Department of Horticultural Bioscience/Life and Industry Convergence Research Institute, College of Natural Resources and Life Science, Pusan National University, Miryang 50463, Republic of Korea.
Institute of Nano-Bio Convergence, Pusan National University, Busan 46241, Republic of Korea.
Nutrients. 2024 Jul 8;16(13):2171. doi: 10.3390/nu16132171.
This study aimed to investigate the therapeutic potential of extract (CME) in counteracting adipogenesis and its associated metabolic disturbances in murine models. In vitro experiments utilizing 3T3-L1 preadipocytes revealed that CME potently inhibited adipocyte differentiation, as evidenced by a dose-dependent reduction in lipid droplet formation. Remarkably, CME also attenuated glucose uptake and intracellular triglyceride accumulation in fully differentiated adipocytes, suggesting its ability to modulate metabolic pathways in mature adipose cells. Translating these findings to an in vivo setting, we evaluated the effects of CME in C57BL/6N mice fed a high-fat diet (HFD) for 10 weeks. CME administration, concomitantly with the HFD, resulted in a significant attenuation of body weight gain compared to the HFD control group. Furthermore, CME treatment led to substantial reductions in liver weight, total fat mass, and deposits of visceral and retroperitoneal adipose tissue, underscoring its targeted impact on adipose expansion. Histological analyses revealed the remarkable effects of CME on hepatic steatosis. While the HFD group exhibited severe lipid accumulation within liver lobules, CME dose-dependently mitigated this pathology, with the highest dose virtually abolishing hepatic fat deposition. An examination of adipose tissue revealed a progressive reduction in adipocyte hypertrophy upon CME treatment, culminating in a near-normalization of adipocyte morphology at the highest dose. Notably, CME exhibited potent anti-inflammatory properties, significantly attenuating the upregulation of pro-inflammatory cytokines' mRNA levels (TNF-α, IL-1β and IL-6) in the livers of HFD-fed mice. This suggests a potential mechanism through which CME may exert protective effects against inflammation associated with obesity and fatty liver disease.
这项研究旨在探究 提取物(CME)在对抗脂肪生成及其相关代谢紊乱方面的治疗潜力,为此我们在鼠模型中进行了实验。利用 3T3-L1 前脂肪细胞进行的体外实验表明,CME 能够强力抑制脂肪细胞分化,这一点可从其对脂滴形成的剂量依赖性减少得到证明。值得注意的是,CME 还能减弱完全分化的脂肪细胞对葡萄糖的摄取和细胞内三酰甘油的积累,这表明它能够调节成熟脂肪细胞中的代谢途径。将这些发现转化为体内环境,我们评估了 CME 在喂食高脂肪饮食(HFD)10 周的 C57BL/6N 小鼠中的作用。与 HFD 对照组相比,同时给予 CME 治疗可显著抑制体重增加。此外,CME 治疗导致肝重、总脂肪质量以及内脏和腹膜后脂肪组织沉积的显著减少,突出了其对脂肪扩张的靶向影响。组织学分析揭示了 CME 对肝脂肪变性的显著作用。HFD 组肝小叶内出现严重的脂质堆积,而 CME 呈剂量依赖性地减轻了这种病变,最高剂量几乎消除了肝脂肪沉积。对脂肪组织的检查表明,CME 处理后脂肪细胞肥大呈渐进性减少,最高剂量时脂肪细胞形态几乎恢复正常。值得注意的是,CME 表现出强大的抗炎特性,可显著减弱 HFD 喂养小鼠肝脏中促炎细胞因子(TNF-α、IL-1β 和 IL-6)mRNA 水平的上调。这表明 CME 可能通过发挥抗炎作用来预防肥胖和脂肪肝疾病相关的炎症。