| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Department of Genetics, University of Pennsylvania School of Medicine, Philadelphia, PA, USA; Division of Gastroenterology, University of Pennsylvania School of Medicine, Phladelphia, PA, USA
2 Department of Genetics, University of Pennsylvania School of Medicine, Philadelphia, PA, USA
3 Division of Gastroenterology, University of Pennsylvania School of Medicine, Phladelphia, PA, USA
4 Departments of Pharmacology and Physiology, University of Medicine and Dentistry of New Jersey, Newark, NJ, USA
* To whom correspondence should be addressed. E-mail: kaestner{at}mail.med.upenn.edu.
Background and Aims: Mice lacking the mesenchymal winged helix transcription factor Foxl1 exhibit markedly abnormal small intestinal epithelia and postnatal growth retardation. We investigated whether defects in intestinal nutrient uptake and specific transport processes exist in Foxl1-/- mice. Methods: Foxl1-/- mice and controls on a defined genetic background were weighed regularly and sacrificed at 2, 4, and 12 weeks of age. Intestinal uptake studies, quantitative real-time PCR, RNase protection assays, and Western blots were performed. Results: Foxl1-/- mice have dysmorphic small intestinal epithelia and postnatal growth retardation. Foxl1-/- mice demonstrate decreased small intestinal uptake of D-glucose in all age groups studied. Intestinal uptake of D-fructose and two amino acids, L-proline, and L-leucine, is not altered. Consistent with these findings, Foxl1-/- mice show decreased levels of the intestinal D-glucose transporter SGLT1. Expression of sucrase-isomaltase, lactase, GLUT2, and Na+-K+ ATPase are not changed. Conclusions: Foxl1-/- mice demonstrate markedly abnormal intestinal epithelia, postnatal growth retardation, and decreased intestinal uptake of D-glucose. The specific effect of Foxl1 on intestinal D-glucose uptake is due to decreased production of SGLT1 protein in the small intestine. Thus, we identify, for the first time, a link between a mesenchymal factor, Foxl1, and the regulation of a specific epithelial transport process.
This article has been cited by other articles:
|
|
 |
|
  B. G. Goldstein, H.-H. Chao, Y. Yang, Y. A. Yermolina, J. W. Tobias, and J. P. Katz Overexpression of Kruppel-like factor 5 in esophageal epithelia in vivo leads to increased proliferation in basal but not suprabasal cells Am J Physiol Gastrointest Liver Physiol, June 1, 2007; 292(6): G1784 - G1792. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Takano-Maruyama, K. Hase, H. Fukamachi, Y. Kato, H. Koseki, and H. Ohno Foxl1-deficient mice exhibit aberrant epithelial cell positioning resulting from dysregulated EphB/EphrinB expression in the small intestine Am J Physiol Gastrointest Liver Physiol, July 1, 2006; 291(1): G163 - G170. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Ormestad, J. Astorga, H. Landgren, T. Wang, B. R. Johansson, N. Miura, and P. Carlsson Foxf1 and Foxf2 control murine gut development by limiting mesenchymal Wnt signaling and promoting extracellular matrix production Development, March 1, 2006; 133(5): 833 - 843. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
