scholarly journals Diet-related variation in cellular retinol-binding protein type II gene expression in rat jejunum

2005 ◽  
Vol 94 (6) ◽  
pp. 890-895 ◽  
Author(s):  
Kazuhito Suruga ◽  
Masaaki Kitagawa ◽  
Hiromitsu Yasutake ◽  
Sachiko Takase ◽  
Toshinao Goda

Cellular retinol-binding protein type II (CRBPII) is involved in the transport of vitamin A and its metabolism in the small intestine. In the present study, we demonstrated diet-related variations in CRBPII expression in rat jejunum. The CRBPII protein and mRNA levels increased in parallel after the start of feeding period regardless of whether the feeding period was restricted to the hours of darkness or of light. In addition, this variation was observed in the rats fed high-fat diet or low-fat diets, but not in those fed a fat-free diet or in fasted rats. A similar diet-induced variation was seen in the mRNA of liver-type fatty acid-binding protein in rat jejunum. In the transient transfection experiment, unsaturated fatty acid increased rat CRBPII gene promoter activity via the PPARα/retinoid X receptor-α heterodimer. Taken together, these results suggest that the diet-related variation in CRBPII expression in rat jejunum may be brought about by the transcriptional induction of CRBPII gene expression mainly triggered by dietary fatty acids.

1998 ◽  
Vol 274 (4) ◽  
pp. G626-G632 ◽  
Author(s):  
Sachiko Takase ◽  
Kimiko Tanaka ◽  
Kazuhito Suruga ◽  
Masaaki Kitagawa ◽  
Miki Igarashi ◽  
...  

2008 ◽  
Vol 54 (2) ◽  
pp. 130-135 ◽  
Author(s):  
Yuko OGURA ◽  
Hiromitsu YASUTAKE ◽  
Kazuki MOCHIZUKI ◽  
Saori YOSHIKAWA ◽  
Kazuhito SURUGA ◽  
...  

1999 ◽  
Vol 362 (1) ◽  
pp. 159-166 ◽  
Author(s):  
Kazuhito Suruga ◽  
Kazuki Mochizuki ◽  
Masaaki Kitagawa ◽  
Toshinao Goda ◽  
Nobuyuki Horie ◽  
...  

2008 ◽  
Vol 295 (6) ◽  
pp. E1358-E1368 ◽  
Author(s):  
Cynthia F. Zizola ◽  
Gary J. Schwartz ◽  
Silke Vogel

Cellular retinol-binding protein (CRBP) type III (CRBP-III) belongs to the family of intracellular lipid-binding proteins, which includes the adipocyte-binding protein aP2. In the cytosol, CRBP-III binds retinol, the precursor of retinyl ester and the active metabolite retinoic acid. The goal of the present work is to understand the regulation of CRBP-III expression and its role in lipid metabolism. Using EMSAs, luciferase reporter assays, and chromatin immunoprecipitation assays, we found that CRBP-III is a direct target of peroxisome proliferator-activated receptor-γ (PPARγ). Moreover, CRBP-III expression was induced in adipose tissue of mice after treatment with the PPARγ agonist rosiglitazone. To examine a potential role of CRBP-III in regulating lipid metabolism in vivo, CRBP-III-deficient (C-III-KO) mice were maintained on a high-fat diet (HFD). Hepatic steatosis was decreased in HFD-fed C-III-KO compared with HFD-fed wild-type mice. These differences were partly explained by decreased serum free fatty acid levels and decreased free fatty acid efflux from adipose tissue of C-III-KO mice. In addition, the lack of CRBP-III was associated with reduced food intake, increased respiratory energy ratio, and altered body composition, with decreased adiposity and increased lean body mass. Furthermore, expression of genes involved in mitochondrial fatty acid oxidation in brown adipose tissue was increased in C-III-KO mice, and C-III-KO mice were more cold tolerant than wild-type mice fed an HFD. In summary, we demonstrate that CRBP-III is a PPARγ target gene and plays a role in lipid and whole body energy metabolism.


2020 ◽  
Vol 47 (9) ◽  
pp. 6879-6886
Author(s):  
Amedeo Ferlosio ◽  
Elena Doldo ◽  
Sara Agostinelli ◽  
Gaetana Costanza ◽  
Federica Centofanti ◽  
...  

Abstract In recent years, new treatments with novel action mechanisms have been explored for advanced non-small cell lung cancer (NSCLC). Retinoids promote cancer cell differentiation and death and their trafficking and action is mediated from specific cytoplasmic and nuclear receptors, respectively. The purpose of this study was to investigate the effect of Cellular retinol binding protein-1 (CRBP-1) transfection in H460 human NSCLC cell line, normally not expressing CRBP-1. H460 cells were transfected by using a vector pTargeT Mammalian expression system carrying the whole sequence of CRBP-1 gene. For proliferation and apoptosis studies, cells were treated with different concentrations of all-trans Retinoic Acid (atRA) and retinol. AKT-related gene expression was analyzed by using western blot and Signosis array and results analysed by one-way analysis of variance (ANOVA) or by t-student test. CRBP-1+ showed reduced proliferation and viability in basal condition and after atRA treatment when compared to empty-transfected H460 cells. Reduced proliferation in CRBP-1+ H460 cells associated to the down-regulation of pAKT/pERK/pEGFR-related genes. In particular, gene array documented the down-regulation of AKT and Stat-3-related genes, including M-Tor, Akt1, Akt2, Akt3, Foxo1, p27, Jun. Restoration of CRBP-1 expression in H460 cells reduced proliferation and viability in both basal condition and after atRA treatment, likely by down-regulating AKT-related gene level. Further studies are needed to better clarify how those CRBP-1-related intracellular pathways contribute to counteract NSCLC progression in order to suggest a potential tool to improve efficacy of retinoid anti lung cancer adjuvant therapy.


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