PMID- 19637336
OWN - NLM
STAT- MEDLINE
DCOM- 20100302
LR  - 20220408
IS  - 1536-4844 (Electronic)
IS  - 1078-0998 (Print)
IS  - 1078-0998 (Linking)
VI  - 16
IP  - 1
DP  - 2010 Jan
TI  - Increased serum levels of L-arginine in ulcerative colitis and correlation with 
      disease severity.
PG  - 105-11
LID - 10.1002/ibd.21035 [doi]
AB  - BACKGROUND: L-arginine (L-Arg) is a semi-essential amino acid that is the 
      substrate for both nitric oxide and polyamine synthesis. Cellular uptake of L-Arg 
      is an active transport process that is subject to competitive inhibition by 
      L-ornithine (L-Orn) and L-lysine (L-Lys). We investigated L-Arg utilization in 
      patients with ulcerative colitis (UC). METHODS: Serum was collected from 14 
      normal controls and 22 UC patients with pancolitis of moderate or severe activity 
      by histopathology score. The Mayo Disease Activity Index (DAI) and endoscopy 
      subscore were assessed. Serum amino acid levels were measured by high-performance 
      liquid chromatography. Arginine availability index (AAI) was defined as 
      [L-Arg]/([L-Orn] + [L-Lys]). RESULTS: Serum L-Arg levels were significantly 
      associated with histopathologic grade (P = 0.001). L-Arg levels were increased in 
      subjects with severe colitis when compared to those with moderate colitis or 
      normal mucosa. L-Orn + L-Lys levels were also increased in severe colitis, so 
      that AAI was not significantly increased. L-Arg levels were also strongly 
      associated with the endoscopy subscore (P < 0.001). There was a strong 
      correlation between DAI and L-Arg levels (r = 0.656, P < 0.001). CONCLUSIONS: 
      Serum L-Arg levels correlate with UC disease severity but availability is not 
      increased due to competitive inhibition by L-Orn and L-Lys. Our findings suggest 
      that L-Arg uptake by cells in the inflamed colon is defective, which may 
      contribute to the pathogenesis of UC. Studies delineating the mechanism of uptake 
      inhibition could enhance our understanding of UC or lead to novel treatment 
      options.
FAU - Hong, Shih-Kuang S
AU  - Hong SK
AD  - Department of Medicine, Division of Gastroenterology, Hepatology, and Nutrition, 
      Vanderbilt University Medical Center, Nashville, Tennessee 37232-0252, USA.
FAU - Maltz, Brad E
AU  - Maltz BE
FAU - Coburn, Lori A
AU  - Coburn LA
FAU - Slaughter, James C
AU  - Slaughter JC
FAU - Chaturvedi, Rupesh
AU  - Chaturvedi R
FAU - Schwartz, David A
AU  - Schwartz DA
FAU - Wilson, Keith T
AU  - Wilson KT
LA  - eng
GR  - T32 DK007673/DK/NIDDK NIH HHS/United States
GR  - R01 AT004821/AT/NCCIH NIH HHS/United States
GR  - P30 DK058404/DK/NIDDK NIH HHS/United States
GR  - 5T32 DK007673/DK/NIDDK NIH HHS/United States
GR  - UL1 RR024975/RR/NCRR NIH HHS/United States
GR  - R01 AT004821-01/AT/NCCIH NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Inflamm Bowel Dis
JT  - Inflammatory bowel diseases
JID - 9508162
RN  - 0 (Biomarkers)
RN  - 94ZLA3W45F (Arginine)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Aged
MH  - Arginine/*blood
MH  - Biomarkers/*blood
MH  - Case-Control Studies
MH  - Chromatography, High Pressure Liquid
MH  - Colitis, Ulcerative/*blood/*diagnosis
MH  - Colon/*pathology
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Prospective Studies
MH  - Young Adult
PMC - PMC2795785
MID - NIHMS143535
EDAT- 2009/07/29 09:00
MHDA- 2010/03/03 06:00
PMCR- 2011/01/01
CRDT- 2009/07/29 09:00
PHST- 2009/07/29 09:00 [entrez]
PHST- 2009/07/29 09:00 [pubmed]
PHST- 2010/03/03 06:00 [medline]
PHST- 2011/01/01 00:00 [pmc-release]
AID - 10.1002/ibd.21035 [doi]
PST - ppublish
SO  - Inflamm Bowel Dis. 2010 Jan;16(1):105-11. doi: 10.1002/ibd.21035.