Lee Young-Sil, Park Eun-Jung, Park Gun-Seok, Ko Seung-Hyun, Park Juyi, Lee You-Kyung, Kim Jong-Yeon, Lee Daeyoung, Kang Jihee, Lee Hae-Jeung
AtoGen Co., Ltd., Daejeon 34015, Korea.
Department of Food and Nutrition, College of BioNano Technology, Gachon University, Gyeonggi-do 13120, Korea.
Int J Mol Sci. 2021 Nov 23;22(23):12665. doi: 10.3390/ijms222312665.
Obesity is a major health problem. Compelling evidence supports the beneficial effects of probiotics on obesity. However, the anti-obesity effect of probiotics remains unknown. In this study, we investigated the anti-obesity effects and potential mechanisms of ATG-K2 using 3T3-L1 adipocytes and high-fat diet (HFD)-induced obese mice. 3T3-L1 cells were incubated to determine the effect of lipid accumulation with lysate of ATG-K2. Mice were fed a normal fat diet or HFD with ATG-K2 and Orlistat for 8 weeks. ATG-K2 inhibited lipid accumulation in 3T3-L1 adipocytes, and reduced body weight gain, WAT weight, and adipocyte size in HFD-induced obese mice, concurrently with the downregulation of PPARγ, SREBP1c, and FAS and upregulation of PPARα, CTP1, UCP1, Prdm16, and ND5. Moreover, ATG-K2 decreased TG, T-CHO, leptin, and TNF-α levels in the serum, with corresponding gene expression levels in the intestine. ATG-K2 modulated the gut microbiome by increasing the abundance of the family, which increased SCFA levels and branched SCFAs in the feces. ATG-K2 exhibited an anti-obesity effect and anti-hyperlipidemic effect in 3T3-L1 adipocytes and HFD-induced obese mice by alleviating the inflammatory response and regulating lipid metabolism, which may be influenced by modulation of the gut microbiome and its metabolites. Therefore, ATG-K2 can be a preventive and therapeutic agent for obesity.
肥胖是一个主要的健康问题。有力的证据支持益生菌对肥胖有益。然而，益生菌的抗肥胖作用仍不明确。在本研究中，我们使用3T3-L1脂肪细胞和高脂饮食（HFD）诱导的肥胖小鼠研究了ATG-K2的抗肥胖作用及其潜在机制。将3T3-L1细胞与ATG-K2裂解物一起孵育以确定脂质积累的影响。给小鼠喂食正常脂肪饮食或添加了ATG-K2和奥利司他的高脂饮食8周。ATG-K2抑制3T3-L1脂肪细胞中的脂质积累，并减少HFD诱导的肥胖小鼠的体重增加、白色脂肪组织重量和脂肪细胞大小，同时下调PPARγ、SREBP1c和FAS，并上调PPARα、CTP1、UCP1、Prdm16和ND5。此外，ATG-K2降低了血清中的甘油三酯、总胆固醇、瘦素和TNF-α水平，以及肠道中的相应基因表达水平。ATG-K2通过增加该菌属的丰度来调节肠道微生物群，从而增加粪便中的短链脂肪酸水平和支链短链脂肪酸。ATG-K2通过减轻炎症反应和调节脂质代谢，在3T3-L1脂肪细胞和HFD诱导的肥胖小鼠中表现出抗肥胖和抗高血脂作用，这可能受到肠道微生物群及其代谢产物调节的影响。因此，ATG-K2可以成为肥胖的预防和治疗药物。
