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Condition: Fatty Liver Disease (FLD)

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Total 185 results found since Jan 2013.

miR-34a regulates lipid metabolism by targeting SIRT1 in non-alcoholic fatty liver disease with iron overload.
CONCLUSIONS: Our results support the existence of a link between the liver cell mitochondria and miR-34a/SIRT1 signaling. Potential endogenous modulators of NAFLD pathogenesis may ultimately provide new tools for therapeutic intervention. PMID: 33098868 [PubMed - as supplied by publisher]
Source: Archives of Biochemistry and Biophysics - October 21, 2020 Category: Biochemistry Authors: Wang L, Sun M, Cao Y, Ma L, Shen Y, Velikanova AA, Li X, Sun C, Zhao Y Tags: Arch Biochem Biophys Source Type: research

GPR40-Deficiency Is Associated with Hepatic FAT/CD36 Upregulation, Steatosis, Inflammation and Cell Injury in C57BL/6 Mice.
In this study, we fed wild-type or GPR40 knockout C57BL/6 mice high-fat diet (HFD) for 20 weeks and then assessed the effect of GPR40-deficiency on HFD-induced NAFLD. Assays on metabolic parameters showed that HFD increased bodyweight, glucose, insulin, insulin resistance, cholesterol and alanine aminotransferase (ALT), and GPR40-deficiency did not mitigate the HFD-induced metabolic abnormalities. In contrast, we found that GPR40-deficiency was associated with increased bodyweight, insulin, insulin resistance, cholesterol and ALT in control mice fed low fat diet (LFD). Surprisingly, histology and Oil Red O staining showed ...
Source: American Journal of Physiology. Endocrinology and Metabolism - October 26, 2020 Category: Physiology Authors: Lu Z, Li Y, Syn WK, Li AJ, Ritter S, Wank SA, Lopes-Virella MF, Huang Y Tags: Am J Physiol Endocrinol Metab Source Type: research

TXNIP/VDUP1 attenuates steatohepatitis via autophagy and fatty acid oxidation.
Abstract Impaired macroautophagy/autophagy has been implicated in experimental and human nonalcoholic steatohepatitis (NASH). However, the mechanism underlying autophagy dysregulation in NASH is largely unknown. Here, we investigated the role and mechanism of TXNIP/VDUP1 (thioredoxin interacting protein), a key mediator of cellular stress responses, in the pathogenesis of NASH. Hepatic TXNIP expression was upregulated in nonalcoholic fatty liver disease (NAFLD) patients and in methionine choline-deficient (MCD) diet-fed mice, as well as in palmitic acid (PA)-treated hepatocytes. Upregulation of hepatic TXNIP was p...
Source: Autophagy - November 16, 2020 Category: Cytology Authors: Park HS, Song JW, Park JH, Lim BK, Moon OS, Son HY, Lee JH, Gao B, Won YS, Kwon HJ Tags: Autophagy 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

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

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

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

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

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

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

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

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: Am J Physiol Cell Ph... - 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