Department of Food Science and Biotechnology, Gachon University, Seongnam 13120, Gyeonggi-do, Korea.
Department of Food and Nutrition, Gachon University, Seongnam 13120, Gyeonggi-do, Korea.
Int J Mol Sci. 2022 May 24;23(11):5901. doi: 10.3390/ijms23115901.
HAC01 has been shown to effectively treat metabolic diseases. However, the precise pharmacological effects and molecular mechanisms of HAC01 remain unclear. In this study, we investigate the anti-adipogenic effects of HAC01 lysate and its associated mechanism of action. To induce lipid accumulation, 3T3-L1 cells were incubated in differentiation media with or without HAC01 lysate. Our results show that HAC01 lysate treatment not only reduced lipid accumulation during the differentiation of 3T3-L1 cells, but also decreased the expression of adipogenic and lipogenic genes involved in lipid metabolism in a dose-dependent manner. Additionally, HAC01 lysate inhibited CCAAT/enhancer-binding protein (C/EBP) beta within 4 h of differentiation induction and inhibited peroxisome proliferator-activated receptor gamma, C/EBP alpha, and sterol regulatory element-binding proteins within 2 d. Moreover, treatment with HAC01 lysate increased the phosphorylation of adenosine monophosphate-activated protein kinase, an important regulator of energy metabolism, and decreased the phosphorylation of mitogen-activated protein kinase. These results indicate that HAC01 lysate may have anti-adipogenic effects and support its potential as a useful agent for the treatment of obesity.
HAC01 已被证明可有效治疗代谢疾病。然而，HAC01 的确切药理作用和分子机制尚不清楚。在这项研究中，我们研究了 HAC01 裂解物的抗脂肪生成作用及其相关的作用机制。为了诱导脂肪堆积，用或不用 HAC01 裂解物孵育 3T3-L1 细胞进行分化培养。我们的结果表明，HAC01 裂解物处理不仅减少了 3T3-L1 细胞分化过程中的脂质积累，而且还以剂量依赖的方式降低了与脂质代谢相关的脂肪生成和脂肪生成基因的表达。此外，HAC01 裂解物在分化诱导后 4 小时内抑制 CCAAT/增强子结合蛋白（C/EBP）β，在 2 天内抑制过氧化物酶体增殖物激活受体γ、C/EBPα 和固醇调节元件结合蛋白。此外，用 HAC01 裂解物处理可增加对能量代谢有重要调节作用的单磷酸腺苷激活蛋白激酶的磷酸化，并降低丝裂原激活蛋白激酶的磷酸化。这些结果表明，HAC01 裂解物可能具有抗脂肪生成作用，并支持其作为肥胖治疗有用药物的潜力。
