PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 20851881-7 2010 Moreover, FXR(-/-) MEFs displayed both an increased lipolysis and a decreased de novo lipogenesis, resulting in reduced intracellular triglyceride content, even upon PPARgamma activation. Triglycerides 134-146 nuclear receptor subfamily 1, group H, member 4 Mus musculus 10-13 20631352-4 2010 Activation of FXR has been shown to improve plasma lipid profiles, whereas Fxr(-/-) mice have increased plasma triglyceride and very-low-density lipoprotein levels. Triglycerides 111-123 nuclear receptor subfamily 1, group H, member 4 Mus musculus 75-78 20431060-6 2010 FXR activation by a synthetic FXR agonist, 6alpha-ethyl chenodeoxycholic acid (INT-747) inhibited phosphate induced-mineralization and triglyceride accumulation in CVCs. Triglycerides 135-147 nuclear receptor subfamily 1, group H, member 4 Mus musculus 0-3 20431060-6 2010 FXR activation by a synthetic FXR agonist, 6alpha-ethyl chenodeoxycholic acid (INT-747) inhibited phosphate induced-mineralization and triglyceride accumulation in CVCs. Triglycerides 135-147 nuclear receptor subfamily 1, group H, member 4 Mus musculus 30-33 19998408-3 2010 Yet bile salt sequestration is also known to affect triglyceride (TG) metabolism, possibly through signaling pathways involving farnesoid X receptor (FXR) and liver X receptor alpha (LXRalpha). Triglycerides 52-64 nuclear receptor subfamily 1, group H, member 4 Mus musculus 150-153 19998408-3 2010 Yet bile salt sequestration is also known to affect triglyceride (TG) metabolism, possibly through signaling pathways involving farnesoid X receptor (FXR) and liver X receptor alpha (LXRalpha). Triglycerides 66-68 nuclear receptor subfamily 1, group H, member 4 Mus musculus 150-153 18948497-5 2009 FXR deficiency and high-fat feeding increased serum cholesterol and triglycerides. Triglycerides 68-81 nuclear receptor subfamily 1, group H, member 4 Mus musculus 0-3 19776172-5 2009 Treatment of these mice with the highly selective and potent FXR-activating ligand 6-alpha-ethyl-chenodeoxycholic acid (INT-747) ameliorates triglyceride accumulation by modulating fatty acid synthesis and oxidation, improves proteinuria, prevents podocyte loss, mesangial expansion, accumulation of extracellular matrix proteins, and increased expression of profibrotic growth factors and fibrosis markers, and modulates inflammation and oxidative stress. Triglycerides 141-153 nuclear receptor subfamily 1, group H, member 4 Mus musculus 61-64 19136377-1 2009 The nuclear hormone receptor farnesoid X receptor (FXR) plays a critical role in the regulation of bile acid, triglyceride (TG), and cholesterol homeostasis. Triglycerides 110-122 nuclear receptor subfamily 1, group H, member 4 Mus musculus 51-54 19136377-1 2009 The nuclear hormone receptor farnesoid X receptor (FXR) plays a critical role in the regulation of bile acid, triglyceride (TG), and cholesterol homeostasis. Triglycerides 124-126 nuclear receptor subfamily 1, group H, member 4 Mus musculus 51-54 19028791-5 2009 FXR activation reduced the liver expression of sterol regulatory element binding protein 1c, resulting in reduced triglyceride and cholesterol content in the liver and amelioration of hyperlipidemia. Triglycerides 114-126 nuclear receptor subfamily 1, group H, member 4 Mus musculus 0-3 18000141-5 2007 Triglyceride accretion and a deficit in hepatic fatty acid oxidation, features of the aging process in mammals, associate to a deficit in hepatic FXR activity in the SAM-P8 mice. Triglycerides 0-12 nuclear receptor subfamily 1, group H, member 4 Mus musculus 146-149 19126757-4 2009 FXR is activated by bile acids, and FXR-deficient (FXR(-/-)) mice display elevated serum levels of triglycerides and high-density lipoprotein cholesterol, demonstrating a critical role of FXR in lipid metabolism. Triglycerides 99-112 nuclear receptor subfamily 1, group H, member 4 Mus musculus 0-3 19126757-4 2009 FXR is activated by bile acids, and FXR-deficient (FXR(-/-)) mice display elevated serum levels of triglycerides and high-density lipoprotein cholesterol, demonstrating a critical role of FXR in lipid metabolism. Triglycerides 99-112 nuclear receptor subfamily 1, group H, member 4 Mus musculus 36-39 19126757-4 2009 FXR is activated by bile acids, and FXR-deficient (FXR(-/-)) mice display elevated serum levels of triglycerides and high-density lipoprotein cholesterol, demonstrating a critical role of FXR in lipid metabolism. Triglycerides 99-112 nuclear receptor subfamily 1, group H, member 4 Mus musculus 36-39 19126757-5 2009 In an opposite manner, activation of FXR by bile acids (BAs) or nonsteroidal synthetic FXR agonists lowers plasma triglycerides by a mechanism that may involve the repression of hepatic SREBP-1c expression and/or the modulation of glucose-induced lipogenic genes. Triglycerides 114-127 nuclear receptor subfamily 1, group H, member 4 Mus musculus 37-40 19126757-5 2009 In an opposite manner, activation of FXR by bile acids (BAs) or nonsteroidal synthetic FXR agonists lowers plasma triglycerides by a mechanism that may involve the repression of hepatic SREBP-1c expression and/or the modulation of glucose-induced lipogenic genes. Triglycerides 114-127 nuclear receptor subfamily 1, group H, member 4 Mus musculus 87-90 16936198-3 2006 The increase in renal triglyceride content is associated with 1) increased expression of sterol regulatory element-binding protein (SREBP)-1c and carbohydrate response element-binding protein (ChREBP), which collectively results in increased fatty acid synthesis, 2) decreased expression of peroxisome proliferator-activated receptor (PPAR)-alpha and -delta, which results in decreased fatty acid oxidation, and 3) decreased expression of farnesoid X receptor (FXR) and small heterodimer partner (SHP). Triglycerides 22-34 nuclear receptor subfamily 1, group H, member 4 Mus musculus 439-459 17110163-1 2006 Farnesoid X receptor (FXR), a bile-acid-activated member of the nuclear receptor superfamily, is essential in regulating bile-acid, cholesterol, and triglyceride homeostasis. Triglycerides 149-161 nuclear receptor subfamily 1, group H, member 4 Mus musculus 22-25 17110163-2 2006 Disruption of the FXR gene in mice results in a proatherosclerotic lipid profile with increased serum cholesterols and triglycerides. Triglycerides 119-132 nuclear receptor subfamily 1, group H, member 4 Mus musculus 18-21 17110163-8 2006 Compared to ApoE-null mice, the FXR/ApoE double-null mice were found to have less atherosclerotic lesion area in the aorta, despite a further increase in the serum cholesterols and triglycerides. Triglycerides 181-194 nuclear receptor subfamily 1, group H, member 4 Mus musculus 32-35 16936198-5 2006 Our results indicate that in type 1 diabetes, there is altered renal lipid metabolism favoring net accumulation of triglycerides and cholesterol, which are driven by increases in SREBP-1, ChREBP, and SREBP-2 and decreases in FXR, LXR-alpha, and LXR-beta, which may also play a role in the increased expression of profibrotic growth hormones, proinflammatory cytokines, and oxidative stress. Triglycerides 115-128 nuclear receptor subfamily 1, group H, member 4 Mus musculus 225-228 16936198-3 2006 The increase in renal triglyceride content is associated with 1) increased expression of sterol regulatory element-binding protein (SREBP)-1c and carbohydrate response element-binding protein (ChREBP), which collectively results in increased fatty acid synthesis, 2) decreased expression of peroxisome proliferator-activated receptor (PPAR)-alpha and -delta, which results in decreased fatty acid oxidation, and 3) decreased expression of farnesoid X receptor (FXR) and small heterodimer partner (SHP). Triglycerides 22-34 nuclear receptor subfamily 1, group H, member 4 Mus musculus 461-464 16844773-6 2006 FXR KO mice also exhibit a biphasic lipid profile after bile duct ligation, with an increase in high-density lipoprotein cholesterol and triglycerides by day 6. Triglycerides 137-150 nuclear receptor subfamily 1, group H, member 4 Mus musculus 0-3 16844773-7 2006 The expression of apolipoprotein AV was reduced in these mice, implicating FXR in triglyceride regulation. Triglycerides 82-94 nuclear receptor subfamily 1, group H, member 4 Mus musculus 75-78 14729567-2 2004 Here we show that PGC-1alpha regulates triglyceride metabolism through both farnesoid X receptor (FXR)-dependent and -independent pathways. Triglycerides 39-51 nuclear receptor subfamily 1, group H, member 4 Mus musculus 98-101 15721319-6 2005 In addition, treatment of mice with an FXR agonist significantly increased hepatic PDK4 expression, while concomitantly decreasing plasma triglyceride levels. Triglycerides 138-150 nuclear receptor subfamily 1, group H, member 4 Mus musculus 39-42 15146238-0 2004 Bile acids lower triglyceride levels via a pathway involving FXR, SHP, and SREBP-1c. Triglycerides 17-29 nuclear receptor subfamily 1, group H, member 4 Mus musculus 61-64 14729567-0 2004 Peroxisome proliferator-activated receptor-gamma coactivator 1alpha (PGC-1alpha) regulates triglyceride metabolism by activation of the nuclear receptor FXR. Triglycerides 91-103 nuclear receptor subfamily 1, group H, member 4 Mus musculus 153-156 14729567-2 2004 Here we show that PGC-1alpha regulates triglyceride metabolism through both farnesoid X receptor (FXR)-dependent and -independent pathways. Triglycerides 39-51 nuclear receptor subfamily 1, group H, member 4 Mus musculus 76-96 12421815-4 2003 FXR(-/-) mice also have increased: (i) plasma non-HDL cholesterol and triglyceride levels, (ii) apolipoprotein B-containing lipoprotein synthesis, and (iii) intestinal cholesterol absorption. Triglycerides 70-82 nuclear receptor subfamily 1, group H, member 4 Mus musculus 0-3 12891557-4 2003 METHODS: The influence of bile acids and synthetic FXR activators on Apo CIII and triglyceride metabolism was studied in vivo by using FXR wild-type and FXR-deficient mice and in vitro by using human primary hepatocytes and HepG2 cells. Triglycerides 82-94 nuclear receptor subfamily 1, group H, member 4 Mus musculus 51-54 12891557-5 2003 RESULTS: In mice, treatment with the FXR agonist taurocholic acid strongly decreased serum triglyceride levels, an effect associated with reduced Apo CIII serum and liver messenger RNA levels. Triglycerides 91-103 nuclear receptor subfamily 1, group H, member 4 Mus musculus 37-40 11030617-2 2000 FXR/BAR null mice were distinguished from wild-type mice by elevated serum bile acid, cholesterol, and triglycerides, increased hepatic cholesterol and triglycerides, and a proatherogenic serum lipoprotein profile. Triglycerides 103-116 nuclear receptor subfamily 1, group H, member 4 Mus musculus 0-3 11579204-0 2001 Farnesoid X-activated receptor induces apolipoprotein C-II transcription: a molecular mechanism linking plasma triglyceride levels to bile acids. Triglycerides 111-123 nuclear receptor subfamily 1, group H, member 4 Mus musculus 0-30 11579204-8 2001 These results identify a mechanism whereby FXR and its ligands lower plasma triglyceride levels. Triglycerides 76-88 nuclear receptor subfamily 1, group H, member 4 Mus musculus 43-46 11030617-2 2000 FXR/BAR null mice were distinguished from wild-type mice by elevated serum bile acid, cholesterol, and triglycerides, increased hepatic cholesterol and triglycerides, and a proatherogenic serum lipoprotein profile. Triglycerides 152-165 nuclear receptor subfamily 1, group H, member 4 Mus musculus 0-3 32604760-5 2020 Significant decreases in the levels of hepatomegaly, hepatic damage-associated diagnostic markers, hepatic triglycerides, and total bile acids were found in Fxr-null mice fed with a selenoneine-rich diet. Triglycerides 107-120 nuclear receptor subfamily 1, group H, member 4 Mus musculus 157-160 34986301-8 2021 CONCLUSION: Loss of FXR is associated with aggravation of atherosclerosis and hepatic steatosis in ApoE-deficient mice, which could be reversed by a PPARalpha agonist through induction of fatty acid uptake, beta-oxidation, and triglyceride hydrolysis. Triglycerides 227-239 nuclear receptor subfamily 1, group H, member 4 Mus musculus 20-23 34778346-8 2021 In contrast, the expression levels of the ileum farnesoid X receptor (Fxr) and fibroblast growth factor 15 (Fgf15), which inhibit the expression of liver CYP7A1, were significantly reduced in the SCO-PL group than the SOY-TG group. Triglycerides 222-224 nuclear receptor subfamily 1, group H, member 4 Mus musculus 48-68 34778346-8 2021 In contrast, the expression levels of the ileum farnesoid X receptor (Fxr) and fibroblast growth factor 15 (Fgf15), which inhibit the expression of liver CYP7A1, were significantly reduced in the SCO-PL group than the SOY-TG group. Triglycerides 222-224 nuclear receptor subfamily 1, group H, member 4 Mus musculus 70-73 32003602-8 2020 FXR agonism also reduced intestinal triglyceride content and activity of microsomal triglyceride transfer protein, involved in chylomicron assembly. Triglycerides 36-48 nuclear receptor subfamily 1, group H, member 4 Mus musculus 0-3 32003602-8 2020 FXR agonism also reduced intestinal triglyceride content and activity of microsomal triglyceride transfer protein, involved in chylomicron assembly. Triglycerides 84-96 nuclear receptor subfamily 1, group H, member 4 Mus musculus 0-3 32062620-3 2020 Significant decreases in the levels of hepatic damage-associated diagnostic markers, hepatic triglycerides, non-esterified fatty acids, and total bile acids were found in Fxr-null mice that had drunk water containing 0.5% taurine for four weeks. Triglycerides 93-106 nuclear receptor subfamily 1, group H, member 4 Mus musculus 171-174 32006644-7 2020 Combined with the results of Oil Red staining and quantitative detection of triglycerides in fresh tissue blocks, we hypothesized that FXR knockout aggravates diabetes-induced cardiac lipid accumulation. Triglycerides 76-89 nuclear receptor subfamily 1, group H, member 4 Mus musculus 135-138 29986186-1 2018 Bile acids, initially discovered as endogenous ligands of farnesoid X receptor (FXR), play a central role in the regulation of triglyceride and cholesterol metabolism and have recently emerged as a privileged structure for interacting with nuclear receptors relevant to a large array of metabolic processes. Triglycerides 127-139 nuclear receptor subfamily 1, group H, member 4 Mus musculus 80-83 29142166-6 2017 There was a significant decrease in the levels of hepatic damage-associated diagnostic markers, hepatic and serum bile acids, triglycerides, free fatty acids, and total cholesterol levels in Fxr-null mice because of fish oil feeding. Triglycerides 126-139 nuclear receptor subfamily 1, group H, member 4 Mus musculus 191-194 28378930-5 2017 Liver-specific Fxr/Shp double knockout mice fully phenocopied the DKO mice, with lower hepatic triglyceride accumulation, improved glucose/insulin tolerance, and accelerated fatty acid use. Triglycerides 95-107 nuclear receptor subfamily 1, group H, member 4 Mus musculus 15-18 29216638-15 2017 CONCLUSIONS: The present results indicate that miR-122 plays an important role in lipid (particularly TG) accumulation in the liver by reducing YY1 mRNA stability to upregulate FXR-SHP signaling. Triglycerides 102-104 nuclear receptor subfamily 1, group H, member 4 Mus musculus 177-180 25500885-5 2015 Compared with control mice, animals with intestine-specific Fxr disruption had reduced hepatic triglyceride accumulation in response to a HFD. Triglycerides 95-107 nuclear receptor subfamily 1, group H, member 4 Mus musculus 60-63 26909306-9 2015 FXRalpha2 expression in Fxr(-/-) mouse liver activates a similar gene program and robustly decreases hepatic triglyceride levels. Triglycerides 109-121 nuclear receptor subfamily 1, group H, member 4 Mus musculus 24-27 25156247-10 2015 Hepatic Fxr knockouts were characterized by elevated triglycerides and bile acid levels. Triglycerides 53-66 nuclear receptor subfamily 1, group H, member 4 Mus musculus 8-11 25425577-4 2015 In vivo studies utilizing acetylation-mimic and acetylation-defective K217 mutants and gene expression profiling revealed that FXR acetylation increased proinflammatory gene expression, macrophage infiltration, and liver cytokine and triglyceride levels, impaired insulin signaling, and increased glucose intolerance. Triglycerides 234-246 nuclear receptor subfamily 1, group H, member 4 Mus musculus 127-130 24747563-4 2014 We found that FXR deficient (FXR(-/-)) mice fed methionine- and choline-deficient (MCD) diet had higher serum ALT and AST activities and lower hepatic triglyceride levels than wild-type (WT) mice fed MCD diet. Triglycerides 151-163 nuclear receptor subfamily 1, group H, member 4 Mus musculus 14-17 24747563-8 2014 The super-physiological concentrations of hepatic bile acids in FXR(-/-)/MCD mice inhibited the expression of genes involved in fatty acid uptake and triglyceride accumulation, which may be an explanation for less steatosis in FXR(-/-)/MCD mice in contrast to WT/MCD mice. Triglycerides 150-162 nuclear receptor subfamily 1, group H, member 4 Mus musculus 64-67 24747563-4 2014 We found that FXR deficient (FXR(-/-)) mice fed methionine- and choline-deficient (MCD) diet had higher serum ALT and AST activities and lower hepatic triglyceride levels than wild-type (WT) mice fed MCD diet. Triglycerides 151-163 nuclear receptor subfamily 1, group H, member 4 Mus musculus 29-32 22197325-5 2012 Accordingly, pharmacological activation of Fxr with GW4064 overcomes the BA imbalance, restoring hepatic and plasma TG levels of FoxO1-deficient mice to normal levels. Triglycerides 116-118 nuclear receptor subfamily 1, group H, member 4 Mus musculus 43-46 24038130-3 2014 However, the mechanism by which activation of FXR lowers hepatic triglyceride (TG) levels remains unknown. Triglycerides 65-77 nuclear receptor subfamily 1, group H, member 4 Mus musculus 46-49 24038130-3 2014 However, the mechanism by which activation of FXR lowers hepatic triglyceride (TG) levels remains unknown. Triglycerides 79-81 nuclear receptor subfamily 1, group H, member 4 Mus musculus 46-49 24038130-8 2014 Activation of FXR induced hepatic CES1, and reduced the levels of hepatic and plasma TG as well as plasma cholesterol in a CES1-dependent manner. Triglycerides 85-87 nuclear receptor subfamily 1, group H, member 4 Mus musculus 14-17 22197325-4 2012 These changes are associated with deficiency of 12alpha-hydroxylated BAs and their synthetic enzyme, Cyp8b1, that hinders the TG-lowering effects of the BA receptor, Fxr. Triglycerides 126-128 nuclear receptor subfamily 1, group H, member 4 Mus musculus 166-169 24548803-10 2014 This resulted in a similar decrease in liver triglycerides, indicating that the effect seen in bile salt fed Hrn animals is FXR dependent. Triglycerides 45-58 nuclear receptor subfamily 1, group H, member 4 Mus musculus 124-127 21862726-10 2011 These findings suggest that farnesol could improve metabolic abnormalities in mice via both PPARalpha-dependent and -independent pathways and that the activation of FXR by farnesol might contribute partially to the PPARalpha-independent hepatic triglyceride content-lowering effect. Triglycerides 245-257 nuclear receptor subfamily 1, group H, member 4 Mus musculus 165-168 22540009-1 2012 Farnesoid X receptor (FXR) is a nuclear receptor and a key regulator of liver cholesterol and triglyceride homeostasis. Triglycerides 94-106 nuclear receptor subfamily 1, group H, member 4 Mus musculus 22-25