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Condition: Fatty Liver Disease (FLD)

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Total 185 results found since Jan 2013.

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

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

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

Hesperetin protects against palmitate-induced cellular toxicity via induction of GRP78 in hepatocytes.
In conclusion, hesperetin protected against palmitate-induced hepatic cell death via activation of the sXBP1/GRP78 signaling pathway, thus inhibiting palmitate-induced ER stress. Moreover, high concentrations of hesperetin induce ER stress and subsequently cause cell death in hepatocytes. PMID: 32763355 [PubMed - as supplied by publisher]
Source: Toxicology and Applied Pharmacology - August 4, 2020 Category: Toxicology Authors: Geng Y, Wu Z, Buist-Homan M, Blokzijl H, Moshage H Tags: Toxicol Appl Pharmacol Source Type: research

Gut-Derived Serotonin Contributes to the Progression of Non-Alcoholic Steatohepatitis via the Liver HTR2A/PPAR γ2 Pathway
The precipitous increase in occurrence of non-alcoholic steatohepatitis (NASH) is a serious threat to public health worldwide. The pathogenesis of NASH has not yet been thoroughly studied. We aimed to elucidate the interplay between serotonin (5-hydroxytryptamine, 5-HT) and NASH. The serum 5-HT levels in patients with non-alcoholic fatty liver disease (NAFLD) and a rat fed with high fat-sucrose diet (HFSD) were evaluated using liquid chromatography-hybrid quadrupole time-of-flight mass spectrometry (LC-QTOF MS)/MS. The peripheral Tph1 inhibitor, LP533401, and a tryptophan (TRP)-free diet were administered to rats with NASH...
Source: Frontiers in Pharmacology - May 13, 2020 Category: Drugs & Pharmacology Source Type: research

Humanin attenuates palmitate-induced hepatic lipid accumulation and insulin resistance via AMPK-mediated suppression of the mTOR pathway.
This study aim was to investigate effects of HN on lipid accumulation in the hepatocytes and insulin signaling, and explore the underlying mechanisms. Protein expression levels were analyzed by Western blotting. Hepatic lipid accumulation was confirmed by Oil red-O staining. We found that HN-treatment ameliorated palmitate-induced lipid accumulation, expression of lipogenesis-associated genes (processed SREBP1, FAS, and SCD1), cell death, and caspase 3 activity in hepatocytes in a dose-dependent manner. Additionally, HN attenuated palmitate-induced impairment of insulin signaling. HN enhanced AMPK phosphorylation, whereas ...
Source: Biochemical and Biophysical Research communications - March 30, 2020 Category: Biochemistry Authors: Kwon C, Sun JL, Jeong JH, Jung TW Tags: Biochem Biophys Res Commun Source Type: research

Purple sweet potato color protects against hepatocyte apoptosis through Sirt1 activation in high-fat-diet-treated mice.
Conclusion: PSPC protected against HFD-induced hepatic apoptosis by promoting Sirt1- dependent inhibition of p53-apoptotic pathway and facilitation of Akt survival pathway. This study indicates that PSPC is a candidate for nutritional intervention of NAFLD. PMID: 32110174 [PubMed - as supplied by publisher]
Source: Food and Nutrition Research - February 29, 2020 Category: Nutrition Authors: Su W, Zhang C, Chen F, Sui J, Lu J, Wang Q, Shan Q, Zheng G, Lu J, Sun C, Fan S, Wu D, Zhang Z, Zheng Y Tags: Food Nutr Res Source Type: research

Role of ATP-binding cassette transporter A1 in suppressing lipid accumulation by glucagon-like peptide-1 agonist in hepatocytes
ConclusionsOur data reveals that exendin-4 stimulates hepatic ABCA1 expression and reduces lipid accumulation by the CaMKK/CaMKIV/PREB pathway, suggesting that ABCA1 and PREB might be the therapeutic targets in fatty liver disease.Graphical abstract
Source: Molecular Metabolism - January 7, 2020 Category: Endocrinology Source Type: research

PNPLA3 I148M mediates the regulatory effect of NF-kB on inflammation in PA-treated HepG2 cells.
This study aimed to elucidate whether PNPLA3 I148M is involved in NF-kB-related inflammation regulation in NAFLD. HepG2 cells homozygous for the PNPLA3 I148M mutation were used. The human PNPLA3 promoter sequence was screened for NF-kB binding sites using the MATCH and PATCH tools. NF-kB-mediated transcriptional regulation of the PNPLA3 gene was assessed by luciferase reporter assay, EMSA and ChIP-qPCR. Wild-type (I148I) and mutant (M148M) PNPLA3 were overexpressed using stable lentivirus-mediated transfection. The pCMV vector and siRNA were transiently transfected into cells to direct NF-kB overexpression and PNPLA3 silen...
Source: J Cell Mol Med - December 2, 2019 Category: Molecular Biology Authors: Yuan S, Liu H, Yuan D, Xu J, Chen Y, Xu X, Xu F, Liang H Tags: J Cell Mol Med Source Type: research

Liraglutide ameliorates non-alcoholic steatohepatitis by inhibiting NLRP3 inflammasome and pyroptosis activation via mitophagy.
Abstract Non-alcoholic steatohepatitis (NASH) is a key step in the progression of non-alcoholic fatty liver disease (NAFLD), which causes serious health problems worldwide. The nucleotide-binding oligomerization domain, leucine-rich repeat-containing receptor-containing pyrin domain 3 (NLRP3) inflammasome and pyroptosis play crucial roles in the progression of NASH. Our team has provided clinical evidence of the effects of glucagon-like peptide-1 (GLP-1) on the improvement in liver function and histological resolution of NAFLD. Preliminary work has demonstrated that GLP-1 inhibited NLRP3 inflammasome activation in...
Source: European Journal of Pharmacology - October 4, 2019 Category: Drugs & Pharmacology Authors: Yu X, Hao M, Liu Y, Ma X, Lin W, Xu Q, Zhou H, Shao N, Kuang H Tags: Eur J Pharmacol Source Type: research

Circulating ectodysplasin A is a potential biomarker for nonalcoholic fatty liver disease
ConclusionsEDA aggravates steatosis by striking balance between lipid deposition and elimination. It was a potential biomarker of NAFLD.
Source: Clinica Chimica Acta - September 15, 2019 Category: Laboratory Medicine Source Type: research

Allyl isothiocyanate ameliorates lipid accumulation and inflammation in nonalcoholic fatty liver disease via the Sirt1/AMPK and NF- κB signaling pathways.
CONCLUSION: AITC significantly ameliorates hepatic steatosis and inflammation by activating the Sirt1/AMPK pathway and inhibiting the NF-κB pathway. Therefore, AITC is a potential therapeutic agent for NAFLD. PMID: 31558861 [PubMed - in process]
Source: World Journal of Gastroenterology : WJG - September 13, 2019 Category: Gastroenterology Authors: Li CX, Gao JG, Wan XY, Chen Y, Xu CF, Feng ZM, Zeng H, Lin YM, Ma H, Xu P, Yu CH, Li YM Tags: World J Gastroenterol Source Type: research

Circulating ectodysplasin A is a potential biomarker for nonalcoholic fatty liver disease.
CONCLUSIONS: EDA aggravates steatosis by striking balance between lipid deposition and elimination. It was a potential biomarker of NAFLD. PMID: 31526774 [PubMed - as supplied by publisher]
Source: International Journal of Clinical Chemistry - September 13, 2019 Category: Chemistry Authors: Yang J, Zhou W, Zhu J, Wu Y, Xu L, Wang Y, Zhang Q, Yang Y Tags: Clin Chim Acta Source Type: research

M3 Muscarinic receptor activation reduces hepatocyte lipid accumulation via CaMKK β/AMPK pathway.
In conclusion, this proof-of-concept study demonstrates that M3R has protective effects against hepatocyte lipid accumulation by activating AMPK pathway and is a potential therapeutic target for non-alcoholic fatty liver disease. PMID: 31445019 [PubMed - as supplied by publisher]
Source: Biochemical Pharmacology - August 20, 2019 Category: Drugs & Pharmacology Authors: Jadeja RN, Chu X, Wood C, Bartoli M, Khurana S Tags: Biochem Pharmacol Source Type: research

Hypoxia exacerbates non-alcoholic fatty liver disease via HIF-2 α/PPARα pathway.
This study aimed to investigate whether hypoxia can affect non-alcoholic fatty liver disease (NAFLD) progression and the associated mechanisms, specifically regarding the HIF-2α / PPARα pathway in vitro and vivo. Recent studies have reported that, compared with HIF-1α, HIF-2α has different effects on lipid metabolism. We propose hypoxia may exacerbate NAFLD by the HIF-2α upregulation-induced suppression of PPARα in the liver. To verify this hypothesis, a steatotic human hepatocyte (L02) cell line treated with free fatty acids and a mouse model of NAFLD fed a high-fat diet were used. Steatotic hepatocytes were treated...
Source: American Journal of Physiology. Endocrinology and Metabolism - August 19, 2019 Category: Physiology Authors: Chen J, Chen J, Fu H, Li Y, Wang L, Luo S, Lu H Tags: Am J Physiol Endocrinol Metab Source Type: research