratory Animal Resource Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), 125 Gwahak-ro, Yuseong-gu, Daejeon 34141, Republic of Korea.
Department of Functional Genomics, KRIBB School of Bioscience, University of Science and Technology (UST), 217 Gajeong-ro, Yuseong-gu, Daejeon, Korea.
Int J Med Sci. 2020 Mar 5;17(6):787-798. doi: 10.7150/ijms.42247. eCollection 2020.
Obesity is a medical condition in which excess body fat has accumulated to a serious extent. It is a chronic disease that can lead to dyslipidemia, insulin resistance, and type 2 diabetes. In the present study, we investigated the anti-obesity effects of (SA) extract on a high-fat diet (HFD)-induced C57BL/6J obese mice. The mice were divided into vehicle and three SA groups (25, 50, and 100 mg/kg body weight). The mice were fed a HFD with or without SA for 12 weeks. The oral administration of SA reduced body and adipose tissue weight in HFD-fed mice compared to those in the vehicle group (<0.05). Adipocyte size and inflammation significantly decreased in the SA-administered groups in a dose-dependent manner. In particular, adipocytes larger than 5000 µm were remarkably reduced by around 50% in the SA-treated groups (<0.05). In addition, SA contributes towards reducing insulin resistance (measured as the HOMA-IR index) and glucose intolerance in HFD-induced obese mice (<0.05; Vehicle 21.5±3.1 vs. SA100 4.7±0.4). These beneficial effects of SA on obesity may be linked to the suppression of lipogenesis and stimulating energy metabolism in white adipose tissue and muscle. In white adipose tissue and muscle, the administration of SA activated AMPK pathway, leading to the inhibition of the development of pathophysiological conditions associated with obesity, including lipogenesis and inflammation. These findings suggest that SA may prevent obesity through inhibiting fat accumulation in HFD-induced obese mice. Therefore, SA is able to exert metabolic benefits in the prevention of obesity and insulin resistance.
肥胖是一种身体脂肪积累过多的医学病症。它是一种慢性疾病,可以导致血脂异常、胰岛素抵抗和 2 型糖尿病。在本研究中,我们研究了(SA)提取物对高脂肪饮食(HFD)诱导的 C57BL/6J 肥胖小鼠的抗肥胖作用。将小鼠分为载体组和三个 SA 组(25、50 和 100mg/kg 体重)。将小鼠用 HFD 喂养或不服用 SA 喂养 12 周。与载体组相比,SA 的口服给药降低了 HFD 喂养小鼠的体重和脂肪组织重量(<0.05)。脂肪细胞大小和炎症在 SA 给药组中呈剂量依赖性显著降低。特别是,SA 处理组中大于 5000 µm 的脂肪细胞减少了约 50%(<0.05)。此外,SA 有助于降低 HFD 诱导的肥胖小鼠的胰岛素抵抗(用 HOMA-IR 指数测量)和葡萄糖不耐受(<0.05;载体 21.5±3.1 对 SA100 4.7±0.4)。SA 对肥胖的这些有益影响可能与抑制白色脂肪组织和肌肉中的脂肪生成和刺激能量代谢有关。在白色脂肪组织和肌肉中,SA 的给药激活 AMPK 途径,导致抑制与肥胖相关的病理生理状况的发展,包括脂肪生成和炎症。这些发现表明,SA 可以通过抑制 HFD 诱导的肥胖小鼠体内脂肪积累来预防肥胖。因此,SA 能够在预防肥胖和胰岛素抵抗方面发挥代谢益处。