Department of Food Science and Nutrition, Gwangju University, Gwangju 61743, Republic of Korea.
Nutrients. 2024 Oct 24;16(21):3614. doi: 10.3390/nu16213614.
Several Previous studies indicate that consuming krill oil may aid in reducing hypercholesterolemia and improving cholesterol metabolism. Therefore, our study was designed to investigate the effectiveness of Antarctic krill oil () (ESKO) in combating obesity and lowering fat/lipid/cholesterol levels.
The study aimed to investigate the molecular docking model targeting 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) using ESKO-derived eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and astaxanthin. In this study, histological alterations in the liver of the obesity model (ICR male mouse), obesity-related or antioxidant markers in both liver and serum, the molecular mechanisms in HepG2 cells and liver tissue, and HMGCR activity were analyzed.
Our findings revealed that a high-fat diet (HFD) significantly led to increased oxidative stress, obesity-related indicators, and cardiovascular-associated risk indices. However, ESKO effectively mitigated HFD-induced oxidative stress, fat accumulation, and the suppression of low-density lipoprotein receptor (LDLR) or activation of related molecular pathways. This was achieved through improvements in metabolic parameters, including CD36/liver X receptor α (LXRα)/sterol regulatory element-binding protein 1c (SREBP1c), proprotein convertase subtilsin/kexin type 9 (PCSK-9), and HMGCR, ultimately ameliorating HFD-induced hypercholesterolemia and obesity.
These beneficial findings indicate that ESKO might have significant potential for preventing and treating obesity-related disorders.
几项先前的研究表明，食用磷虾油可能有助于降低高胆固醇血症和改善胆固醇代谢。因此，我们的研究旨在调查南极磷虾油（）（ESKO）在对抗肥胖和降低脂肪/脂质/胆固醇水平方面的有效性。
本研究旨在研究 ESKO 衍生的二十碳五烯酸（EPA）、二十二碳六烯酸（DHA）和虾青素针对 3-羟基-3-甲基戊二酰辅酶 A 还原酶（HMGCR）的分子对接模型。在这项研究中，分析了肥胖模型（ICR 雄性小鼠）肝脏的组织学改变、肝脏和血清中的肥胖相关或抗氧化标志物、HepG2 细胞和肝组织中的分子机制以及 HMGCR 活性。
我们的研究结果表明，高脂肪饮食（HFD）显著导致氧化应激增加、肥胖相关指标和心血管相关风险指数增加。然而，ESKO 有效地减轻了 HFD 诱导的氧化应激、脂肪积累以及低密度脂蛋白受体（LDLR）的抑制或相关分子途径的激活。这是通过改善代谢参数来实现的，包括 CD36/肝 X 受体 α（LXRα）/固醇调节元件结合蛋白 1c（SREBP1c）、脯氨酸羧肽酶/肠激酶 9（PCSK-9）和 HMGCR，最终改善了 HFD 诱导的高胆固醇血症和肥胖。
这些有益的发现表明，ESKO 可能具有预防和治疗肥胖相关疾病的巨大潜力。
