Postoperative alterations in interorgan glutamine exchange in enterectomized dogs

Wiley W. Souba, Patrick Roughneen, Diane L. Goldwater, Julian C. Williams, Brian J. Rowlands

Research output: Contribution to journalArticle

37 Citations (Scopus)

Abstract

The effect of enterectomy on postoperative visceral organ glutamine exchange was studied in order to gain further understanding of the role of the intestinal tract in the altered glutamine metabolism that occurs following catabolic illness. In addition to studying glutamine, which transports 1 3 of whole blood amino acid nitrogen, we determined the fluxes of glutamate and alanine across the gastrointestinal tract, liver, and kidneys in 18 postoperative dogs. Arterial glutamine and glutamate were significantly higher in enterectomized animals than in controls. With enterectomy the gut became an organ of glutamine balance while in control dogs the GI tract consumed glutamine (0.11 ± 0.04 vs 1.67 ± 0.14 μmole/kg · min, P <0.001). The gut switched from an organ of glutamate release to one of net glutamate uptake following enterectomy and intestinal alanine release simultaneously fell by 50%. Simultaneously, the liver reduced its uptake of alanine and became an organ of glutamine release. Renal glutamine consumption was also diminished in enterectomy animals. The interorgan exchange of glutamine and other amino acids is altered by enterectomy. The increase in circulating glutamine levels in enterectomized animals suggests that the accelerated intestinal glutamine consumption that characterizes catabolic illnesses contributes to the low glutamine levels in these stress states. In addition, it becomes apparent that the gut is an important supplier of alanine to the liver, which supports gluconeogenesis. Metabolic adaptation and cooperation between organs is essential during organ absence or dysfunction if the organism is to survive critical illness.

Original languageEnglish (US)
Pages (from-to)117-125
Number of pages9
JournalJournal of Surgical Research
Volume42
Issue number2
DOIs
StatePublished - 1987
Externally publishedYes

Fingerprint

Glutamine
Dogs
Alanine
Glutamic Acid
Gastrointestinal Tract
Liver
Kidney
Amino Acids
Gluconeogenesis
Critical Illness
Nitrogen

ASJC Scopus subject areas

  • Surgery

Cite this

Postoperative alterations in interorgan glutamine exchange in enterectomized dogs. / Souba, Wiley W.; Roughneen, Patrick; Goldwater, Diane L.; Williams, Julian C.; Rowlands, Brian J.

In: Journal of Surgical Research, Vol. 42, No. 2, 1987, p. 117-125.

Research output: Contribution to journalArticle

Souba, Wiley W. ; Roughneen, Patrick ; Goldwater, Diane L. ; Williams, Julian C. ; Rowlands, Brian J. / Postoperative alterations in interorgan glutamine exchange in enterectomized dogs. In: Journal of Surgical Research. 1987 ; Vol. 42, No. 2. pp. 117-125.
@article{fff6d1f5a4224afb8cdbc3e10d7e3c15,
title = "Postoperative alterations in interorgan glutamine exchange in enterectomized dogs",
abstract = "The effect of enterectomy on postoperative visceral organ glutamine exchange was studied in order to gain further understanding of the role of the intestinal tract in the altered glutamine metabolism that occurs following catabolic illness. In addition to studying glutamine, which transports 1 3 of whole blood amino acid nitrogen, we determined the fluxes of glutamate and alanine across the gastrointestinal tract, liver, and kidneys in 18 postoperative dogs. Arterial glutamine and glutamate were significantly higher in enterectomized animals than in controls. With enterectomy the gut became an organ of glutamine balance while in control dogs the GI tract consumed glutamine (0.11 ± 0.04 vs 1.67 ± 0.14 μmole/kg · min, P <0.001). The gut switched from an organ of glutamate release to one of net glutamate uptake following enterectomy and intestinal alanine release simultaneously fell by 50{\%}. Simultaneously, the liver reduced its uptake of alanine and became an organ of glutamine release. Renal glutamine consumption was also diminished in enterectomy animals. The interorgan exchange of glutamine and other amino acids is altered by enterectomy. The increase in circulating glutamine levels in enterectomized animals suggests that the accelerated intestinal glutamine consumption that characterizes catabolic illnesses contributes to the low glutamine levels in these stress states. In addition, it becomes apparent that the gut is an important supplier of alanine to the liver, which supports gluconeogenesis. Metabolic adaptation and cooperation between organs is essential during organ absence or dysfunction if the organism is to survive critical illness.",
author = "Souba, {Wiley W.} and Patrick Roughneen and Goldwater, {Diane L.} and Williams, {Julian C.} and Rowlands, {Brian J.}",
year = "1987",
doi = "10.1016/0022-4804(87)90108-9",
language = "English (US)",
volume = "42",
pages = "117--125",
journal = "Journal of Surgical Research",
issn = "0022-4804",
publisher = "Academic Press Inc.",
number = "2",

}

TY - JOUR

T1 - Postoperative alterations in interorgan glutamine exchange in enterectomized dogs

AU - Souba, Wiley W.

AU - Roughneen, Patrick

AU - Goldwater, Diane L.

AU - Williams, Julian C.

AU - Rowlands, Brian J.

PY - 1987

Y1 - 1987

N2 - The effect of enterectomy on postoperative visceral organ glutamine exchange was studied in order to gain further understanding of the role of the intestinal tract in the altered glutamine metabolism that occurs following catabolic illness. In addition to studying glutamine, which transports 1 3 of whole blood amino acid nitrogen, we determined the fluxes of glutamate and alanine across the gastrointestinal tract, liver, and kidneys in 18 postoperative dogs. Arterial glutamine and glutamate were significantly higher in enterectomized animals than in controls. With enterectomy the gut became an organ of glutamine balance while in control dogs the GI tract consumed glutamine (0.11 ± 0.04 vs 1.67 ± 0.14 μmole/kg · min, P <0.001). The gut switched from an organ of glutamate release to one of net glutamate uptake following enterectomy and intestinal alanine release simultaneously fell by 50%. Simultaneously, the liver reduced its uptake of alanine and became an organ of glutamine release. Renal glutamine consumption was also diminished in enterectomy animals. The interorgan exchange of glutamine and other amino acids is altered by enterectomy. The increase in circulating glutamine levels in enterectomized animals suggests that the accelerated intestinal glutamine consumption that characterizes catabolic illnesses contributes to the low glutamine levels in these stress states. In addition, it becomes apparent that the gut is an important supplier of alanine to the liver, which supports gluconeogenesis. Metabolic adaptation and cooperation between organs is essential during organ absence or dysfunction if the organism is to survive critical illness.

AB - The effect of enterectomy on postoperative visceral organ glutamine exchange was studied in order to gain further understanding of the role of the intestinal tract in the altered glutamine metabolism that occurs following catabolic illness. In addition to studying glutamine, which transports 1 3 of whole blood amino acid nitrogen, we determined the fluxes of glutamate and alanine across the gastrointestinal tract, liver, and kidneys in 18 postoperative dogs. Arterial glutamine and glutamate were significantly higher in enterectomized animals than in controls. With enterectomy the gut became an organ of glutamine balance while in control dogs the GI tract consumed glutamine (0.11 ± 0.04 vs 1.67 ± 0.14 μmole/kg · min, P <0.001). The gut switched from an organ of glutamate release to one of net glutamate uptake following enterectomy and intestinal alanine release simultaneously fell by 50%. Simultaneously, the liver reduced its uptake of alanine and became an organ of glutamine release. Renal glutamine consumption was also diminished in enterectomy animals. The interorgan exchange of glutamine and other amino acids is altered by enterectomy. The increase in circulating glutamine levels in enterectomized animals suggests that the accelerated intestinal glutamine consumption that characterizes catabolic illnesses contributes to the low glutamine levels in these stress states. In addition, it becomes apparent that the gut is an important supplier of alanine to the liver, which supports gluconeogenesis. Metabolic adaptation and cooperation between organs is essential during organ absence or dysfunction if the organism is to survive critical illness.

UR - http://www.scopus.com/inward/record.url?scp=0023094225&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0023094225&partnerID=8YFLogxK

U2 - 10.1016/0022-4804(87)90108-9

DO - 10.1016/0022-4804(87)90108-9

M3 - Article

VL - 42

SP - 117

EP - 125

JO - Journal of Surgical Research

JF - Journal of Surgical Research

SN - 0022-4804

IS - 2

ER -