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Biomedical subjects

S E Kong

Publications and source records attributed to S E Kong.

15 recordsLinked to original sources
PubMed2001

Pretreatment with glycine reduces the severity of warm intestinal ischemic-reperfusion injury in the rat.

Free jejunal flaps may experience adverse effects immediately after revascularization because of ischemic-reperfusion injury. In this study the authors evaluated the ability of glycine to protect the small intestine against the effects of a warm ischemic-reperfusion injury. Male Wistar rats (N = 30) were randomized to either a baseline group (no intervention), a control group (local arterial infusion with normal saline), or a glycine group (local arterial infusion with 20% glycine). Pretreatment with 20% glycine increased significantly (p < 0.05) mucosal protein and deoxyribonucleic acid content, reduced intestinal myeloperoxidase activity, and maintained mucosal glutaminase activity. These results indicate that some of the indicators of ischemic-reperfusion injury are improved by pretreatment with a 20% glycine solution.

Animals↗
PubMed2000

Glutamine-enriched parenteral nutrition regulates the activity and expression of intestinal glutaminase.

The aim of this study was to examine the effect of glutamine-enriched parenteral nutrition on the activity, expression and distribution of glutaminase mRNA within the small intestine of rats. Central venous lines were inserted into 30 male Wistar rats before they were fed for 6 days with either: (a) conventional parenteral nutrition, (b) 2.5% glutamine-enriched parenteral nutrition, or (c) rat food ad libitum. Jejunal glutaminase activity per milligram of dry matter was greatest in the animals fed rat food (0.94+/-0.29), intermediate in the glutamine supplemented rats (0.69+/-0.19) and least in the rats nourished with conventional parenteral nutrition (0.55+/-0.24) (P<0.05). The data for glutaminase expression exhibited a similar trend (P<0.05). In situ hybridisation analysis confirmed that glutaminase is expressed in the mucosa along the whole length of the small intestine. It was concluded that provision of glutamine alters the activity and expression of glutaminase in intestinal enterocytes. The results suggest that glutamine increases glutaminase activity by promoting the accumulation of intestinal glutaminase mRNA.

Animals↗
PubMed2000

Branched-chain amino acids.

The branched-chain amino acids (BCAA), isoleucine, leucine and valine, are unique in that they are principally metabolized extrahepatically in the skeletal muscle. This observation led to the investigation of these nutrients in a number of clinical scenarios. By far the most intensively studied applications for BCAA have been in patients with liver failure and/or patients in catabolic disease states. However, the resulting studies have not demonstrated a clear clinical benefit for BCAA nutritional supplements. In patients with liver failure, the BCAA did improve nitrogen retention and protein synthesis, but their effect on patient outcome was less clear. Similarly, in critically ill septic patients, BCAA did not improve either survival or morbidity. The BCAA are important nutrients, and it seems that any specific benefits associated with their use will be based upon a greater understanding of the underlying cellular biology. Potential areas of further research may include the combination of BCAA supplements with other anabolic factors (e.g. growth hormone) in managing patients with catabolic disease states.

Amino Acids, Branched-Chain↗
PubMed1998

Quantitation of glutaminase mRNA in enterocytes using competitive RT-PCR.

The concentration of mRNA within the intestinal mucosa is usually measured by either Northern blot analysis or semi-quantitative reverse transcription polymerase chain reaction (RT-PCR). However, these methods are limited by a lack of valid internal controls, low sensitivity, and large differences in the concentration of the internal control and target gene. The authors present an alternative method using competitive RT-PCR to measure glutaminase mRNA in isolated enterocytes.

Animals↗
PubMed1998

The role of enterocytes in gut dysfunction.

Stem cells in the intestinal epithelium give rise to enterocytes, goblet cells, enteroendocrine cells, and Paneth cells. Each of these cell lines plays a role in cytoprotection of the intestinal mucosa. In particular, it has been demonstrated that mature enterocytes can act as antigen presenting cells. Parenteral and enteral nutrition are used to nourish critically ill patients. However, these regimens are unfortunately associated with gut atrophy. Glutamine, the preferred intestinal nutrient, reverses this gut atrophy and plays a key role in maintaining the barrier function of the gut. Specific nutrients (putrescine, spermidine, spermine) have been used to modulate intestinal adaption. In addition, ornithine has been shown to act as a regulator of intestinal adaption. In this review, we discuss the relationship between the biology of enterocytes and failure of the gut barrier.

Animals↗
PubMed1998

Influence of ischaemia-reperfusion injury on CD44 expression in rat small intestine.

BACKGROUND: CD44 is an adhesion molecule expressed by neutrophils and lymphocytes which is involved in cell-cell and cell-matrix binding. In this study, the effect of ischaemia-reperfusion injury on CD44 messenger RNA (mRNA) and cell surface immunohistochemical expression of CD44 in the rat small intestine was evaluated. METHODS: Wistar rats (n=16) were randomized to either serve as controls (sham surgery) or to be subjected to a standardized ischaemia-reperfusion injury (suprarenal aorta occluded for 1 h followed by 1 h of reperfusion). Standardized segments of jejunum were harvested after ischaemia-reperfusion injury (ischaemic and reperfused samples) to measure the mucosal protein and DNA content, mRNA expression of CD44 and the immunohistochemical expression of CD44. RESULTS: Reperfusion significantly damaged the jejunal mucosa, e.g. mucosal protein content was lower after reperfusion compared with that in the control group (z=-2.31, P=0.02) and the ischaemic samples (z=-2.52, P=001). The expression of cell surface CD44 protein was also significantly decreased after ischaemic injury (z=-1.99, P=0.04); this coincided with a decrease in the amount of cytoplasmic CD44 mRNA within isolated enterocytes (z=-2.31, P=0.02). CONCLUSION: Ischaemia-reperfusion injury decreases the expression of CD44 within the jejunal mucosa. This may contribute to the failure of the gut barrier after such injury.

Animals↗
PubMed1998

The influence of ischemia/reperfusion injury on the jejunum.

Ischemia/reperfusion injury (IRI) after free tissue transfer of the small intestine results in transmural tissue damage. This study examined the effects of IRI on the jejunum. Wistar rats served either as controls (N=10) or underwent clamping of the infrarenal aorta for 1 hour followed by 1 hour of reperfusion (N=10). Both ischemia and reperfusion reduced the protein and deoxyribonucleic acid content of the jejunal mucosa (p < 0.05). Myeloperoxidase activity in the jejunal mucosa remained relatively low. The expression of leukocyte function-associated antigen 1 and intercellular adhesion molecule 1 (ICAM-1) on the surface of mucosal cells was not altered significantly by the ischemic insult, but was reduced after the period of reperfusion (p < 0.05). This coincided with an increase in messenger ribonucleic acid (mRNA) for ICAM-1 within isolated mucosal cells (p < 0.05). The specific activity of glutaminase in isolated jejunal mucosal cells was diminished after ischemia and reperfusion (p < 0.05), and this was not associated with an appreciable change in glutaminase mRNA expression. These results have identified some molecular mechanisms underlying IRI of the small intestine that are possible candidates for therapeutic intervention.

Animals↗
PubMed1998

The effect of minimum luminal nutrition on mucosal cellularity and immunity of the gut.

Many catabolic patients can only consume small volumes of enteral nutrients. The aim of this study was to evaluate markers of cellularity and immunity in the small intestine of rats randomized to receive 6 days of parenteral nutrition, 25% enteral and 75% parenteral nutrition (i.e. minimum luminal nutrition) or enteral nutrition. The same glutamine-enriched solution was used for both parenteral and enteral nutrition. Enteral nutrition was associated with the least amount of jejunal atrophy (P<0.01), with the results from the minimum luminal nutrition group approximating those of the parenteral nutrition group. Parenteral nutrition was associated with the greatest number of CD2+ cells (P< 0.05) and the lowest CD4/CD8 cell ratio (P< 0.01) in the jejunal mucosa. In essence, we failed to demonstrate that there are any appreciable benefits associated with the enteral consumption of 25% of a nutrient load.

Animals↗
PubMed1998

Ischaemia-reperfusion injury to the intestine.

Ischaemia-reperfusion injury (IRI) is of obvious relevance in situations where there is an interruption of blood supply to the gut, as in vascular surgery, or in the construction of free intestinal grafts. It is now appreciated that IRI also underlies the guy dysfunction that occurs in early shock, sepsis, and trauma. The events that occur during IRI are complex. However, recent advances in cellular biology have started to unravel these underlying processes. The aim of this review is to provide an outline of current knowledge on the mechanisms and consequences of IRI. Initially, IRI appears to be mediated by reactive oxygen metabolites and, at a later stage, by the priming and activation of polymorphonuclear neutrophils (PMN). Ischaemia-reperfusion injury can diminish the barrier function of the gut, and can promote an increase in the leakage of molecules (intestinal permeability) or the passage of microbes across the wall of the bowel (bacterial translocation). Ischaemia-reperfusion injury to the gut can result in the generation of molecules that may also harm distant tissues.

Bacterial Translocation↗
PubMed1997

Method for measuring a comprehensive energy budget in a proliferating cell system over multiple cell cycles.

Isolated cell systems are now being used very effectively to study a range of important biochemical questions, but their energy metabolism has never been comprehensively investigated. We have developed a system, using J2E cells, which enables us to measure total ATP turnover and the contribution of various fuels and pathways to this total in a dynamic, proliferating preparation. Cells are cultured in 500 ml airtight glass containers which enables (1) the measurement of oxygen consumption, (2) the collection and measurement of 14CO2 production from labelled fuels, and (3) the measurement of metabolite utilization and production. Data on cell numbers are then used to produce a curve of cell number vs. time, the area under which (cell numbers x hour) is used as a base by which all measurements and experiments are compared. To our knowledge this is the first time a comprehensive energy budget has been measured in a proliferating cell system over a period that covers multiple cell cycles.

Adenosine Triphosphate↗
PubMed1993

Induction of manganese-containing superoxide dismutase in anaerobic Escherichia coli by diamide and 1,10-phenanthroline: sites of transcriptional regulation.

Transcriptional regulation of the sodA gene, a member of the soxRS regulon encoding the manganese-containing superoxide dismutase (MnSOD; superoxide:superoxide oxidoreductase, EC 1.15.1.1) of Escherichia coli, was examined in a variety of regulatory mutants. Diamide, an oxidant that causes the anaerobic biosynthesis of the MnSOD polypeptide and also facilitates insertion of manganese at the active site, was found to anaerobically induce MnSOD in both soxRS and fur arcA fnr strains. Metal chelating agents also caused anaerobic induction of MnSOD in a fur arcA fnr triple mutant; however, this induction of MnSOD and of glucose-6-phosphate dehydrogenase (G6PD) by 1,10-phenanthroline was dependent on an intact soxRS locus. A strain of E. coli bearing a fusion of the soxS promoter to lacZ was used to demonstrate that both diamide and 1,10-phenanthroline caused anaerobic activation of soxS transcription. These results indicate that (i) both diamide and 1,10-phenanthroline induce the soxRS regulon anaerobically by stimulation of soxS transcription; (ii) diamide, but not metal chelators, also induces MnSOD biosynthesis by a soxRS-independent mechanism, perhaps mediated by effects on fur, arcA, or fnr-mediated repression of sodA; and (iii) the soxRS locus contains a metal-binding component and is responsive to the redox status of the cell.

Diamide↗
PubMedDate not supplied

Starvation alters the activity and mRNA level of glutaminase and glutamine synthetase in the rat intestine.

The metabolism of glutamine, the main respiratory fuel of enterocytes, is governed by the activity of glutaminase and glutamine synthetase. Because starvation induces intestinal atrophy, it might alter the rate of intestinal glutamine utilization. This study examined the effect of starvation on the activity, level of mRNA, and distribution of mRNA of glutaminase and glutamine synthetase in the rat intestine. Rats were randomized into groups and were either: (1) fed for 2 days with rat food ad libitum or (2) starved for 2 days. Standardized segments of jejunum and ileum were removed for the estimation of enzyme activity, level of mRNA, and in situ hybridization analysis. The jejunum of the fed rats had a greater activity of both enzymes per centimeter of intestine (P < 0.01), a greater glutaminase specific activity (1.97 +/- 0.45 vs. 1.09 +/- 0.34 micromol/hr/mg protein, P < 0.01), and a lower level of glutaminase and glutamine synthetase mRNA. The ileum of the fed rats had a greater activity of glutamine synthetase per centimeter of intestine (162.9 +/- 50.6 vs. 91.0 +/- 23.1 nmol/hr/cm bowel, P < 0.01), a lower level of glutaminase mRNA, and a greater level of glutamine synthetase mRNA. In situ hybridization analysis showed that starvation does not alter the distribution of glutaminase and glutamine synthetase mRNA in the intestinal mucosa. This study confirms that starvation decreases the total intestinal activity per centimeter of both glutaminase and glutamine synthetase. More importantly, the results indicate that the intestine adapts to starvation by accumulating glutaminase mRNA. This process prepares the intestine for a restoration of intake.

Journal Article↗
PubMedDate not supplied

The role of glutaminase in the small intestine.

Glutaminase is the enzyme which hydrolyses glutamine, the main respiratory fuel of the intestine, to yield glutamate and ammonia. Glutaminase has a central role in intestinal metabolism: the products of the reaction catalyzed by glutaminase can be transaminated, catabolized to yield energy or used for the biosynthesis of pyrimidine nucleotides. Experimental treatments which deprive the intestine of glutamine induce intestinal atrophy. In this review, attention is paid to the role of glutaminase in intestinal metabolism. Background information on the structure, kinetics and distribution of glutaminase precede a discussion of the metabolism of glutamine within the intestine. In closing, we review the factors known to regulate glutaminase activity and emphasise that the regulation of glutaminase within the intestine is poorly understood.

Caco-2 Cells↗
PubMedDate not supplied

Glutamine and nucleotide metabolism within enterocytes.

Glutamine has an important role as a source of energy for enterocytes. However, it may also have a key role as a source of nitrogen for the synthesis of nucleotides. The relative contribution of de novo synthesis and salvage pathways seems to be affected by the position of enterocytes within the crypt-villus axis as well as the dietary intake of nucleic acids and glutamine. Nucleotides are especially important to enterocytes during intestinal development, maturation, and repair. Hence an understanding of nucleotide metabolism within enterocytes has important implications regarding both the composition and route of administration of nutrient solutions. Many important questions remain unanswered, in particular: Does glutamine stimulate intestinal de novo pyrimidine synthesis via the action of carbamoyl phosphate synthetase I? Can de novo purine synthesis maintain intestinal purine pools in the absence of dietary nucleic acids? And, what are the specific effects of parenterally administered nucleotides on the metabolism and well-being of enterocytes? A greater understanding of these issues will lead to a more rational approach toward the nutritional modulation of gut dysfunction.

Glutamine↗