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ChREBP regulates gene transcription related to glucose and lipid metabolism. Findings from knockout mice and human subjects suggest that ChREBP helps to induce hepatic steatosis, dyslipidemia, and glucose intolerance. [review]
ChREBP and FGF21 constitute a signaling axis likely conserved in humans that mediates an essential adaptive response to fructose ingestion that may participate in the pathogenesis of NAFLD and liver fibrosis.
The results of this population-based study provide evidence for a relationship between lipid regulatory gene polymorphisms including GCKR (rs780094), GCKR (rs1260333), FADS (rs174547), and MLXIPL (rs3812316) with dyslipidemia in an Iranian population.
Data (including data from studies using tissues/cells from transgenic mice) suggest that ChREBPalpha up-regulates expression and activity of NRF2, initiating mitochondrial biogenesis in beta-cells; induction of NRF2 is required for ChREBPalpha-mediated effects and for glucose-stimulated beta-cell proliferation. [NRF2 = nuclear factor (erythroid-derived 2)-like 2 protein]
ChREBP was initially studied as a master regulator of lipogenesis in liver and fat tissue, it is now clear that ChREBP functions as a central metabolic coordinator in a variety of cell types in response to environmental and hormonal signals, with wide implications in health and disease.
A nutrient-sensitive mTOR/ChREBP regulated transcriptional network could be a novel target to improve beta cell survival and glucose homeostasis in diabetes.
these findings support a carbohydrate-mediated, ChREBP-driven mechanism that contributes to hepatic insulin resistance.
results indicated that the age and total cholesterol concentrations were independent influential factors of ChREBP methylation and DNMT1 variants could probably influence LDL-C to further modify ChREBP DNA methylation
p = 6.69 x 10(-9) ] on chr7 at the carbohydrate-responsive element-binding protein-encoding (MLXIPL) gene locus displayed significant protective characteristics, while another variant rs6982502 [0.76 (0.68-0.84); p = 5.31 x 10(-7) ] on chr8 showed similar but weaker properties.
ChREBP role in non-alcoholic fatty liver disease.The involvement of ChREBP in FASN promoter histone modification.
This cross-sectional study suggests that MLXIPL rs3812316 genotypes may be associated with Triglyceride levels. there were significantly different genotype distributions in two TG categories: (1) subjects with normal TG values had a significantly higher G allele frequency than those with elevated TG levels
The results revealed the novel mechanism by which HNF-4alpha promoted ChREBP transcription in response to glucose, and also demonstrated that ChREBP-alpha and HNF-4alpha synergistically increased ChREBP-beta transcription.
High glucose-mediated induction of PDGF-C via ChREBP in mesangial cells contributes to the development of glomerular mesangial expansion in diabetes.
Diet-induced obesity increases basal expression of ChREBPbeta, which may increase the risk of developing hepatic steatosis, and fructose-induced activation is independent of gluconeogenesis.
Evaluation of the conservation of ChREBP and MondoA sequences demonstrate that MondoA is better conserved and potentially mediates more ancient function in glucose metabolism.
Metformin down-regulates high-glucose-induced TXNIP transcription by inactivating ChREBP and FOXO1 in endothelial cells, partially through AMP-activated protein kinase activation
Data suggest that expression of ChREBPbeta isoform is up-regulated in pancreatic beta-cells in response to elevated levels of glucose (i.e., hyperglycemic conditions).
Polymorphisms in lipid level modifier MLXIPL, GCKR, GALNT2, CILP2, ANGPTL3 and TRIB1 genes are highly associated with plasma lipid level changes.
Single-nucleotide polymorphisms alleles near MLXIPL that were associated with higher coffee consumption.
A major function of Mio in mitosis is to regulate the activation/deactivation of Plk1 and Aurora A.
This gene encodes a basic helix-loop-helix leucine zipper transcription factor of the Myc/Max/Mad superfamily. This protein forms a heterodimeric complex and binds and activates, in a glucose-dependent manner, carbohydrate response element (ChoRE) motifs in the promoters of triglyceride synthesis genes. The gene is deleted in Williams-Beuren syndrome, a multisystem developmental disorder caused by the deletion of contiguous genes at chromosome 7q11.23.
MLX interacting protein-like
, carbohydrate response element binding protein variant 1
, carbohydrate response element binding protein variant 2
, Williams-Beuren syndrome chromosomal region 14 protein homolog
, carbohydrate responsive element binding protein
, williams-Beuren syndrome chromosomal region 14 protein homolog
, MLX-interacting protein-like
, Mlx interactor
, WS basic-helix-loop-helix leucine zipper protein
, Williams Beuren syndrome chromosome region 14
, Williams-Beuren syndrome chromosome region 14 protein 1
, Williams-Beuren syndrome chromosome region 14 protein 2
, carbohydrate response element binding protein
, carbohydrate-responsive element-binding protein
, class D basic helix-loop-helix protein 14
, williams-Beuren syndrome chromosomal region 14 protein
, MLX interacting protein-like beta
, MLX interactor
, Williams-Beuren syndrome chromosome region 14 homolog
, putative hepatic transcription factor
, WBSCR14 protein-like
, Williams-Beuren syndrome chromosomal region 14 protein