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PMID |
Sentence |
1 |
12414791
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The oxysterol receptors LXR (liver X receptor)-alpha and LXRbeta are nuclear receptors that play a key role in regulation of cholesterol and fatty acid metabolism.
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2 |
14749264
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The nuclear receptors liver X receptor (LXR)alpha and LXRbeta are sensors of cholesterol metabolism and lipid biosynthesis.
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3 |
14749264
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LXRalpha is a target gene of the peroxisome proliferator-activated receptor-gamma, a target of drugs used in treating elevated levels of glucose seen in diabetes.
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4 |
14749264
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Furthermore, insulin induces LXRalpha in hepatocytes, resulting in increased expression of lipogenic enzymes and suppression of key enzymes in gluconeogenesis, including PEPCK.
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5 |
14749264
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LXR seems to have an important role in the regulation of glucocorticoid action and a role in the overall energy homeostasis suggested by its putative regulatory effect on leptin and uncoupling protein 1.
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6 |
15220211
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Plausible positional candidate genes include NR1H2 and TULP2.
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7 |
15503871
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The liver X receptors (LXRs), LXRalpha and LXRbeta, are ligand-activated transcription factors of the nuclear receptor superfamily that control the expression of genes involved in cholesterol and fatty acid metabolism.
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8 |
15539633
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The liver X receptors alpha and beta (LXRalpha and LXRbeta) are important regulators of cholesterol homeostasis in liver and macrophages.
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9 |
15539633
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LXR ligands suppressed mitogen-induced degradation of the cyclin-dependent kinase inhibitor p27Kip1, attenuated cyclin D1 and cyclin A expression, and inhibited the expression of S phase-regulatory minichromosome maintenance protein 6.
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10 |
15539633
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Stabilization of p27kip1 by LXR ligands was mediated by supressing the transcriptional activation of the S phase kinase-associated protein 2 (Skp2), an F-box protein that targets p27Kip1 for degradation.
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11 |
15539633
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Inhibition of Rb phosphorylation and G1-->S cell cycle progression by LXR ligands was reversed in VSMCs overexpressing Skp2, indicating that Skp2 as an upstream regulator of p27Kip1 degradation plays a central role in LXR ligand-mediated inhibition of VSMC proliferation.
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12 |
16101409
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Two LXRs (LXRalpha and LXRbeta) were initially characterized as orphan members of this superfamily with disparate patterns of tissue expression.
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13 |
16604185
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In this review, we discuss the molecular pathology of AD, the cholesterol connection and recent data suggesting that the oxysterol receptor, liver X receptor LXR (NR1H2 and NR1H3), may modulate these events.
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14 |
16936198
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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).
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15 |
16936198
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The increase in cholesterol content is associated with 1) increased expression of SREBP-2 and 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase, which results in increased cholesterol synthesis, and 2) decreased expression of liver X receptor (LXR)-alpha, LXR-beta, and ATP-binding cassette transporter-1, which results in decreased cholesterol efflux.
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16 |
16936198
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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.
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17 |
16973760
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The nuclear hormone receptors liver X receptor alpha (LXRalpha) (NR1H3) and LXRbeta (NR1H2) are established regulators of cholesterol, lipid, and glucose metabolism and are attractive drug targets for the treatment of diabetes and cardiovascular disease.
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18 |
17107947
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The liver X receptors, LXRalpha (NR1H3) and LXRbeta (NR1H2), are ligand-activated transcription factors that belong to the nuclear hormone receptor superfamily.
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19 |
17107947
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We show that T0901317 treatment of mice is associated with up-regulation of the ChREBP target gene, liver-type pyruvate kinase.
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20 |
17626048
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Elk1 and SRF transcription factors convey basal transcription and mediate glucose response via their binding sites in the human LXRB gene promoter.
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21 |
17626048
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The nuclear receptors LXRalpha (NR1H3) and LXRbeta (NR1H2) are attractive drug targets for the treatment of diabetes and cardiovascular disease due to their established role as regulators of cholesterol and lipid metabolism.
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22 |
17626048
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A large body of literature has recently indicated their important roles in glucose metabolism and particularly LXRbeta is important for proper insulin production in pancreas.
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23 |
17626048
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The transcription start site of the human LXRB gene was determined and we identified two highly conserved, and functional, ETS and Elk1 binding sites, respectively, in the LXRB gene promoter.
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24 |
17626048
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The Elk1 binding site also bound the serum responsive factor (SRF).
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25 |
17626048
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Furthermore, mutation of the binding sites or siRNA knockdown of SRF and Elk1 significantly reduced the promoter activity and impaired the glucose response.
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26 |
17626048
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Elk1 and SRF transcription factors convey basal transcription and mediate glucose response via their binding sites in the human LXRB gene promoter.
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27 |
17626048
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The nuclear receptors LXRalpha (NR1H3) and LXRbeta (NR1H2) are attractive drug targets for the treatment of diabetes and cardiovascular disease due to their established role as regulators of cholesterol and lipid metabolism.
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28 |
17626048
|
A large body of literature has recently indicated their important roles in glucose metabolism and particularly LXRbeta is important for proper insulin production in pancreas.
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29 |
17626048
|
The transcription start site of the human LXRB gene was determined and we identified two highly conserved, and functional, ETS and Elk1 binding sites, respectively, in the LXRB gene promoter.
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30 |
17626048
|
The Elk1 binding site also bound the serum responsive factor (SRF).
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31 |
17626048
|
Furthermore, mutation of the binding sites or siRNA knockdown of SRF and Elk1 significantly reduced the promoter activity and impaired the glucose response.
|
32 |
17626048
|
Elk1 and SRF transcription factors convey basal transcription and mediate glucose response via their binding sites in the human LXRB gene promoter.
|
33 |
17626048
|
The nuclear receptors LXRalpha (NR1H3) and LXRbeta (NR1H2) are attractive drug targets for the treatment of diabetes and cardiovascular disease due to their established role as regulators of cholesterol and lipid metabolism.
|
34 |
17626048
|
A large body of literature has recently indicated their important roles in glucose metabolism and particularly LXRbeta is important for proper insulin production in pancreas.
|
35 |
17626048
|
The transcription start site of the human LXRB gene was determined and we identified two highly conserved, and functional, ETS and Elk1 binding sites, respectively, in the LXRB gene promoter.
|
36 |
17626048
|
The Elk1 binding site also bound the serum responsive factor (SRF).
|
37 |
17626048
|
Furthermore, mutation of the binding sites or siRNA knockdown of SRF and Elk1 significantly reduced the promoter activity and impaired the glucose response.
|
38 |
17626048
|
Elk1 and SRF transcription factors convey basal transcription and mediate glucose response via their binding sites in the human LXRB gene promoter.
|
39 |
17626048
|
The nuclear receptors LXRalpha (NR1H3) and LXRbeta (NR1H2) are attractive drug targets for the treatment of diabetes and cardiovascular disease due to their established role as regulators of cholesterol and lipid metabolism.
|
40 |
17626048
|
A large body of literature has recently indicated their important roles in glucose metabolism and particularly LXRbeta is important for proper insulin production in pancreas.
|
41 |
17626048
|
The transcription start site of the human LXRB gene was determined and we identified two highly conserved, and functional, ETS and Elk1 binding sites, respectively, in the LXRB gene promoter.
|
42 |
17626048
|
The Elk1 binding site also bound the serum responsive factor (SRF).
|
43 |
17626048
|
Furthermore, mutation of the binding sites or siRNA knockdown of SRF and Elk1 significantly reduced the promoter activity and impaired the glucose response.
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44 |
18769020
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Nuclear hormone receptors liver X receptor (LXRalpha and LXRbeta) ligands are attractive approaches for the treatment of dyslipidemia and atherosclerosis.
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45 |
18769020
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Reduction of LXRalpha transcript levels to 48 +/- 13% compared with control virus transduction resulted in a significant downregulation of the LXRalpha-regulated lipogenic genes sterol-regulatory element binding protein-1c (SREBP1c) and stearoyl CoA desaturase 1 in vivo.
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46 |
18772361
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The high concentration of glucose enhanced the protein expression of the critical cholesterol transporter NPC1L1 and that of CD36 (P < 0.02) and concomitantly decreased SR-BI protein mass (P < 0.02).
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47 |
18772361
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No significant changes were observed in the protein expression of ABCA1 and ABCG8, which act as efflux pumps favoring cholesterol export out of absorptive cells.
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48 |
18772361
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Finally, increases were noted in the transcription factors LXR-alpha, LXR-beta, PPAR-beta, and PPAR-gamma along with a drop in the protein expression of SREBP-2.
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49 |
19690071
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Separate and overlapping metabolic functions of LXRalpha and LXRbeta in C57Bl/6 female mice.
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50 |
19690071
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The two liver X receptors (LXRs), LXRalpha and LXRbeta, are transcriptional regulators of cholesterol, lipid, and glucose metabolism and are both activated by oxysterols.
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51 |
19690071
|
C57Bl/6 female mice were fed a normal or a high-fat diet (HFD) and metabolic responses in wild-type, LXRalpha(-/-), LXRbeta(-/-), and LXRalphabeta(-/-) mice were analyzed.
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52 |
19690071
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Using tolerance tests, we found that, on an HFD, LXRbeta(-/-) mice enhanced their endogenous glucose production and became highly insulin resistant, whereas LXRalpha(-/-) and LXRalphabeta(-/-) mice remained glucose tolerant and insulin sensitive.
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53 |
19690071
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Gene expression profiling confirmed that LXRbeta is the regulator of lipogenic genes in visceral white adipose tissue (WAT) and muscle tissue and, surprisingly, that Ucp1 and Dio2 are not responsible for the protection against diet-induced obesity observed in LXRbeta(-/-) and LXRalphabeta(-/-) mice.
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54 |
19690071
|
LXRalpha is required for the control of cholesterol metabolism in the liver, while LXRbeta appears to be a major regulator of glucose homeostasis and energy utilization and of fat storage in muscle and WAT.
|
55 |
19690071
|
Separate and overlapping metabolic functions of LXRalpha and LXRbeta in C57Bl/6 female mice.
|
56 |
19690071
|
The two liver X receptors (LXRs), LXRalpha and LXRbeta, are transcriptional regulators of cholesterol, lipid, and glucose metabolism and are both activated by oxysterols.
|
57 |
19690071
|
C57Bl/6 female mice were fed a normal or a high-fat diet (HFD) and metabolic responses in wild-type, LXRalpha(-/-), LXRbeta(-/-), and LXRalphabeta(-/-) mice were analyzed.
|
58 |
19690071
|
Using tolerance tests, we found that, on an HFD, LXRbeta(-/-) mice enhanced their endogenous glucose production and became highly insulin resistant, whereas LXRalpha(-/-) and LXRalphabeta(-/-) mice remained glucose tolerant and insulin sensitive.
|
59 |
19690071
|
Gene expression profiling confirmed that LXRbeta is the regulator of lipogenic genes in visceral white adipose tissue (WAT) and muscle tissue and, surprisingly, that Ucp1 and Dio2 are not responsible for the protection against diet-induced obesity observed in LXRbeta(-/-) and LXRalphabeta(-/-) mice.
|
60 |
19690071
|
LXRalpha is required for the control of cholesterol metabolism in the liver, while LXRbeta appears to be a major regulator of glucose homeostasis and energy utilization and of fat storage in muscle and WAT.
|
61 |
19690071
|
Separate and overlapping metabolic functions of LXRalpha and LXRbeta in C57Bl/6 female mice.
|
62 |
19690071
|
The two liver X receptors (LXRs), LXRalpha and LXRbeta, are transcriptional regulators of cholesterol, lipid, and glucose metabolism and are both activated by oxysterols.
|
63 |
19690071
|
C57Bl/6 female mice were fed a normal or a high-fat diet (HFD) and metabolic responses in wild-type, LXRalpha(-/-), LXRbeta(-/-), and LXRalphabeta(-/-) mice were analyzed.
|
64 |
19690071
|
Using tolerance tests, we found that, on an HFD, LXRbeta(-/-) mice enhanced their endogenous glucose production and became highly insulin resistant, whereas LXRalpha(-/-) and LXRalphabeta(-/-) mice remained glucose tolerant and insulin sensitive.
|
65 |
19690071
|
Gene expression profiling confirmed that LXRbeta is the regulator of lipogenic genes in visceral white adipose tissue (WAT) and muscle tissue and, surprisingly, that Ucp1 and Dio2 are not responsible for the protection against diet-induced obesity observed in LXRbeta(-/-) and LXRalphabeta(-/-) mice.
|
66 |
19690071
|
LXRalpha is required for the control of cholesterol metabolism in the liver, while LXRbeta appears to be a major regulator of glucose homeostasis and energy utilization and of fat storage in muscle and WAT.
|
67 |
19690071
|
Separate and overlapping metabolic functions of LXRalpha and LXRbeta in C57Bl/6 female mice.
|
68 |
19690071
|
The two liver X receptors (LXRs), LXRalpha and LXRbeta, are transcriptional regulators of cholesterol, lipid, and glucose metabolism and are both activated by oxysterols.
|
69 |
19690071
|
C57Bl/6 female mice were fed a normal or a high-fat diet (HFD) and metabolic responses in wild-type, LXRalpha(-/-), LXRbeta(-/-), and LXRalphabeta(-/-) mice were analyzed.
|
70 |
19690071
|
Using tolerance tests, we found that, on an HFD, LXRbeta(-/-) mice enhanced their endogenous glucose production and became highly insulin resistant, whereas LXRalpha(-/-) and LXRalphabeta(-/-) mice remained glucose tolerant and insulin sensitive.
|
71 |
19690071
|
Gene expression profiling confirmed that LXRbeta is the regulator of lipogenic genes in visceral white adipose tissue (WAT) and muscle tissue and, surprisingly, that Ucp1 and Dio2 are not responsible for the protection against diet-induced obesity observed in LXRbeta(-/-) and LXRalphabeta(-/-) mice.
|
72 |
19690071
|
LXRalpha is required for the control of cholesterol metabolism in the liver, while LXRbeta appears to be a major regulator of glucose homeostasis and energy utilization and of fat storage in muscle and WAT.
|
73 |
19690071
|
Separate and overlapping metabolic functions of LXRalpha and LXRbeta in C57Bl/6 female mice.
|
74 |
19690071
|
The two liver X receptors (LXRs), LXRalpha and LXRbeta, are transcriptional regulators of cholesterol, lipid, and glucose metabolism and are both activated by oxysterols.
|
75 |
19690071
|
C57Bl/6 female mice were fed a normal or a high-fat diet (HFD) and metabolic responses in wild-type, LXRalpha(-/-), LXRbeta(-/-), and LXRalphabeta(-/-) mice were analyzed.
|
76 |
19690071
|
Using tolerance tests, we found that, on an HFD, LXRbeta(-/-) mice enhanced their endogenous glucose production and became highly insulin resistant, whereas LXRalpha(-/-) and LXRalphabeta(-/-) mice remained glucose tolerant and insulin sensitive.
|
77 |
19690071
|
Gene expression profiling confirmed that LXRbeta is the regulator of lipogenic genes in visceral white adipose tissue (WAT) and muscle tissue and, surprisingly, that Ucp1 and Dio2 are not responsible for the protection against diet-induced obesity observed in LXRbeta(-/-) and LXRalphabeta(-/-) mice.
|
78 |
19690071
|
LXRalpha is required for the control of cholesterol metabolism in the liver, while LXRbeta appears to be a major regulator of glucose homeostasis and energy utilization and of fat storage in muscle and WAT.
|
79 |
19690071
|
Separate and overlapping metabolic functions of LXRalpha and LXRbeta in C57Bl/6 female mice.
|
80 |
19690071
|
The two liver X receptors (LXRs), LXRalpha and LXRbeta, are transcriptional regulators of cholesterol, lipid, and glucose metabolism and are both activated by oxysterols.
|
81 |
19690071
|
C57Bl/6 female mice were fed a normal or a high-fat diet (HFD) and metabolic responses in wild-type, LXRalpha(-/-), LXRbeta(-/-), and LXRalphabeta(-/-) mice were analyzed.
|
82 |
19690071
|
Using tolerance tests, we found that, on an HFD, LXRbeta(-/-) mice enhanced their endogenous glucose production and became highly insulin resistant, whereas LXRalpha(-/-) and LXRalphabeta(-/-) mice remained glucose tolerant and insulin sensitive.
|
83 |
19690071
|
Gene expression profiling confirmed that LXRbeta is the regulator of lipogenic genes in visceral white adipose tissue (WAT) and muscle tissue and, surprisingly, that Ucp1 and Dio2 are not responsible for the protection against diet-induced obesity observed in LXRbeta(-/-) and LXRalphabeta(-/-) mice.
|
84 |
19690071
|
LXRalpha is required for the control of cholesterol metabolism in the liver, while LXRbeta appears to be a major regulator of glucose homeostasis and energy utilization and of fat storage in muscle and WAT.
|
85 |
19933273
|
Nuclear receptor liver X receptor is O-GlcNAc-modified in response to glucose.
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86 |
19933273
|
In the present study, we show for the first time that LXRalpha and LXRbeta are targets for glucose-hexosamine-derived O-GlcNAc modification in human Huh7 cells.
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87 |
19933273
|
Importantly, induction of LXRalpha O-GlcNAcylation in both mouse models was concomitant with increased expression of the lipogenic gene SREBP-1c (sterol regulatory element-binding protein 1c).
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88 |
21042792
|
Genetic variation within the NR1H2 gene encoding liver X receptor β associates with insulin secretion in subjects at increased risk for type 2 diabetes.
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89 |
21042792
|
We hypothesized that common variants in the NR1H2 and NR1H3 genes, encoding LXR-β and -α, respectively, may alter pancreatic β-cell function.
|
90 |
21042792
|
One thousand five hundred seventy-four subjects of European ancestry with elevated risk for type 2 diabetes were genotyped for the two NR1H2 single nucleotide polymorphisms (SNPs) rs2248949 and rs1405655 and for the four NR1H3 SNPs rs11039149, rs3758673, rs12221497 and rs2279238, and association studies with metabolic traits were performed.
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91 |
21042792
|
One hundred per cent of common genetic variation (minor allele frequency ≥1%) within the NR1H2 and NR1H3 loci (D' = 1.0; r² ≥ 0.8) were covered by the six chosen tagging SNPs.
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92 |
21042792
|
NR1H2 rs2248949 was nominally associated with OGTT-derived first-phase insulin secretion and proinsulin conversion to insulin and significantly associated with the AUC of insulin levels during the IVGTT (p = 0.007) after adjustment for age, gender, BMI and insulin sensitivity in the dominant model, with the minor allele conferring reduced pancreatic β-cell function to the carriers.
|
93 |
21042792
|
In subjects of European ancestry at increased risk for type 2 diabetes, common variation within the NR1H2 gene impaired insulin secretion, which may facilitate the development of type 2 diabetes.
|
94 |
21042792
|
Genetic variation within the NR1H2 gene encoding liver X receptor β associates with insulin secretion in subjects at increased risk for type 2 diabetes.
|
95 |
21042792
|
We hypothesized that common variants in the NR1H2 and NR1H3 genes, encoding LXR-β and -α, respectively, may alter pancreatic β-cell function.
|
96 |
21042792
|
One thousand five hundred seventy-four subjects of European ancestry with elevated risk for type 2 diabetes were genotyped for the two NR1H2 single nucleotide polymorphisms (SNPs) rs2248949 and rs1405655 and for the four NR1H3 SNPs rs11039149, rs3758673, rs12221497 and rs2279238, and association studies with metabolic traits were performed.
|
97 |
21042792
|
One hundred per cent of common genetic variation (minor allele frequency ≥1%) within the NR1H2 and NR1H3 loci (D' = 1.0; r² ≥ 0.8) were covered by the six chosen tagging SNPs.
|
98 |
21042792
|
NR1H2 rs2248949 was nominally associated with OGTT-derived first-phase insulin secretion and proinsulin conversion to insulin and significantly associated with the AUC of insulin levels during the IVGTT (p = 0.007) after adjustment for age, gender, BMI and insulin sensitivity in the dominant model, with the minor allele conferring reduced pancreatic β-cell function to the carriers.
|
99 |
21042792
|
In subjects of European ancestry at increased risk for type 2 diabetes, common variation within the NR1H2 gene impaired insulin secretion, which may facilitate the development of type 2 diabetes.
|
100 |
21042792
|
Genetic variation within the NR1H2 gene encoding liver X receptor β associates with insulin secretion in subjects at increased risk for type 2 diabetes.
|
101 |
21042792
|
We hypothesized that common variants in the NR1H2 and NR1H3 genes, encoding LXR-β and -α, respectively, may alter pancreatic β-cell function.
|
102 |
21042792
|
One thousand five hundred seventy-four subjects of European ancestry with elevated risk for type 2 diabetes were genotyped for the two NR1H2 single nucleotide polymorphisms (SNPs) rs2248949 and rs1405655 and for the four NR1H3 SNPs rs11039149, rs3758673, rs12221497 and rs2279238, and association studies with metabolic traits were performed.
|
103 |
21042792
|
One hundred per cent of common genetic variation (minor allele frequency ≥1%) within the NR1H2 and NR1H3 loci (D' = 1.0; r² ≥ 0.8) were covered by the six chosen tagging SNPs.
|
104 |
21042792
|
NR1H2 rs2248949 was nominally associated with OGTT-derived first-phase insulin secretion and proinsulin conversion to insulin and significantly associated with the AUC of insulin levels during the IVGTT (p = 0.007) after adjustment for age, gender, BMI and insulin sensitivity in the dominant model, with the minor allele conferring reduced pancreatic β-cell function to the carriers.
|
105 |
21042792
|
In subjects of European ancestry at increased risk for type 2 diabetes, common variation within the NR1H2 gene impaired insulin secretion, which may facilitate the development of type 2 diabetes.
|
106 |
21042792
|
Genetic variation within the NR1H2 gene encoding liver X receptor β associates with insulin secretion in subjects at increased risk for type 2 diabetes.
|
107 |
21042792
|
We hypothesized that common variants in the NR1H2 and NR1H3 genes, encoding LXR-β and -α, respectively, may alter pancreatic β-cell function.
|
108 |
21042792
|
One thousand five hundred seventy-four subjects of European ancestry with elevated risk for type 2 diabetes were genotyped for the two NR1H2 single nucleotide polymorphisms (SNPs) rs2248949 and rs1405655 and for the four NR1H3 SNPs rs11039149, rs3758673, rs12221497 and rs2279238, and association studies with metabolic traits were performed.
|
109 |
21042792
|
One hundred per cent of common genetic variation (minor allele frequency ≥1%) within the NR1H2 and NR1H3 loci (D' = 1.0; r² ≥ 0.8) were covered by the six chosen tagging SNPs.
|
110 |
21042792
|
NR1H2 rs2248949 was nominally associated with OGTT-derived first-phase insulin secretion and proinsulin conversion to insulin and significantly associated with the AUC of insulin levels during the IVGTT (p = 0.007) after adjustment for age, gender, BMI and insulin sensitivity in the dominant model, with the minor allele conferring reduced pancreatic β-cell function to the carriers.
|
111 |
21042792
|
In subjects of European ancestry at increased risk for type 2 diabetes, common variation within the NR1H2 gene impaired insulin secretion, which may facilitate the development of type 2 diabetes.
|
112 |
21042792
|
Genetic variation within the NR1H2 gene encoding liver X receptor β associates with insulin secretion in subjects at increased risk for type 2 diabetes.
|
113 |
21042792
|
We hypothesized that common variants in the NR1H2 and NR1H3 genes, encoding LXR-β and -α, respectively, may alter pancreatic β-cell function.
|
114 |
21042792
|
One thousand five hundred seventy-four subjects of European ancestry with elevated risk for type 2 diabetes were genotyped for the two NR1H2 single nucleotide polymorphisms (SNPs) rs2248949 and rs1405655 and for the four NR1H3 SNPs rs11039149, rs3758673, rs12221497 and rs2279238, and association studies with metabolic traits were performed.
|
115 |
21042792
|
One hundred per cent of common genetic variation (minor allele frequency ≥1%) within the NR1H2 and NR1H3 loci (D' = 1.0; r² ≥ 0.8) were covered by the six chosen tagging SNPs.
|
116 |
21042792
|
NR1H2 rs2248949 was nominally associated with OGTT-derived first-phase insulin secretion and proinsulin conversion to insulin and significantly associated with the AUC of insulin levels during the IVGTT (p = 0.007) after adjustment for age, gender, BMI and insulin sensitivity in the dominant model, with the minor allele conferring reduced pancreatic β-cell function to the carriers.
|
117 |
21042792
|
In subjects of European ancestry at increased risk for type 2 diabetes, common variation within the NR1H2 gene impaired insulin secretion, which may facilitate the development of type 2 diabetes.
|
118 |
21042792
|
Genetic variation within the NR1H2 gene encoding liver X receptor β associates with insulin secretion in subjects at increased risk for type 2 diabetes.
|
119 |
21042792
|
We hypothesized that common variants in the NR1H2 and NR1H3 genes, encoding LXR-β and -α, respectively, may alter pancreatic β-cell function.
|
120 |
21042792
|
One thousand five hundred seventy-four subjects of European ancestry with elevated risk for type 2 diabetes were genotyped for the two NR1H2 single nucleotide polymorphisms (SNPs) rs2248949 and rs1405655 and for the four NR1H3 SNPs rs11039149, rs3758673, rs12221497 and rs2279238, and association studies with metabolic traits were performed.
|
121 |
21042792
|
One hundred per cent of common genetic variation (minor allele frequency ≥1%) within the NR1H2 and NR1H3 loci (D' = 1.0; r² ≥ 0.8) were covered by the six chosen tagging SNPs.
|
122 |
21042792
|
NR1H2 rs2248949 was nominally associated with OGTT-derived first-phase insulin secretion and proinsulin conversion to insulin and significantly associated with the AUC of insulin levels during the IVGTT (p = 0.007) after adjustment for age, gender, BMI and insulin sensitivity in the dominant model, with the minor allele conferring reduced pancreatic β-cell function to the carriers.
|
123 |
21042792
|
In subjects of European ancestry at increased risk for type 2 diabetes, common variation within the NR1H2 gene impaired insulin secretion, which may facilitate the development of type 2 diabetes.
|
124 |
12435796
|
Liver X receptor (LXR) alpha and LXRbeta are nuclear oxysterol receptors whose biological function has so far been elucidated only with respect to cholesterol and lipid metabolism.
|
125 |
12435796
|
Notably, LXR agonist treatment up-regulated CYP4A10 and CYP4A14 together with cytochrome P450 reductase, indicating a possible enhancement of microsomal lipid peroxidation.
|