Heat-Killed <i>Enterococcus faecalis</i> Inhibit FL83B Hepatic Lipid Accumulation and High Fat Diet-Induced Fatty Liver Damage in Rats by Activating Lipolysis through the Regulation the AMPK Signaling Pathway
Continuous consumption of high-calorie meals causes lipid accumulation in the liver and liver damage, leading to non-alcoholic fatty liver disease (NAFLD). A case study of the hepatic lipid accumulation model is needed to identify the mechanisms underlying lipid metabolism in the liver. In this stud...
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MDPI AG
2023-02-01
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| Series: | International Journal of Molecular Sciences |
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| Online Access: | https://www.mdpi.com/1422-0067/24/5/4486 |
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| author | Jin-Ho Lee Keun-Jung Woo Joonpyo Hong Kwon-Il Han Han Sung Kim Tack-Joong Kim |
| author_facet | Jin-Ho Lee Keun-Jung Woo Joonpyo Hong Kwon-Il Han Han Sung Kim Tack-Joong Kim |
| author_sort | Jin-Ho Lee |
| collection | DOAJ |
| description | Continuous consumption of high-calorie meals causes lipid accumulation in the liver and liver damage, leading to non-alcoholic fatty liver disease (NAFLD). A case study of the hepatic lipid accumulation model is needed to identify the mechanisms underlying lipid metabolism in the liver. In this study, the prevention mechanism of lipid accumulation in the liver of <i>Enterococcus faecalis</i> 2001 (EF-2001) was extended using FL83B cells (FL83Bs) and high-fat diet (HFD)-induced hepatic steatosis. EF-2001 treatment inhibited the oleic acid (OA) lipid accumulation in FL83B liver cells. Furthermore, we performed lipid reduction analysis to confirm the underlying mechanism of lipolysis. The results showed that EF-2001 downregulated proteins and upregulated AMP-activated protein kinase (AMPK) phosphorylation in the sterol regulatory element-binding protein 1c (SREBP-1c) and AMPK signaling pathways, respectively. The effect of EF-2001 on OA-induced hepatic lipid accumulation in FL83Bs enhanced the phosphorylation of acetyl-CoA carboxylase and reduced the levels of lipid accumulation proteins SREBP-1c and fatty acid synthase. EF-2001 treatment increased the levels of adipose triglyceride lipase and monoacylglycerol during lipase enzyme activation, which, when increased, contributed to increased liver lipolysis. In conclusion, EF-2001 inhibits OA-induced FL83B hepatic lipid accumulation and HFD-induced hepatic steatosis in rats through the AMPK signaling pathway. |
| first_indexed | 2024-03-11T07:23:37Z |
| format | Article |
| id | doaj.art-75a5ca39f62d41e1ac206686556ac58f |
| institution | Directory Open Access Journal |
| issn | 1661-6596 1422-0067 |
| language | English |
| last_indexed | 2024-03-11T07:23:37Z |
| publishDate | 2023-02-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | International Journal of Molecular Sciences |
| spelling | doaj.art-75a5ca39f62d41e1ac206686556ac58f2023-11-17T07:49:08ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672023-02-01245448610.3390/ijms24054486Heat-Killed <i>Enterococcus faecalis</i> Inhibit FL83B Hepatic Lipid Accumulation and High Fat Diet-Induced Fatty Liver Damage in Rats by Activating Lipolysis through the Regulation the AMPK Signaling PathwayJin-Ho Lee0Keun-Jung Woo1Joonpyo Hong2Kwon-Il Han3Han Sung Kim4Tack-Joong Kim5Division of Biological Science and Technology, Yonsei University, Wonju 26493, Republic of KoreaDivision of Biological Science and Technology, Yonsei University, Wonju 26493, Republic of KoreaDivision of Biological Science and Technology, Yonsei University, Wonju 26493, Republic of KoreaDivision of Biological Science and Technology, Yonsei University, Wonju 26493, Republic of KoreaDepartment of Biomedical Engineering, Yonsei University, Wonju 26493, Republic of KoreaDivision of Biological Science and Technology, Yonsei University, Wonju 26493, Republic of KoreaContinuous consumption of high-calorie meals causes lipid accumulation in the liver and liver damage, leading to non-alcoholic fatty liver disease (NAFLD). A case study of the hepatic lipid accumulation model is needed to identify the mechanisms underlying lipid metabolism in the liver. In this study, the prevention mechanism of lipid accumulation in the liver of <i>Enterococcus faecalis</i> 2001 (EF-2001) was extended using FL83B cells (FL83Bs) and high-fat diet (HFD)-induced hepatic steatosis. EF-2001 treatment inhibited the oleic acid (OA) lipid accumulation in FL83B liver cells. Furthermore, we performed lipid reduction analysis to confirm the underlying mechanism of lipolysis. The results showed that EF-2001 downregulated proteins and upregulated AMP-activated protein kinase (AMPK) phosphorylation in the sterol regulatory element-binding protein 1c (SREBP-1c) and AMPK signaling pathways, respectively. The effect of EF-2001 on OA-induced hepatic lipid accumulation in FL83Bs enhanced the phosphorylation of acetyl-CoA carboxylase and reduced the levels of lipid accumulation proteins SREBP-1c and fatty acid synthase. EF-2001 treatment increased the levels of adipose triglyceride lipase and monoacylglycerol during lipase enzyme activation, which, when increased, contributed to increased liver lipolysis. In conclusion, EF-2001 inhibits OA-induced FL83B hepatic lipid accumulation and HFD-induced hepatic steatosis in rats through the AMPK signaling pathway.https://www.mdpi.com/1422-0067/24/5/4486<i>Enterococcus faecalis</i>EF-2001lipid metabolismhigh-fat dietAMPK signaling |
| spellingShingle | Jin-Ho Lee Keun-Jung Woo Joonpyo Hong Kwon-Il Han Han Sung Kim Tack-Joong Kim Heat-Killed <i>Enterococcus faecalis</i> Inhibit FL83B Hepatic Lipid Accumulation and High Fat Diet-Induced Fatty Liver Damage in Rats by Activating Lipolysis through the Regulation the AMPK Signaling Pathway International Journal of Molecular Sciences <i>Enterococcus faecalis</i> EF-2001 lipid metabolism high-fat diet AMPK signaling |
| title | Heat-Killed <i>Enterococcus faecalis</i> Inhibit FL83B Hepatic Lipid Accumulation and High Fat Diet-Induced Fatty Liver Damage in Rats by Activating Lipolysis through the Regulation the AMPK Signaling Pathway |
| title_full | Heat-Killed <i>Enterococcus faecalis</i> Inhibit FL83B Hepatic Lipid Accumulation and High Fat Diet-Induced Fatty Liver Damage in Rats by Activating Lipolysis through the Regulation the AMPK Signaling Pathway |
| title_fullStr | Heat-Killed <i>Enterococcus faecalis</i> Inhibit FL83B Hepatic Lipid Accumulation and High Fat Diet-Induced Fatty Liver Damage in Rats by Activating Lipolysis through the Regulation the AMPK Signaling Pathway |
| title_full_unstemmed | Heat-Killed <i>Enterococcus faecalis</i> Inhibit FL83B Hepatic Lipid Accumulation and High Fat Diet-Induced Fatty Liver Damage in Rats by Activating Lipolysis through the Regulation the AMPK Signaling Pathway |
| title_short | Heat-Killed <i>Enterococcus faecalis</i> Inhibit FL83B Hepatic Lipid Accumulation and High Fat Diet-Induced Fatty Liver Damage in Rats by Activating Lipolysis through the Regulation the AMPK Signaling Pathway |
| title_sort | heat killed i enterococcus faecalis i inhibit fl83b hepatic lipid accumulation and high fat diet induced fatty liver damage in rats by activating lipolysis through the regulation the ampk signaling pathway |
| topic | <i>Enterococcus faecalis</i> EF-2001 lipid metabolism high-fat diet AMPK signaling |
| url | https://www.mdpi.com/1422-0067/24/5/4486 |
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