|
Non-alcoholic Fatty Liver Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
In summary, our study identifies Nogo-B as a new molecular target of PPARγ, and suggests increased Nogo-B might be a potential indicator for NAFLD.
|
31654717 |
2020 |
|
Non-alcoholic Fatty Liver Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
Telmisartan is a potential treatment for NAFLD due to its ability to improve insulin sensitivity and decrease hepatic fat accumulation via modulation of PPARγ, and to suppress hepatic fibrosis by blocking angiotensin II receptors.
|
30850637 |
2019 |
|
Non-alcoholic Fatty Liver Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
Western blot revealed that PP1 inhibited the lipid accumulation and fatty acid synthesis in 3T3-L1 adipocytes in two pathways, primarily: nonalcoholic fatty liver disease (NAFLD) pathway (C/EBPα, SREBP-1c, AMPKα) and AMPK signaling pathway (SREBP-1c, PPARγ, AMPKα).
|
31569521 |
2019 |
|
Non-alcoholic Fatty Liver Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
Overexpression of miR-130a and PPARγ antagonist GW9662 inhibited lipogenesis and TG secretion, and PPARγ agonist GW1929 reversed this change induced by miR-130a up-regulation.<b>Conclusion:</b> Knockdown of H19 alleviated hepatic lipogenesis via directly regulating miR-130a/PPARγ axis, which is a novel mechanistic role of H19 in the regulation of NAFLD.
|
31064820 |
2019 |
|
Non-alcoholic Fatty Liver Disease
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Abbreviations: WAT: white adipose tissue; PPAR: Peroxisome proliferators-activated receptor; RXR: retinoid X receptors; mTORC1: mechanistic target of rapamycin complex 1; PPRE: PPAR-responsive regulatory elements; NAFLD: nonalcoholic fatty liver disease; LPL: lipoprotein lipase; FGF21: fibroblast growth factor 21; BAT: brown adipose tissue; UCP1: uncoupling protein 1; LPC(16:0): 1-palmitoyl lysophosphatidylcholine; C/EBP: CCAAT-enhancer binding proteins; STAT5A: signal transduction and activator of transcription 5A; APO apolipoptotein; CBP: cAMP response element-binding protein-binding protein; PGC1A: PPARγ coactivator protein 1a; HFD: high-fat diet; TG: triglyceride; VLDL: very low density lipoprotein; HDL: high density lipoprotein.
|
30572788 |
2019 |
|
Non-alcoholic Fatty Liver Disease
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Further, among the 10 SNPs negatively associated with NAFLD, the four-locus model (rs13431696 and rs3856806 in PPARγ, and rs5182, rs1492100 in ATGR1) and the five-locus model (rs9817428, rs1175543, rs13433696, and rs2920502 in PPARγ, and rs1492100 in ATGR1) were closely related with NAFLD susceptibility (p = 0.019 and p = 0.048, respectively).
|
30793973 |
2019 |
|
Non-alcoholic Fatty Liver Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
Downregulation of LXRα, PPARγ and iNOS by QWTX were both observed in the 3T3-L1 adipocytes and NAFLD model.
|
30851372 |
2019 |
|
Non-alcoholic Fatty Liver Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
This MiniReview explores adipose- and liver-specific actions of PPARγ, and how this knowledge may contribute in the search for new treatment modalities in NAFLD/NASH.
|
30561132 |
2019 |
|
Non-alcoholic Fatty Liver Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
Both PPARγ and SOCS3 play a role in NAFLD through regulating IR, while it is unclear whether these two proteins interact to regulate hepatic steatosis.
|
29550470 |
2018 |
|
Non-alcoholic Fatty Liver Disease
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
CHLZT and AICAR increased the levels of p-AMPKα and PPARγ in the NAFLD liver tissues and HepG2 cells, but decreased the levels of ACC-α, p-ACC-α, SREBP-2, and 3-hydroxyl-3-methylglutaryl-coenzyme A reductase (HMGR).
|
30291215 |
2018 |
|
Non-alcoholic Fatty Liver Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
Some new pharmacological strategies act broadly to alter energy balance or influence pathways that contribute to NAFLD (e.g., agonists for PPAR γ, PPAR α/δ, FXR and analogs for FGF-21, and GLP-1).
|
28867301 |
2018 |
|
Non-alcoholic Fatty Liver Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
These findings indicate new mechanisms of action for both PPARα and PPARγ, and new potential treatment options for nonalcoholic fatty liver disease (NAFLD) and steatosis.This article has an associated First Person interview with the first author of the paper.
|
30171034 |
2018 |
|
Non-alcoholic Fatty Liver Disease
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Our findings demonstrated that the therapeutic effects of 50% ME among NAFLD rats, were associated with a significant increase in serum adiponectin, reduction in the serum levels of RBP4, vaspin, progranulin, TNF-α, IL-6, and significant downregulation of the hepatic gene expression of PPARγ, SLC10A2, and Collα1.Concomitantly, 50% ME of <i>P. niruri</i> has exhibited a potent antiangiogenic activity on ring assay, cell migration, vascular endothelial growth factor (VEGF), and tube formation, without any cytotoxic effect.
|
30096951 |
2018 |
|
Non-alcoholic Fatty Liver Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
With further validation, plasma DNA methylation of PPARγ could potentially be used to non-invasively stratify liver fibrosis severity in patients with NAFLD.
|
27002005 |
2017 |
|
Non-alcoholic Fatty Liver Disease
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Moreover, we found that hepatic sirtuin1 and peroxisome proliferator-activated receptor-γ coactivator-1α expression levels are downregulated, and acetylated peroxisome proliferator-activated receptor-γ coactivator-1α expression levels are upregulated in patients and dairy cows with non-alcoholic fatty liver disease, as well as in high-fat diet and ob/ob mice.
|
29207650 |
2017 |
|
Non-alcoholic Fatty Liver Disease
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
These findings suggest that manipulation of PPAR-γ activity has the potential to balance lipid-induced M1/M2 macrophage/Kupffer cell polarization, and leading to prevent the development of NAFLD.
|
28300213 |
2017 |
|
Non-alcoholic Fatty Liver Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
The results suggest that consumption of a white corn/bean snack (70%/30% blend) attenuates weight gain, fat mass accumulation, adipocyte size and nonalcoholic fatty liver disease in HFD-fed mice by inhibiting PPARγ and SREBF2.
|
28965030 |
2017 |
|
Non-alcoholic Fatty Liver Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
The suggestion of this Expert Panel is that, pending forthcoming randomized clinical trials, physicians should consider using a PPARgamma agonist, such as pioglitazone, or, statin use in those with NAFLD/NASH at high CVD or HCC risk, alone and/or preferably in combination with each other or with ezetimibe, for the primary or secondary prevention of CVD, and the avoidance of cirrhosis, liver transplantation or HCC, bearing in mind that CVD is the main cause of death in NAFLD/NASH patients.
|
28521870 |
2017 |
|
Non-alcoholic Fatty Liver Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
Apigenin, a modulator of PPARγ, attenuates HFD-induced NAFLD by regulating hepatocyte lipid metabolism and oxidative stress via Nrf2 activation.
|
28414138 |
2017 |
|
Non-alcoholic Fatty Liver Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
However, PPARγ activation may induce obesity and nonalcoholic fatty liver disease (NAFLD), one of the most challenging medical conditions.
|
26775807 |
2016 |
|
Non-alcoholic Fatty Liver Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
Currently, there is no approved pharmacological treatment for this disease, but improvement of insulin resistance using peroxisome proliferator-activated receptor-γ (PPARγ) agonists, such as thiazolidinediones (TZDs), has been shown to reduce steatosis and steatohepatitis effectively and to improve liver function in patients with obesity-related NAFLD.
|
26858440 |
2016 |
|
Non-alcoholic Fatty Liver Disease
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
This unique antagonistic regulation of PPARγ by distinct AP-1 dimers occurs at the transcriptional level and establishes AP-1 as a link between obesity, hepatic lipid metabolism, and NAFLD.
|
24411941 |
2014 |
|
Non-alcoholic Fatty Liver Disease
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Our meta-analysis demonstrates that the PPARγ Pro12Ala polymorphism is associated with susceptibility to NAFLD in East Asians, but not in European populations.
|
24697566 |
2014 |
|
Non-alcoholic Fatty Liver Disease
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
We investigated the association of polymorphisms C161T and Pro12Ala of peroxisome proliferator-activated receptor gamma (PPARγ) with clinical and biochemical parameters in Asian Indians with NAFLD.
|
23031808 |
2013 |
|
Non-alcoholic Fatty Liver Disease
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
A common variant in the peroxisome proliferator-activated receptor-γ coactivator-1α gene is associated with nonalcoholic fatty liver disease in obese children.
|
23269818 |
2013 |