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l-Glutamine enhances enterocyte growth via activation of the mTOR signaling pathway independently of AMPK.
- Source :
-
Amino Acids . Jan2015, Vol. 47 Issue 1, p65-78. 14p. - Publication Year :
- 2015
-
Abstract
- Neonates (including human infants) require l-glutamine (Gln) for optimal intestinal health. This study tested the hypothesis that Gln enhances enterocyte growth via both mammalian target of rapamycin (mTOR) and AMP-activated kinase (AMPK) signaling pathways. Intestinal porcine epithelial cells (IPEC-1) were cultured for 3 days in Gln-free Dulbecco's modified Eagle medium containing 0 or 2 mM Gln. To determine the role of mTOR and AMPK on cell growth, additional experiments were conducted where medium contained 2 mM Gln and 10 nM rapamycin (Rap, an inhibitor of mTOR) or 1 μM compound C (an inhibitor of AMPK). IPEC-1 cell growth increased with increasing concentrations of Gln from 0 to 2 mM. Compared with 0 mM Gln, 2 mM Gln increased ( P < 0.05) the amounts of phosphorylated 4E-binding protein 1 (4E-BP1) and ribosomal protein S6 kinase (p70S6 kinase) proteins but did not affect abundances of total or phosphorylated AMPK protein. Gln also increased mRNA levels for Bcl-2, mTOR, p70S6 kinase, 4E-BP1, COX7C, ASCT2, ODC, SGLT-1, CFTR, Na/K-ATPase, HSP70, and ZO-1. Similarly, cells cultured with Rap and Gln exhibited higher ( P < 0.05) abundances of phosphorylated 4E-BP1 and p70S6 kinase proteins than the Rap-only group, whereas abundances of phosphorylated mTOR and 4E-BP1 proteins were increased when AMPK was inhibited by compound C. Conversely, the amount of phosphorylated AMPK increased when mTOR was inhibited by Rap, suggesting a negative cross-talk between mTOR and AMPK. Collectively, these results indicate that Gln stimulates enterocyte growth by activating the mTOR signaling pathway independently of AMPK. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 09394451
- Volume :
- 47
- Issue :
- 1
- Database :
- Academic Search Index
- Journal :
- Amino Acids
- Publication Type :
- Academic Journal
- Accession number :
- 100239544
- Full Text :
- https://doi.org/10.1007/s00726-014-1842-8