PMID- 8203529
OWN - NLM
STAT- MEDLINE
DCOM- 19940707
LR  - 20180109
IS  - 0002-9513 (Print)
IS  - 0002-9513 (Linking)
VI  - 266
IP  - 5 Pt 1
DP  - 1994 May
TI  - L-glutamine and L-asparagine stimulate Na+ -H+ exchange in porcine jejunal 
      enterocytes.
PG  - G828-38
AB  - L-Glutamine (Gln) is a major respiratory fuel and substrate for nucleic acid 
      synthesis in mammalian intestinal cells. The structurally related amino acid, 
      L-asparagine (Asn), stimulates the proliferative enzyme ornithine decarboxylase 
      in colonocytes, an effect that is blocked by the Na+-H+ exchange inhibitor 
      amiloride. In an epithelial cell line derived from newborn piglet jejunum 
      (IPEC-J2 cells), we determined intracellular pH (pHi) by computer-assisted 
      microfluorimetry in single cells loaded with pH-sensitive dye 
      2',7'-bis(2-carboxyethyl)5-(6)- carboxyfluorescein. Resting pHi in 
      N-2-hydroxyethylpiperazine-N'-2- ethanesulfonic acid-buffered NaCl Ringer was 
      7.06 +/- 0.02. Removal of external Na+ caused reversible acidification; recovery 
      of pHi from NH+4-induced acid load was Na+ dependent, amiloride inhibitable, and 
      Cl-independent. Asn and Gln had no measurable effect on resting pHi, but 
      pretreatment with Asn or Gln induced a consistent twofold increase in pHi 
      recovery from an acid challenge that was not seen with L-proline, D-glutamine, or 
      L-phenylalanine. Inhibition of Gln metabolism by aminooxyacetate abolished the 
      stimulatory effect of Gln on the exchanger. The tumor promotor phorbol 
      12-myristate 13-acetate (PMA) stimulated recovery rate from acid load and also 
      increased resting pHi. The effects of PMA and Gln on Na+-H+ exchange from acid 
      load were additive. Stimulation of Na+-H+ exchange by PMA, but not by Gln, was 
      inhibited by protein kinase C (PKC) inhibitor 
      1-(5-isoquinolinylsulfonyl)-2-methylpeperazine. We conclude that Gln metabolism 
      stimulates Na+-H+ exchange of acid-loaded porcine enterocytes by a mechanism not 
      requiring activation of PKC.
FAU - Rhoads, J M
AU  - Rhoads JM
AD  - Department of Pediatrics, North Carolina State University School of Veterinary 
      Medicine, Chapel Hill 27599.
FAU - Chen, W
AU  - Chen W
FAU - Chu, P
AU  - Chu P
FAU - Berschneider, H M
AU  - Berschneider HM
FAU - Argenzio, R A
AU  - Argenzio RA
FAU - Paradiso, A M
AU  - Paradiso AM
LA  - eng
GR  - KO8-HD-00945/HD/NICHD NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Am J Physiol
JT  - The American journal of physiology
JID - 0370511
RN  - 0 (Fluoresceins)
RN  - 0 (Fluorescent Dyes)
RN  - 0 (Isoquinolines)
RN  - 0 (Piperazines)
RN  - 0 (Sodium-Hydrogen Exchangers)
RN  - 01Q9PC255D (Ammonium Chloride)
RN  - 0RH81L854J (Glutamine)
RN  - 117464-70-7 (2',7'-bis-(2-carboxyethyl)-5(6)-carboxyfluorescein acetoxymethyl 
      ester)
RN  - 3OWL53L36A (Mannitol)
RN  - 6HG8UB2MUY (Meglumine)
RN  - 7006-34-0 (Asparagine)
RN  - 7DZO8EB0Z3 (Amiloride)
RN  - 84477-87-2 (1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine)
RN  - 9NEZ333N27 (Sodium)
RN  - EC 2.7.11.13 (Protein Kinase C)
RN  - NI40JAQ945 (Tetradecanoylphorbol Acetate)
SB  - IM
MH  - 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine
MH  - Acid-Base Equilibrium/drug effects/physiology
MH  - Amiloride/pharmacology
MH  - Ammonium Chloride/pharmacology
MH  - Animals
MH  - Asparagine/*pharmacology
MH  - Cell Line
MH  - Epithelium/drug effects/metabolism
MH  - Fluoresceins
MH  - Fluorescent Dyes
MH  - Glutamine/*pharmacology
MH  - *Hydrogen-Ion Concentration
MH  - Isoquinolines/pharmacology
MH  - Jejunum/drug effects/*metabolism
MH  - Kinetics
MH  - Mannitol/pharmacology
MH  - Meglumine/pharmacology
MH  - Piperazines/pharmacology
MH  - Protein Kinase C/antagonists & inhibitors
MH  - Sodium/*metabolism
MH  - Sodium-Hydrogen Exchangers/drug effects/*metabolism
MH  - Swine
MH  - Tetradecanoylphorbol Acetate/pharmacology
MH  - Time Factors
EDAT- 1994/05/01 00:00
MHDA- 1994/05/01 00:01
CRDT- 1994/05/01 00:00
PHST- 1994/05/01 00:00 [pubmed]
PHST- 1994/05/01 00:01 [medline]
PHST- 1994/05/01 00:00 [entrez]
AID - 10.1152/ajpgi.1994.266.5.G828 [doi]
PST - ppublish
SO  - Am J Physiol. 1994 May;266(5 Pt 1):G828-38. doi: 10.1152/ajpgi.1994.266.5.G828.