scholarly journals Curcumin diminishes the impacts of hyperglycemia on the activation of hepatic stellate cells by suppressing membrane translocation and gene expression of glucose transporter-2

2011 ◽  
Vol 333 (2) ◽  
pp. 160-171 ◽  
Author(s):  
Jianguo Lin ◽  
Anping Chen
Author(s):  
Shigenari Hozawa ◽  
Haruko Suzuki ◽  
Sachiko Kagawa ◽  
Ayako Higuchi ◽  
Tetsu Watanabe ◽  
...  

2003 ◽  
Vol 39 (5) ◽  
pp. 749-755 ◽  
Author(s):  
Naoki Uyama ◽  
Yasuyuki Shimahara ◽  
Hiroaki Okuyama ◽  
Norifumi Kawada ◽  
Shoko Kamo ◽  
...  

2013 ◽  
Vol 125 (6) ◽  
pp. 281-289 ◽  
Author(s):  
Daniela F. Pinheiro ◽  
Patricia F. F. Pinheiro ◽  
José Buratini ◽  
Anthony C. S. Castilho ◽  
Paula F. Lima ◽  
...  

Intrauterine dietary restriction may cause changes in the functioning of offspring organs and systems later in life, an effect known as fetal programming. The present study evaluated mRNA abundance and immunolocalization of nutrient transporters as well as enterocytes proliferation in the proximal, median and distal segments of small intestine of rats born to protein-restricted dams. Pregnant rats were fed hypoproteic (6% protein) or control (17% protein) diets, and offspring rats were evaluated at 3 and 16 weeks of age. The presence of SGLT1 (sodium–glucose co-transporter 1), GLUT2 (glucose transporter 2), PEPT1 (peptide transporter 1) and the intestinal proliferation were evaluated by immunohistochemical techniques and the abundance of specific mRNA for SGLT1, GLUT2 and PEPT1 was assessed by the real-time PCR technique. Rats born to protein-restricted dams showed higher cell proliferation in all intestinal segments and higher gene expression of SGLT1 and PEPT1 in the duodenum. Moreover, in adult animals born to protein-restricted dams the immunoreactivity of SGLT1, GLUT2 and PEPT1in the duodenum was more intense than in control rats. Taken together, the results indicate that changes in the small intestine observed in adulthood can be programmed during the gestation. In addition, they show that this response is caused by both up-regulation in transporter gene expression, a specific adaptation mechanism, and intestinal proliferation, an unspecific adaptation mechanism.


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