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Condition: Fatty Liver Disease (FLD)
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Total 185 results found since Jan 2013.
Nicotinamide N-methyltransferase (NNMT) upregulation via the mTORC1-ATF4 pathway activation contributes to palmitate-induced lipotoxicity in hepatocytes
In this study, using AML12 cells, a non-transformed murine hepatocyte cell line, exposed to palmitate (a 16-C saturated fatty acid) as an experimental model, we investigated the role and mechanisms of nicotinamide N-methyltransferase (NNMT), a methyltransferase catalyzing nicotinamide methylation and degradation, in hepatic lipotoxicity. We initially identified activating transcription factor 4 (ATF4) as a major transcription factor for hepatic NNMT expression. Here, we demonstrated that palmitate upregulates NNMT expression via activating ATF4 in a mechanistic target of rapamycin complex 1 (mTORC1)-dependent mechanism in ...
Source: American Journal of Physiology. Cell Physiology - August 11, 2021 Category: Cytology Authors: Alexandra Griffiths Jun Wang Qing Song Iredia D Iyamu Lifeng Liu Jooman Park Yuwei Jiang Rong Huang Zhenyuan Song Source Type: research
Thymosin beta 4 alleviates non-alcoholic fatty liver by inhibiting ferroptosis via up-regulation of GPX4
This study revealed that Tβ4 protects hepatocytes by inhibiting the GPX4-mediated ferroptosis pathway, which provides a new strategy and target for the treatment of NAFLD.PMID:34280397 | DOI:10.1016/j.ejphar.2021.174351
Source: European Journal of Pharmacology - July 19, 2021 Category: Drugs & Pharmacology Authors: Zixin Zhu Ya Zhang Xinhao Huang Li Can Xueke Zhao Yinghui Wang Jing Xue Mingliang Cheng Lili Zhu Source Type: research
Caveolin-1 Alleviates Acetaminophen-Induced Fat Accumulation in Non-Alcoholic Fatty Liver Disease by Enhancing Hepatic Antioxidant Ability via Activating AMPK Pathway
In this study, seven-week-old C57BL/6 male mice (18–20 g) were raised under similar conditions for in vivo experiment. In vitro, L02 cells were treated with A/O (alcohol and oleic acid mixture) for 48 h, and APAP was added at 24 h for further incubation. The results showed that the protein expression of the AMPK/Nrf2 pathway was enhanced after CAV1 upregulation. The effects of CAV1 on fat accumulation, ROS, and the AMPK/Nrf2 anti-oxidative pathway were reduced after the application of CAV1-siRNA. Finally, treatment with compound C (an AMPK inhibitor) prevented CAV1 plasmid-mediated alleviation of oxidative stress and ...
Source: Frontiers in Pharmacology - July 7, 2021 Category: Drugs & Pharmacology Source Type: research
Research Articles Hepatocyte TLR4 triggers inter-hepatocyte Jagged1/Notch signaling to determine NASH-induced fibrosis
Aberrant hepatocyte Notch activity is critical to the development of nonalcoholic steatohepatitis (NASH)–induced liver fibrosis, but mechanisms underlying Notch reactivation in developed liver are unclear. Here, we identified that increased expression of the Notch ligand Jagged1 (JAG1) tracked with Notch activation and nonalcoholic fatty liver disease (NAFLD) activity score (NAS) in human liver biopsy specimens and mouse NASH models. The increase in Jag1 was mediated by hepatocyte Toll-like receptor 4 (TLR4)–nuclear factor B (NF-B) signaling in pericentral hepatocytes. Hepatocyte-specific Jag1 overexpression ex...
Source: Science Translational Medicine - June 23, 2021 Category: Biomedical Science Authors: Yu, J., Zhu, C., Wang, X., Kim, K., Bartolome, A., Dongiovanni, P., Yates, K. P., Valenti, L., Carrer, M., Sadowski, T., Qiang, L., Tabas, I., Lavine, J. E., Pajvani, U. B. Tags: Research Articles Source Type: research
Olanzapine leads to nonalcoholic fatty liver disease through the apolipoprotein A5 pathway
This study investigated whether apolipoprotein A5 (apoA5) and sortilin, two interactive factors involved in NAFLD pathogenesis, are implicated in olanzapine-induced NAFLD. In our study, at week 8, olanzapine treatment successfully induced hepatic steatosis in female C57 BL/6 J mice, which was independent of body weight gain. Likewise, olanzapine effectively mediated hepatocyte steatosis in HepG2 cells characterized by substantially elevated intracellular lipid droplets. Increased plasma triglyceride concentration and decreased plasma apoA5 levels were observed in mice treated with 8-week olanzapine. Surprisingly, olanzapin...
Source: Biomedicine and pharmacotherapy = Biomedecine and pharmacotherapie - June 19, 2021 Category: Drugs & Pharmacology Authors: Rong Li Wenqiang Zhu Piaopiao Huang Yang Yang Fei Luo Wen Dai Li Shen Wenjing Pei Xiansheng Huang Source Type: research
Lipotoxicity reduces DDX58/Rig-1 expression and activity leading to impaired autophagy and cell death
This study uncovers the unexpected role of immune surveillance protein DDX58/Rig-1 (DExD/H box helicase 58) in activating macroautophagy/autophagy and protecting from lipotoxicity associated with NAFLD. Here we show for the first time that DDX58 protein is significantly reduced in nonalcoholic steatohepatitis (NASH) mouse model, an aggressive form of NAFLD characterized by inflammation and fibrosis of the liver. In addition to decreased expression of DDX58, we found that DDX58 activity can be attenuated by treatments with palmitic acid (PA), a saturated fatty acid. To investigate whether PA inhibition of DDX58 is harmful t...
Source: Autophagy - May 10, 2021 Category: Cytology Authors: Karla K Frietze Alyssa M Brown Dividutta Das Raymond G Franks Jessie Lee Cunningham Michael Hayward Joseph T Nickels Source Type: research
Mesenchymal stromal cells protect hepatocytes from lipotoxicity through alleviation of endoplasmic reticulum stress by restoring SERCA activity.
Abstract
The aim of this study was to investigate how mesenchymal stromal cells (MSCs) modulate metabolic balance and attenuate hepatic lipotoxicity in the context of non-alcoholic fatty liver disease (NAFLD). In vivo, male SD rats were fed with high-fat diet (HFD) to develop NAFLD; then, they were treated twice by intravenous injections of rat bone marrow MSCs. In vitro, HepG2 cells were cocultured with MSCs by transwell and exposed to palmitic acid (PA) for 24 hours. The endoplasmic reticulum (ER) stressor thapsigargin and sarco/ER Ca2+ -ATPase (SERCA2)-specific siRNA were used to explore the regulation of ER s...
Source: J Cell Mol Med - February 16, 2021 Category: Molecular Biology Authors: Li L, Zeng X, Liu Z, Chen X, Li L, Luo R, Liu X, Zhang J, Liu J, Lu Y, Cheng J, Chen Y Tags: J Cell Mol Med Source Type: research
Empagliflozin Alleviates Hepatic Steatosis by Activating the AMPK-TET2-Autophagy Pathway in vivo and in vitro
Conclusion: Empagliflozin improves hepatic steatosis through the AMPK-TET2-autophagy pathway. The use of empagliflozin as a treatment for preventing and treating MAFLD in patients with T2DM warrants further study.
Source: Frontiers in Pharmacology - January 20, 2021 Category: Drugs & Pharmacology Source Type: research
Src-mediated Tyr353 phosphorylation of IP3R1 promotes its stability and causes apoptosis in palmitic acid-treated hepatocytes.
Conclusion: PA promotes the Tyr353 phosphorylation of IP3R1 by activating the src pathway and increasing the protein stability of IP3R1, which consequently results in mitochondrial Ca2+ overload and mitochondrial dysfunction in hepatic cells. Our results also suggested that inhibition of the src/IP3R1 pathway, such as by SU6656, may be a novel potential therapeutic approach for the treatment of NAFLD.
PMID: 33358861 [PubMed - as supplied by publisher]
Source: Experimental Cell Research - December 21, 2020 Category: Cytology Authors: Yu T, Zheng E, Li Y, Li Y, Xia J, Ding Q, Hou Z, Ruan XZ, Zhao L, Chen Y Tags: Exp Cell Res Source Type: research
Activation of the AMPK-SIRT1 pathway contributes to protective effects of Salvianolic acid A against lipotoxicity in hepatocytes and NAFLD in mice
Conclusion: Our data uncover a novel mechanism for hepatoprotective effects of Sal A against lipotoxicity both in livers from HFCD-fed mice and palmitic acid-treated hepatocytes.
Source: Frontiers in Pharmacology - November 30, 2020 Category: Drugs & Pharmacology Source Type: research
