Suryaningtyas Indyaswan Tegar, Je Jae-Young
Department of Nutrition, Pukyong National University, Busan 48513, Republic of Korea; Research Center for Food Technology and Processing, National Research and Innovation Agency, Yogyakarta 55861, Indonesia.
Major of Human Bioconvergence, Division of Smart Healthcare, Pukyong National University, Busan 48513, Republic of Korea.
Tissue Cell. 2024 Dec;91:102630. doi: 10.1016/j.tice.2024.102630. Epub 2024 Nov 21.
Non-alcoholic fatty liver disease (NAFLD) is a progressive condition, advancing from simple hepatic lipid accumulation to inflammation, fibrosis, and increased risk of mortality. This study explores the therapeutic efficacy of bioactive peptides PIISVYWK (P1) and FSVVPSPK (P2) in ameliorating NAFLD in both oleic acid-treated HepG2 cells and high-fat diet (HFD)-induced mice. Our findings demonstrated that P1 and P2 significantly reduced hepatic fat deposition, enhanced lipolysis by promoting the release of free glycerol and free fatty acids, and suppressed key de novo lipogenesis-related proteins, including peroxisome proliferator-activated receptor γ (PPARγ), CCAAT-enhancer-binding protein α (C/EBPα), sterol regulatory element-binding protein 1 (SREBP-1), and fatty acid synthase (FAS). Furthermore, both peptides stimulated fatty acid oxidation via phosphorylation of AMP-activated protein kinase (AMPK) and hormone-sensitive lipase (HSL). Notably, reductions in body and liver weight, along with improved cholesterol profiles and liver function markers (alanine transaminase and aspartate aminotransferase), were observed in HFD mice. Additionally, P1 and P2 significantly attenuated the production of pro-inflammatory cytokines, such as tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) in both in vitro and in vivo models. Collectively, these results highlight the potent therapeutic potential of P1 and P2 in mitigating NAFLD progression, offering a promising intervention for this increasingly prevalent metabolic disorder.
非酒精性脂肪性肝病(NAFLD)是一种进行性疾病,从单纯的肝脏脂质积累发展为炎症、纤维化,并增加死亡风险。本研究探讨了生物活性肽PIISVYWK(P1)和FSVVPSPK(P2)在改善油酸处理的HepG2细胞和高脂饮食(HFD)诱导的小鼠的NAFLD方面的治疗效果。我们的研究结果表明,P1和P2显著减少肝脏脂肪沉积,通过促进游离甘油和游离脂肪酸的释放增强脂肪分解,并抑制关键的从头脂肪生成相关蛋白,包括过氧化物酶体增殖物激活受体γ(PPARγ)、CCAAT增强子结合蛋白α(C/EBPα)、固醇调节元件结合蛋白1(SREBP-1)和脂肪酸合酶(FAS)。此外,两种肽都通过激活AMP激活蛋白激酶(AMPK)和激素敏感性脂肪酶(HSL)的磷酸化来刺激脂肪酸氧化。值得注意的是,在HFD小鼠中观察到体重和肝脏重量减轻,同时胆固醇水平和肝功能指标(丙氨酸转氨酶和天冬氨酸转氨酶)得到改善。此外,P1和P2在体外和体内模型中均显著减轻促炎细胞因子如肿瘤坏死因子α(TNF-α)、白细胞介素-1β(IL-1β)和白细胞介素-6(IL-6)的产生。总体而言,这些结果突出了P1和P2在减轻NAFLD进展方面的强大治疗潜力,为这种日益普遍的代谢紊乱提供了一种有前景 的干预措施。