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Leptin affects intestinal epithelial cell turnover in correlation with leptin receptor expression along the villus-crypt axis after massive small bowel resection in a rat.

Authors: Sukhotnik, I  Coran, AG  Mogilner, JG  Shamian, B  Karry, R  Lieber, M  Shaoul, R 
Citation: Sukhotnik I, etal., Pediatr Res. 2009 Dec;66(6):648-53.
Pubmed: (View Article at PubMed) PMID:19730157
DOI: Full-text: DOI:10.1203/PDR.0b013e3181be9f84

In this study, we examine the responsiveness of intestinal epithelial cell turnover to leptin (LEP) in correlation with leptin receptor (LEPr) expression along the villus-crypt axis in a rat with short bowel syndrome (SBS). Adult rats underwent either a 75% intestinal resection or a transection. SBS-LEP rats underwent bowel resection and were treated with LEP starting from the fourth postoperative day. Parameters of intestinal adaptation, enterocyte proliferation, and enterocyte apoptosis were determined at sacrifice. RT-PCR technique was used to determine Bax and Bcl-2 gene expression in ileal mucosa. Villus tips, lateral villi, and crypts were separated using laser capture microdissection. LEPr expression for each compartment was assessed by quantitative real-time PCR (Taqman). Treatment with LEP significantly stimulated all parameters of adaptation. LEPr expression in crypts significantly increased in SBS rats (vs Sham rats) and was accompanied by a significant increase in enterocyte proliferation and decreased apoptosis after LEP administration. A significant increase in LEPr expression at the tip of the villus in SBS rats was accompanied by decreased cell apoptosis. In conclusion LEP accelerated enterocyte turnover and stimulated intestinal adaptation. The effect of LEP on enterocyte proliferation and enterocyte apoptosis correlated with receptor expression along the villus-crypt axis.


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RGD Object Information
RGD ID: 5128624
Created: 2011-03-14
Species: All species
Last Modified: 2011-03-14
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.