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Cunniffe, B, Papageorgiou, M, O'Brien, B, Davies, NA, Grimble, GK, and Cardinale, M. Acute citrulline-malate supplementation and high-intensity cycling performance. J Strength Cond Res 30(9): 2638-2647, 2016-Dietary L-citrulline-malate (CM) consumption has been suggested to improve skeletal muscle metabolism and contractile efficiency, which would be expected to predispose exercising individuals to greater fatigue resistance. The purpose of this study was to examine the effects of CM supplementation on acid-base balance and high-intensity exercise performance. In a double-blind, placebo-controlled, crossover study, 10 well-trained males consumed either 12 g of CM (in 400 ml) or lemon sugar-free cordial (placebo [PL]) 60 minutes before completion of 2 exercise trials. Each trial consisted of subjects performing 10 (×15 seconds) maximal cycle sprints (with 30-second rest intervals) followed by 5 minutes recovery before completing a cycle time-to-exhaustion test (TTE) at 100% of individual peak power (PP). Significant increases in plasma concentrations of citrulline (8.8-fold), ornithine (3.9-fold), and glutamine (1.3-fold) were observed 60 minutes after supplementation in the CM trial only (p ≤ 0.05) and none of the subjects experienced gastrointestinal side-effects during testing. Significantly higher exercise heart rates were observed in CM condition (vs. PL) although no between trial differences in performance related variables (TTE: [120 ± 61 seconds CM vs. 113 ± 50 seconds PL]), PP or mean power, ([power fatigue index: 36 ± 16% CM vs. 28 ± 18% PL]), subjective rating of perceived exertion or measures of acid-base balance (pH, lactate, bicarbonate, base-excess) were observed (p > 0.05). This study demonstrated that acute supplementation of 12 g CM does not provide acute ergogenic benefits using the protocol implemented in this study in well-trained males.

Intestinal failure (IF) is a well identified clinical condition, which is characterised by the reduction of functional gut capacity below the minimum needed for adequate digestion and absorption of nutrients for normal growth in children. Short bowel syndrome (SBS) is the leading cause of IF in neonates, infants and young children usually as a result of extensive intestinal resection during the neonatal period. Simultaneously maintaining optimal nutritional status and achieving intestinal adaptation is a clinical challenge in short bowel patients. Both growth and development of the child as well as gut adaptation should be considered synergistically as primary outcome parameters. Enteral nutrition (EN) can be introduced orally and/or by tube feeding (TF). Several controversies over nutritional treatment of children with SBS related intestinal failure remain. As reported from different centres around the world, most practices are more "experienced based" rather than "evidence based". This is partly due to the small number of patients with this condition. This review (based on a consensus) discusses the physiological principles and nutritional management, including the type of diet and route of delivery. Perspectives in optimizing intestinal adaptation and reducing the consequences of small intestinal bacterial overgrowth are also discussed.

Batch syntheses of isomaltooligosaccharides (IMO) from sucrose, using the enzymes dextransucrase and dextranase were performed with the aim of understanding the reaction mechanism and the parameters which affect product characteristics and molecular size. Both activities described for dextransucrase (dextran formation and acceptor reaction) achieved synthesis whilst the hydrolytic activity of dextranase regulated the product molecular size and acceptor availability. Depending on the reaction conditions, the product oligosaccharide mixtures contained mainly sugars (up to 36%) with degrees of polymerization (DP) varying between 10 and 60 together with lower concentrations of both lower and higher molecular weight sugars. Alterations in substrate and dextranase concentrations (50-400 mg ml(-1) and 2.5-46 U ml(-1), respectively) affected the molecular weight of IMO, the reaction rate and the formation of leucrose. This permitted manipulation of the product characteristics. It was found that higher substrate and dextranase concentrations gave rise to products with lower molecular sizes and a dextransucrase:dextranase ratio of 1: 1 or 1:2 appeared to produce a polymer with a molecular weight which is desirable for prebiotic use. (C) 2004 Elsevier Inc. All rights reserved.

OBJECTIVE: To determine whether critically ill children are hypermetabolic and to calculate whether predictive equations are appropriate for critically ill children. DESIGN: Prospective, clinical study. SETTING: Pediatric intensive care unit. PATIENTS: A total of 57 children (39 boys) aged 9 months to 15.8 yrs. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: The median resting energy expenditure measurement measured by indirect calorimetry was 37.2 (range, 11.9-66.6) kcal x kg(-1) x day(-1). This was significantly lower than would be predicted using either the Schofield (42.7 [26.9-65.4] kcal x kg(-1) x day(-1)) or Fleisch equations (42.8 [20.9-66.2] kcalx kg(-1)-1 x day(-1), p < .001) but significantly higher than the White equation developed specifically for pediatric intensive care units (26.2 [8.5-70.1] kcal x kg(-1),day(-1), p < .0001). Methods comparison analysis showed the limits of agreement were -484 to 300, -461 to 319, and -3.2 to 854 kcal/day, respectively. Multivariate analysis indicated the following factors contribute to hypometabolism and hypermetabolism: age (p = .006), sex (p = .034), time spent in the pediatric intensive care unit (p = .001), diagnosis (p = .015), weight (p = .009), temperature (p = .04), continuous infusion for sedation (p = .04), and neuromuscular blockade (p = .03). CONCLUSION: Children do not become hypermetabolic during critical illness. These data suggest that agreement between resting energy expenditure and the predictive equations are so broad that they are inappropriate for use in critically ill children.

The success of nasoenteral nutrition support can be limited by intestinal impairment. In particular, reduced absorptive area, mucosal atrophy and abnormal motility may reduce absorption of macronutrients and micronutrients, and diarrhoea remains a commonly encountered complication. We review how basic physiological techniques can be used to investigate such pathophysiology. Lumenal nutrients control mucosal growth, expression of mucosal transporters and regional gut motility. Cell biology techniques now complement classical intestinal perfusion methods in determining the 'safety factor' of excess absorptive capacity. The controversial role of the sodium-glucose linked transporter in dietary glucose assimilation is described in terms of its control, its true function and its role in uptake of other solutes. Techniques that involve brush-border membrane vesicles, Caco-2 cells, mucosal immunohistochemistry and gene expression probes are described. Together, these techniques describe a picture of an organ with remarkable ability to maintain digestive and absorptive function in response to a wide variety of nutritional intakes, often in the face of inflammatory illness.

Dietary nucleotides, like glutamine, have attracted attention as a key ingredient missing from nutritional formulae for many years. They are the building blocks of tissue RNA and DNA and of ATP and their presence in breast milk has stimulated research in babies which has indicated that supplementation of infant formula milk leads to improved growth and reduced susceptibility to infection. Animal studies have confirmed some of these data. In particular, dietary nucleotides modulate immune function, promote faster intestinal healing and have trophic effects on the intestine of parenterally-fed rats which are similar to those resulting from glutamine supplementation, but at much lower intakes. Nucleotide supplementation has also been shown to improve some aspects of tissue recovery from ischaemia/reperfusion injury or radical resection. There is, however, a fundamental paradox. The intestine and liver possess powerful homeostatic mechanisms which degrade intake of purines and pyrimidines (i.e. salvage) and replace it with de novo synthesised output. It is possible that peripheral tissues receive only small amounts of nucleotides of dietary origin. Previously, nucleotides have been proposed as being conditionally-essential nutrients that provide an adequate supply of purines and pyrimidines for nucleic acid synthesis in neonates or in the stressed patient. This review explores this puzzle in the light of recent data from nutritional studies and from research into purinergic signalling in the intestine, heart and cells of the immune system. We propose that dietary nucleotides should be considered within a pharmacological and metabolic framework.

Measuring RNA turnover is important because of the significance of rRNA, tRNA and mRNA in tissue protein synthesis. Changes in turnover of each of these species precede important cellular events such as hormone or cytokine action or cell-division itself. Isotopic methods have relied on decay of pulse-labelled RNA or on incorporation of isotopically-labelled precursors. However, recycling of labels may lead to under or overestimation of synthesis rates respectively. The labelling of the intracellular precursor pool must be known if accurate RNA synthesis rates are to be calculated from the degree of incorporation. However, the intracellular nucleotide pools may be anatomically or metabolically compartmented (i.e. via de novo or salvage synthesis routes) and this complicates many study designs. The use of[methyl-14C]- or [methyl-3H]methionine as a means of labelling methylated nucleosides in RNA and protein simultaneously is described in addition to new stable isotopic techniques based on 13C-glycine as a de novo label. Urinary excretion of the numerous modified nucleosides in cellular RNA can be used to calculate whole-body turnover rates of each of the major RNA species. Examples of the effects of critical-illness and glutamine supplementation on RNA turnover are given. We conclude by suggesting that whole-body RNA turnover rates have been significantly underestimated and that this has implications for nutritional therapy, especially with regard to nucleotide supplementation.

Severe protein-calorie malnutrition is a major problem in many intensive care (ICU) patients, due to the increased catabolic state often associated with acute severe illness and the frequent presence of prior chronic wasting conditions. Nutritional support is thus an important part of these patient's management. Over the years, enteral nutrition (EN) has gained considerable popularity, due to its favorable effects on the digestive tract and its lower cost and rate of complications compared to parenteral nutrition. However, clinicians caring for ICU patients are often faced with contradictory data and difficult decision-making when having to determine the optimal timing and modalities of EN administration, estimation of patient requirements and choice of formulas. The purpose of this paper is to provide practical guidelines on these various aspects of enteral nutritional support, based on presently available evidence.

This study aimed to evaluate whether food fortification and snacks could increase the energy and protein intakes of hospital patients. The control group of 82 consecutive admissions on medical, elderly care and orthopaedic wards ate freely from the hospital menu. Subsequently, an intervention group of 62 patients were offered fortified food and snacks, providing an extra 22.2|g protein/day and 966 kcal/day in addition to the standard menu. Fortification significantly increased energy intake in the intervention group (P = 0.007, independent samples t-test), having the greatest effect on groups with the lowest energy intake, that is male and female orthopaedic, female medical and female elderly patients (84 cent of total). The increases in energy intake were 21.3 cent, 21.4 cent, 23 cent and 19.6 cent respectively. Although the increased energy and protein intake represented 25.6 cent and 22.5 cent respectively, of the supplements given, and suggested that wastage was high, it was nevertheless sufficient to remove energy deficit. We therefore propose that provision of fortified food and snacks is a convenient method of improving the nutritional intakes of hospital patients.

International audience; Severe protein-calorie malnutrition is a major problem in many intensive care (ICU) patients, due to the increased catabolic state often associated with acute severe illness and the frequent presence of prior chronic wasting conditions. Nutritional support is thus an important part of these patient's management. Over the years, enteral nutrition (EN) has gained considerable popularity, due to its favorable effects on the digestive tract and its lower cost and rate of complications compared to parenteral nutrition. However, clinicians caring for ICU patients are often faced with contradictory data and difficult decision-making when having to determine the optimal timing and modalities of EN administration, estimation of patient requirements and choice of formulas. The purpose of this paper is to provide practical guidelines on these various aspects of enteral nutritional support, based on presently available evidence.

Pro-inflammatory cytokines mediate widespread changes in protein metabolism. Amino acids released from peripheral tissues fulfill a number of functions. They act as substrate for acute phase protein and immunoglobulin synthesis and, together with polyamines, in the replication of immune cells. Demands for specific amino acids may outstrip the supply from endogenous sources. A number of strands of evidence suggest that sulphur amino acids, and amino acids that are metabolically related to them, may be required in increased amounts. Protein deficiency impairs the acute phase response. However, sulfur amino acid insufficiency compromises glutathione synthesis, to a greater extent than hepatic protein synthesis, in the presence and absence of an inflammatory stimulus. The resulting effect may be compromised antioxidant defences. Functioning of T cells is dependent on intracellular glutathione concentrations and may also be affected by sulphur amino acid insufficiency. It has been suggested that the increased N excretion, which occurs during the immune response, is a reflection of a relative imbalance in the profile of amino acids released from peripheral tissues and the requirements imposed by the synthesis of substances involved in the acute phase response. Phenylalanine, tyrosine, tryptophan serine, and cysteine are released in amounts closest to requirements. Polyamine synthesis may be important for the fidelity of the enhanced level DNA transcription and RNA translation that occurs in response to infection and during tissue repair, gut growth after surgery, and in gut barrier functions. Although synthesized de novo from ornithine, arginine and S-adenosyl methionine (SAM), substantial recycling is a key feature of polyamine metabolism. The recycling may be a reflection of the need to maintain adequate tissue SAM during periods of rapid cell growth. During an immune/inflammatory response the combination of enhanced utilization of cysteine for glutathione synthesis and cell replication may lead to depletion of cellular SAM. A relatively small addition of polyamines to the diet may improve gut-associated aspects of the hosts' antibacterial defenses.

The urinary catabolites, N2,N2-dimethylguanosine (DMG), pseudouridine (PSU) and 7-methylguanine (m7-Gua) are formed from post-transcriptional methylation of RNA bases and are not reincorporated into RNA upon its degradation. Their quantitative urinary excretion may be used to determine rates of whole body degradation of individual RNA species since DMG occurs exclusively in tRNA, PSU occurs in rRNA and tRNA and m7-Gua occurs in all RNA species. Conventional HPLC analysis has several drawbacks since pre-analytical steps may involve selective losses and, under certain conditions, other urinary analytes may co-elute. In the present paper, we report analysis of these compounds by high-field 1H-nuclear magnetic resonance (1H-NMR) spectroscopy. Urinary concentrations of these metabolites were found to be in agreement with previously published HPLC and ELISA determinations. However, NMR analysis required minimal sample preparation (other than lyophilisation and reconstitution) and was capable of the simultaneous determination of other relevant analytes such as creatinine. This technique was therefore applied to urine samples from patients who had undergone surgical stress and insulin-like growth factor-1 (IGF-I) therapy. Surgical stress increased the excretion of DMG and m7-Gua. Degradation rates for tRNA and mRNA were also higher in surgically stressed subjects when compared with controls but degradation rates of rRNA decreased by approx. 30%. However, injection of IGF-I (40 micrograms/kg s.c.) had no significant effect on the excretion of these nucleosides. These data indicated that IGF-I therapy has no marked effects on RNA turnover following trauma. We suggest that this technique can be applied to study of RNA metabolism in any surgical or medical condition. Furthermore, since only 0.6 ml of urine is required, studies in neonates seem to be feasible.

Patients who were previously considered candidates for total parenteral nutrition are increasingly being considered as suitable for enteral feeding. This change has occurred for physiologic (trophism of intestinal luminal nutrients), pathophysiologic (possible reduction in bacterial translocation), or economic (enteral feeds are cheaper) reasons. Although the obvious inadequacies in the technique are being resolved leg, by percutaneous gastrostomy feeding), there is much suboptimal practice in identifying malnourished patients, in formulation of diets and their amino acid adequacy, and in addition of the so-called 'novel substrates' (ie, glutamine, arginine, and nucleotides) to diets. Furthermore, the cost benefit of feeding those patients who require extensive hospitalization, by the enteral rather than the parenteral route, may prove illusory.

Clinical glutamine supplements are a curious phenomenon, being more akin to bicarbonate to correct acidosis than to antibiotics to cure infection. The amino acid glutamine, a central compound in amino acid and intermediary metabolism, is made and consumed in large amounts by the body each day. Although supplements will not correct a “nutritional deficiency” of glutamine, nevertheless, the particular metabolic features of the intestine, skeletal muscle, and cells of the immune system suggest that they have a dependency on the metabolism of this amino acid. Animal studies suggest that glutamine supplements can reverse the atrophy of the small intestine that occurs during total parenteral nutrition. Similarly, improvements in the immune function of injured animals have been noted. Several clinical studies have also demonstrated positive effects on clinical outcome and patient well-being.

Dietary fiber is known to influence bowel habit and gastrointestinal mucosal cell morphology and function. large-bowel function is particularly influenced by insoluble, poorly fermentable fiber sources, whereas mucosal function is affected by fiber sources that are soluble and highly fermentable. The aim of the present study was to compare bowel function during consumption of a self-selected diet, a fiber-free enteral diet, and three polymeric enteral diets, each supplemented with a fiber with different fermentation characteristics. The fiber sources used were oat, soy oligosaccharide, and soy polysaccharide.Seven healthy subjects consumed four diets in random order for 4 to 7 days. These were a self-selected diet, a 2-L polymeric enteral diet, and a 2-L polymeric enteral diet supplemented with 15 g of total dietary fiber per liter derived from either soy oligosaccharide fiber (75 g/L) or oat fiber (15 g/L). An additional six healthy subjects were randomly assigned to three diets (4 to 7 days): a self-selected diet, a 2-L polymeric enteral diet, or the same 2-L polymeric enteral diet supplemented with 20 g of soy polysaccharide fiber per liter (15 g of total dietary fiber per liter). Bowel function was assessed by measuring whole-gut transit time, mean daily stool wet weights, and bowel movement frequency per day. Fermentation characteristics of the different fiber sources were determined quantitatively and qualitatively by measuring short-chain fatty acids produced during in vitro stool culture.Total short-chain fatty acid and butyric acid production with soy oligosaccharide fiber were significantly higher compared with values observed for soy polysaccharide fiber (p.003), oat fiber (p.005), and self-selected (control) diet (p.003). Compared with the fiber-free diet, consumption of the soy polysaccharide, oat, and soy oligosaccharide-fiber-supplemented enteral diets did not significantly (p.05) alter whole-gut transit time or stool wet weight. However, bowel frequency was significantly improved by consumption of the soy polysaccharide-fiber-supplemented diet but not the oat fiber or soy oligosaccharide-fiber-supplemented diets.Compared with a fiber-free polymeric enteral diet, the daily consumption of an enteral diet supplemented with 30 g of total dietary fiber per day derived from a poorly fermentable oat fiber, a highly fermentable soy oligosaccharide fiber, or a moderately fermentable soy polysaccharide fiber has little impact, if any, on bowel function.

The informational aspects of nucleic acid synthesis have attracted much more attention than the quantitative significance of DNA, rRNA, tRNA, and nucleotide synthesis. Animal and human studies suggest that in energetic terms, 5-10% of the energy used in synthesising tissue protein is expended in manufacturing an appropriate amount of synthetic machinery, that is the ribosome and tRNA. The two sources for synthesis of nucleotides are salvage of nucleotides released by intracellular degradation or derived from the diet, and nucleotides synthesised de novo from amino acids (for example, glutamine) and sugars (glucose). The comparative importance of these two processes is not well defined, but rRNA production requires a high de novo input in cell types with the capacity for rapid division (for example, lymphocytes). The gut is unusual in requiring a ready arterial supply of nucleotides synthesised by hepatic de novo pathways. Animal studies show that an exogenous supply of nucleotides (salvage) can improve liver regrowth, immune responsiveness to a microbial challenge, and gut morphology in diarrhoea models. Humans adapt to dietary nucleotide intake by downregulating de novo pathways. All total parental nutrition regimens, and most enteral regimens lack nucleotides, which may predispose to an inadequate supply of preformed nucleotides to gut and immune cells in the critically ill, artificially fed patient. Unfortunately, there are no clinical studies that answer this point at present.

This prospective double blind randomised seven day crossover controlled clinical trial was carried out to determine whether enterally fed patients with moderately impaired gastrointestinal function require a predigested nitrogen (N) source compared with whole protein. Twelve malnourished patients with varying gastrointestinal abnormalities, who required enteral feeding, received 2.25 l of one of two isocaloric isonitrogenous enteral diets (1 kcal/ml, 4.8 g nitrogen/l) containing either predominantly medium chain peptides (tetra or higher peptides) or whole protein as the nitrogen source. Nitrogen absorption and balance were calculated from dietary intake and analysis of 24 hour total urinary and faecal nitrogen for the last five days of each study period. There was no significant difference in either stool weight (110 (SEM) (49) v 111 (32) g/d), nitrogen absorption (91 (2) v 89 (2)%) or nitrogen balance (+1.0 (1.3) v +0.6 (1.4) g nitrogen/d) between the peptide and whole protein nitrogen sources when all patients are considered. There was, however, evidence to suggest a nutritional advantage from administering an enteral diet whose nitrogen source comprises oligopeptides, rather than whole protein, to a subgroup of patients with small bowel disease.

The hypothesis of the present study was that reducing the sweetness of ONS would alter older individualOs perception and preference ofthe products. Alternative saccharides were used in a model recipe of vanilla ONS. The sensory proÞles of the modiÞed ONS wereevaluated by an analytical sensory panel ( n 8) and correlated with acceptability data (nine-point hedonic scale) collected from a healthyolder volunteer group ( n 25; age range 65Ð84 years). Complete replacement of sucrose with Palatinose

Oral supplements of arginine and citrulline increase local nitric oxide (NO) production in the small intestine and this may be harmful under certain circumstances. Gastrointestinal toxicity was therefore reviewed with respect to the intestinal physiology of arginine, citrulline, ornithine, and cystine (which shares the same transporter) and the many clinical trials of supplements of the dibasic amino acids or N-acetylcysteine (NAC). The human intestinal dibasic amino acid transport system has high affinity and low capacity. L-arginine (but not lysine, ornithine, or D-arginine) induces water and electrolyte secretion that is mediated by NO, which acts as an absorbagogue at low levels and as a secretagogue at high levels. The action of many laxatives is NO mediated and there are reports of diarrhea following oral administration of arginine or ornithine. The clinical data cover a wide span of arginine intakes from 3 g/d to>100 g/d, but the standard of reporting adverse effects (e.g. nausea, vomiting, and diarrhea) was variable. Single doses of 3-6 g rarely provoked side effects and healthy athletes appeared to be more susceptible than diabetic patients to gastrointestinal symptoms at individual doses>9 g. This may relate to an effect of disease on gastrointestinal motility and pharmacokinetics. Most side effects of arginine and NAC occurred at single doses of >9 g in adults (>140 mg/kg) often when part of a daily regime of approximately>30 g/d (>174 mmol/d). In the case of arginine, this compares with the laxative threshold of the nonabsorbed disaccharide alcohol, lactitol (74 g or 194 mmol). Adverse effects seemed dependent on the dosage regime and disappeared if divided doses were ingested (unlike lactitol). Large single doses of poorly absorbed amino acids seem to provoke diarrhea. More research is needed to refine dosage strategies that reduce this phenomenon. It is suggested that dipeptide forms of arginine may meet this criterion.

Studies suggest clinical benefit of glutamine-supplemented parenteral nutrition. The aim was to determine if the inclusion of 10 g of glutamine as part of the nitrogen source of home parenteral nutrition (HPN) reduces infectious complications.Thirty-five patients on HPN were recruited and 22 completed the study. Patients were randomized to receive either standard HPN or glutamine-supplemented HPN. Patients were assessed at randomization, 3 and 6 months later then they were crossed over to the alternative HPN and reassessed at 3 and 6 months. Assessments included plasma amino acid concentrations, intestinal permeability and absorption, nutritional status, oral and parenteral intake, quality of life, routine biochemistry and haematology.No difference was seen between the groups at randomization. No difference was detected between the treatment phases for infective complications (55% in the standard treatment phase and 36% in the glutamine-supplemented phase P=0.67). There were no differences in nutritional status, intestinal permeability, plasma glutamine concentrations or quality of life.Although limited by the sample size, the study has shown that glutamine as part of the nitrogen source of parenteral nutrition can be given to patients on HPN for 6 months without any adverse effects.

BACKGROUND & AIMS: Enteral nutrition is the feeding method of choice during critical illness, but in some cases as few as 25% are fed appropriately. The aim was to retrospectively review the administration of nutrition to critically ill children. METHODS: The notes of 95 children over the age of 1 year who were in PICU>or=3 days were reviewed and information related to the delivery of nutrition was obtained. RESULTS: Fifty-nine per cent were fed within 24h of admission. Enteral nutrition was administered 54% of the time, 10% required parenteral nutrition and 9.5% received no nutritional support. Children only received a median 58.8 (range 0-277)% of their energy requirements, which could not be optimised until the 10th intensive care day. Energy intake was greater when supplemented with parenteral nutrition. Parenteral nutrition administration was interrupted 3 times while enteral nutrition was stopped 264 times, mainly to allow other clinical procedures to take place. For 75% of the study time, children had abnormal bowel patterns. Seventy-nine per cent were constipated for 3-21 days and 43% had diarrhoea of unknown aetiology. CONCLUSION: This was a retrospective study to describe the efficiency of nutritional support in critically ill children. We have shown that it is possible to administer enteral nutrition safely. However, the difference between desirable intake and actual intake achieved suggests that a more pro-active approach should be adopted.

Objective To determine how artificial nutrition support is used in hospitals inthe United Kingdom and to determine whether there have been any alterations in practice when compared to similar studies in 1988 (1) and 1991 (2). Design A 94-question survey about artificial nutrition support (ANS) was sent to all districtdietitians registered with the British Dietetic Association on 1 January 1994. Information was collected additionally from pharmacists, nutrition nurses and clinicians. Results 66.6% of questionnaires distributed were returned with analysable information. Ofthe respondents, 37.3% had access to nutrition support teams, compared with 27% in 1988. The documentation of usage of nutrition support was poor, only 33% of respondents being able to accurately quantify administration of enteral nutrition (EN), and 53% parenteral nutrition (PN). Conclusions Despite increasing awareness about the role of artificial nutrition support, and the value of nutrition support teams there has only been a modest increase in the provision and monitoring of NSTs in the last 3 years. This has important implications when considering audit of such practices.

Diarrhoea complicating enteral feeding is a common clinical problem affecting up to 25% of patients. Its pathogenesis remains unknown. A new technique of human in vivo segmental colonic perfusion was used to investigate colonic water and electrolyte movement in response to enteral feeding. Four groups of studies were performed in which low and high load polymeric enteral diet infusions were undertaken, either intragastrically or intraduodenally (n = 6 each group). Net absorption of sodium, chloride, and water occurred during fasting throughout the colon in all groups. There was a significant net secretion of sodium, chloride, and water in the ascending colon during low load (sodium: -42 mmol/h; 95% confidence limits -52 to -19, Chloride: -18 mmol/h; -50 to +16, water: -174 ml/h; -348 to -30) and high load (sodium: -24 mmol/h; -60 to +8, chloride: -18 mmol/h; -31 to +16, water: -120 ml/h; -246 to +6) gastric feeding, and during high load duodenal feeding (sodium: -12 mmol/h; -22 to -6, chloride; -6 mmol/h; -16 to +3, water: -72 ml/h; -144 to -6). Net secretion persisted in the distal colon only during high load gastric feeding. In the other three groups there was a net absorption in the distal colon. This study identified a significant colonic secretory response to enteral feeding, which is related to the site and load of the diet infusion. This response may play an important part in the pathogenesis of enteral feeding related diarrhoea.

Tissue Pathologl Unit , , ' , The , Roehampton Institute, West Hill, London, Departments of Clinical Biochemistry and Ilmmunology, 3The Institute of Liver Studies, Kin 's College School of Medicine and Dentistry, Bessenier Road, London %acuity of Medicine, University of Southampton, Southampton, 4Department of Gastroenterology and Nutrition, Central Middlesex Hospital, Park Royal, London and 5Department of Pathology, The Maudsley Hospital, Denmark Hill, London. Acute ethanol administration reduces the synthesis rates of both, smooth and skeletal muscle proteins [ 1-31. Chronic ethanol feeding studies have been shown to lead to reductions in the relative amounts of smooth and skeletal muscle proteins [4-61. I t is possible that mediating factors may include cytokines, derived from macrophages and other mononuclear cells, in response to both acute and chronic ethanol toxicity. Tumour necrosis factor alpha (TNF-a) and some interleukins, induce a variety of cellular and biochemical changes, including loss of skeletal muscle protein [7] and increased nitrogen excretion, which are also characteristics of chronic ethanol toxicity. Changes in protein synthesis in response to cytokines have also been reported. As cytokine production has been reported to be influenced by acute and chronic ethanol toxicity, some of the pathological changes observed in our rat models of alcohol toxicity, may be mediated by cytokine production. To test this hypothesis we measured plasma levels of interleukin-6 (IL-6) and TNF-a in rats acutelyand chronically-treated with ethanol. However, chronic ethanol intake characteristically leads to a retardation in normal growth rates and growth hormone (GH) levels have been shown to be suppressed by acute and chronic ethanol administration. The receptor for GH is a member of the cytokine receptor superfamily and it is possible that tissue responsiveness to cytokines is modulated by changes in receptor expression. In this regard we also measured plasma GH-BP levels, since GH-BP is derived from the extracellular portion of the GH receptor and should therefore provide an indirect measure of GH receptor expression. Male Wistar rats (100 g body weight) were subjected to either acute or chronic ethanol treatment. In acute studies rats were injected with an intraperitoneal (i.p.) dose of ethanol ( I m1/100 g body weight; 75 mmol/kg body weight). Controls were injected with isovolumetric saline (0. I5 mol/l NaCl i.p.). Rats were killed by decapitation after 2.5 hr and the blood collected into heparinised tubes and plasma extracted after centrifugation. In chronic studies, treated rats were fed a nutritionally complete liquid diet, containing 35% of total calories as either ethanol or glucose. as previously described 161. Controls were pair-fed identical amounts of the same diet in which ethanol was replaced by isocaloric glucose. At 3 weeks rats were killed by decapitation, and the blood collected as for acute studies. Levels of 11,-6 were measured in a bioassay using specific cell target. the B9 cell line. Cell proliferation was assessed using a rapid and sensitive modified colorimetric method [ S ] , which is based on the ability of viable cells to cleave 3-(4,5-dimethylthiazol-2-yl)-2.5diphenyl tetrazolium bromide. IL-6 activity was expressed in U/ml, defined as the dilution giving half maximal proliferation of B9 cells. Plasma TNF-a was measured using a bioassay. Cultures of L-929 tumorigenic murine fibroblasts were seeded at 4 x 10 cells/well in 50 pl of RPMl (Gibco. U.K.) supplemented with 10% fetal calf serum (Gibco. I1.K.) in 96-well flat-bottomed plates. After 4 h r of culture at 37°C i n 5% carbon dioxide samples and three-fold dilutions of rccombinant human TNF standard (Eurocetus, USA) were added to L.929 cells at a volume of 50 pliwell with 2 pg actinomycin D. Standard curve range was from 1.000 pg/ml to 4 pgiml. The specificity of the assay was checked by neutralisation o f the bioactivity with anti-serum to TNF. After 20 hours of culture, medium was removed and the monolayers stained for 10 min with crystal violet (0.5% in methano1:water). The plate was washed with water and the cells solubilised in 20% acetic acid and absorbance measured at 570 nm using a Dynatech MR5000 microtitrc plate reader. Plasma GH-BP activity was assayed by gel chromatography csscntially as described previously 191. Various analytes, as indicated in Table I were assayed by standard laboratory tests. MICHAEL NORM AN^, ADRIAN B. BONNER, MUNTHER J.

Glycine has been regarded as a poor source of nitrogen for total parenteral nutrition. Two prospective randomised cross over controlled clinical trials were undertaken to compare the efficacy of high and low glycine containing amino acid solutions in parenterally fed malnourished hypoalbuminaemic patients with gastrointestinal disease. In the first study (n = 9), amino acid solutions in which glycine accounted for 23% and 4% of total nitrogen were compared. No statistically significant difference was found in urea nitrogen/total urinary nitrogen excretion (mean (SEM) 83.4 (1.4) v 81.6 (1.7)%, p = 0.31), nitrogen balance (-1.9 (2.4) v -0.6 (2.0) g/day, p = 0.31) or plasma protein concentrations and blood urea nitrogen. In the second extended study (n = 5), there was no significant difference in net whole body protein synthesis (+1.3 (4.7) v-0.2 (3.7) mg/kg/hour, p = 0.69) or fractional (0.403 (0.070) v 0.480 (0.41)%/hour, p = 0.68) and absolute albumin synthesis rates (6.0 (0.9) v 7.2 (0.06) mg/kg/hour, p = 0.22), on comparing solutions of 25% and 8% glycine nitrogen. In addition, a significantly higher proportion of total urinary nitrogen comprised urea when patients received the low glycine containing amino acid source (81.4 (2.5) v 83.8 (3.2)%, p = 0.04). It is concluded that there are no apparent short term nutritional or metabolic disadvantages to using amino acid solutions that contain up to 25% of nitrogen as glycine in total parenteral nutrition.

Sixty nine patients with non-ulcer dyspepsia have been studied with endoscopy, biopsy, quick urease (CLO) test, Helicobacter pylori culture, and the 13C-urea breath test before and after treatment with tripotassium dicitratobismuthane (DeNol) two tablets twice daily for four weeks. Symptoms of non-ulcer dyspepsia were recorded using a standard questionnaire. Using H pylori culture as the gold standard, the sensitivity of the 13C-urea breath test was 90%, the specificity 98.6%, and the accuracy 94.8% with a positive predictive value of 98.2% and a negative predictive value of 92.5%. Conversion rate from H pylori positive to negative status after treatment with tripotassium dicitratobismuthate was 17.9%. Symptoms of non-ulcer dyspepsia improved appreciably after treatment irrespective of H pylori status. The 13C-urea breath test is an accurate research tool suitable for serial testing and population surveys.

103.6 ± 17.1 85.0 ± 3.1 90.2± 18 'ascending colon'. This had the effect of displacing coliforms and clostridia in this chamber after 6 days. DAG levels were reduced 20 fold (1st chamber) and 70-100 fold (2nd and 3rd chambers) compared with the control, and were associated with a moderate drop in coliforms and Clostridium perfringens. A slight increase in lactobacilli also occurred. DAG was also detected in the feces of healthy human volunteers. Consumption of lactitol resulted in an acute increase in fermentative activity in the large bowel and a significant reduction in the numbers of Cl. perfringens in stools, but did not significantly lower fecal DAG. Conclusion: The potential for lactitol to modify colonic conditions and to suppress the formation of DAG was demonstrated in vitro, but not in human feces. This lack of response in vivo may be due to rapid utilisation of lactitol by the highly saccharolytic microbial flora of the ascending colon. Other prebiotics that act more distally may have a greater effect on DAG. Acknowledgement: The work was funded by grants from the BBSRC, the UK Ministry of Agriculture Fisheries and Food, and the World Cancer Research Fund.