Objective The authors randomized patients to an enteral diet containing glutamine, arginine, omega-3 fatty acids, and nucleotides or to an isonitrogenous, isocaloric diet to investigate the effect of septic outcome. A third group of patients, without enteral access but eligible by severity of injury, served as unfed controls and were studied prospectively to determine the risk of infection. Summary Background Data Laboratory and clinical studies suggest that diets containing specialty nutrients, such as arginine, glutamine, nucleotides, and omega-3 fatty acids, reduce septic complications. Unfortunately, most clinical trials have not compared these diets versus isonitrogenous, isocaloric controls. This prospective, blinded study randomized 35 severely injured patients with an Abdominal Trauma Index ≥ 25 or a Injury Severity Score ≥ 21 who had early enteral access to an immune-enhancing diet ([IED] Immun-Aid, McGaw, Inc., Irvine, CA ; n = 17) or an isonitrogenous, isocaloric diet (Promote [Ross Laboratories, Columbus, OH] and Casec [Mead-Johnson Nutritionals, Evansville, IN] ; n = 18) diet. Patients without early enteral access but eligible by severity of injury served as contemporaneous controls (n = 19). Patients were evaluated for septic complications, antibiotic usage, hospital and intensive care unit (ICU) stay, and hospital costs. Results Two patients died in the treatment group and were dropped from the study. Significantly fewer major infectious complications (6%) developed in patients randomized to the IED than patients in the isonitrogenous group (41%, p = 0.02) or the control group (58%, p = 0.002). Hospital stay, therapeutic antibiotics, and the development of intra-abdominal abscess was significantly lower in patients receiving the IED than the other two groups. This improved clinical outcome was reflected in reduced hospital costs. Conclusions An IED significantly reduces major infectious complications in severely injured patients compared with those receiving isonitrogenous diet or no early enteral nutrition. An IED is the preferred diet for early enteral feeding after severe blunt and penetrating trauma in patients at risk of subsequent septic complications. Unfed patients have the highest complication rate.

A randomized trial of isonitrogenous enteral diets after severe trauma. An immune-enhancing diet reduces septic complications.

1. Determination of Total Lipid, Lipid Classes, and Fatty Acids in Aquatic Samples.- 1.1. Introduction.- 1.2. Results and Discussion.- 1.2.1. Sampling and Storage.- 1.2.2. Lipid Extraction.- 1.2.3. Determination of Total Lipid.- 1.2.4. Determination of Lipid Classes.- 1.2.5. Determination of Fatty Acids and Carbon Number Profiles.- 1.3. Conclusion.- References.- 2. Fatty Acids as Trophic and Chemical Markers in Freshwater Ecosystems.- 2.1. Introduction.- 2.2. Nomenclature.- 2.3. Characteristics of Fatty Acid Markers for Trophic Studies.- 2.4. Primary Sources and Trophic Transfer of Fatty Acids.- 2.4.1. Fatty Acid Composition of Algae and Cyanobacteria.- 2.4.2. Fatty Acids as Trophic Markers of Algae and Cyanobacteria.- 2.4.3. Fatty Acid Composition of Bacteria.- 2.4.4. Fatty Acids as Trophic Markers of Bacteria.- 2.4.5. Fatty Acid Markers from Allochthonous Sources.- 2.4.6. Fatty Acids as Trophic Markers in Vertebrates.- 2.5. Research Needs.- 2.6. Conclusions.- References.- 3. Irradiance and Lipid Production in Natural Algal Populations.- 3.1. Introduction.- 3.2. Metabolism and Reallocation.- 3.2.1. Lipids in Relation to Other Macromolecular Classes.- 3.2.2. Diel Versus Light-Phase Allocation and Synthesis.- 3.2.3. Budgets for Overnight Activity.- 3.2.4. Reallocation Among Lipid Classes.- 3.3. Irradiance and Lipid Synthesis.- 3.3.1. Photosynthetic Parameters.- 3.3.2. Light Saturation Parameter, Ik.- 3.3.3. Production Efficiency Parameter, ?.- 3.3.4. Areal Lipid Production.- 3.3.5. Implications of the Irradiance Response.- 3.4. Conclusions.- 3.5. Research Directions.- References.- 4. Lipids in Freshwater Zooplankton: Selected Ecological and Physiological Aspects.- 4.1. Introduction.- 4.2. Usefulness of Areal Energy Reserve Estimates.- 4.3. Time Course of Lipid Deposition/Loss.- 4.4. Lipids as Indices of Stress.- 4.4.1. Ratio of Storage to Membrane Lipids.- 4.4.2. Maternal Lipid Investment.- 4.4.3. Visible Lipid Energy Stores.- 4.4.4. Fatty Acid Composition and Abundance.- 4.5. Ultraviolet Radiation and Zooplankton Lipids.- 4.6. Research Needs and Suggested Future Directions.- 4.6.1. Geographical Disparities.- 4.6.2. Physicochemical Disparities.- 4.6.3. Essential Fatty Acids.- 4.6.4. Effects of Temperature Changes.- 4.6.5. Diapause.- 4.6.6. Lipids as Allelopathic Compounds and Chemical Feeding Deterrents.- 4.7. Conclusions.- References.- 5. Lipid Dietary Dependencies in Zooplankton.- 5.1. Introduction.- 5.2. Methods.- 5.2.1. Microparticle Preparation.- 5.2.2. Dietary Supplement Experiments.- 5.2.3. Characterization of the Natural Algal Diet.- 5.2.4. Algal Counting and Autoradiography.- 5.3. Results.- 5.3.1. Supplement Experiments with Natural Populations.- 5.3.2. Lake Waynewood Experiment: October 1989.- 5.3.2.1. Algal Diet.- 5.3.2.2. Response byDaphnia.- 5.4. Discussion.- References.- 6. Seasonal Dynamics of Lipids in Freshwater Benthic Invertebrates.- 6.1. Introduction.- 6.2. Results and Discussion.- 6.2.1. Slope and Profundal Zones.- 6.2.1.1. Crustacea: Amphipoda.- 6.2.1.2. Mysidacea.- 6.2.2. Shelf and Nearshore Zones.- 6.2.2.1. Crustacea: Amphipoda.- 6.2.2.2. Annelida: Oligochaeta.- 6.2.2.3. Insecta.- 6.2.2.4. Mollusca: Bivalvia.- 6.3. Research Needs.- 6.4. Conclusions.- References.- 7. Ecological Role of Lipids in the Health and Success of Fish Populations.- 7.1. Introduction.- 7.2. Results and Discussion.- 7.2.1. Overwinter Starvation and Survival.- 7.2.2. Energy Allocation Strategies.- 7.2.3. Reproductive Development and Early Life History.- 7.2.4. Lipids and Environmental Stress.- 7.2.4.1. Contaminant Effects.- 7.2.4.2. Thermal Effects.- 7.2.4.3. Other Stressors.- References.- 8. Lipids and Essential Fatty Acids in Aquatic Food Webs: What Can Freshwater Ecologists Learn from Mariculture?.- 8.1. Introduction.- 8.2. Results and Discussion.- 8.2.1. Some Important Lipids and Fatty Acids.- 8.2.1.1. Essential Fatty Acids.- 8.2.1.2. Lipid Classes.- 8.2.2. Methodological Considerations.- 8.2.3. Physiological Requirements of Marine Animals.- 8.2.3.1. General Evaluation of EFA Requirements.- 8.2.3.2. Anabolic Processes and Growth.- 8.2.3.3. Membrane Transport and Metabolism.- 8.2.3.4. Regulation of Metabolism.- 8.2.3.5. General Considerations and Concluding Remarks.- 8.2.4. Methods for Evaluation of EFA Requirements.- 8.2.5. Symptoms of EFA Deficiency.- 8.2.6. Fatty Acid Transport and Metabolism in Food Webs.- 8.2.6.1. Algae.- 8.2.6.1.1. Lipids of Algae.- 8.2.6.1.2. Essential Fatty Acids of Algae.- 8.2.6.1.3. Conclusion.- 8.2.6.2. Zooplankton.- 8.2.6.2.1. Lipid Content and Lipid Composition.- 8.2.6.2.2. Fatty Acids of TAG-Zooplankton.- 8.2.6.3. Fish.- 8.2.6.3.1. Lipid.- 8.2.6.3.2. Fatty Acid Composition.- 8.2.6.4. General Conclusions.- 8.2.7. Relevance of Mariculture Research.- 8.2.8. Evaluation of Ecological Effects of Essential Fatty Acids.- 8.3. Concluding Remarks.- References.- 9. Influence of Lipids on the Bioaccumulation and Trophic Transfer of Organic Contaminants in Aquatic Organisms.- 9.1. Introduction.- 9.1.1. Sources of Contaminant Gain and Loss in Aquatic Systems.- 9.1.2. Organism Adiposity and Internal Distribution of Contaminants.- 9.1.3. Nonlipid Factors Affecting Internal Distributions.- 9.2. Prediction of Bioconcentration and Bioaccumulation.- 9.2.1. Bioconcentration.- 9.2.2. Bioaccumulation.- 9.3. Factors Affecting Prediction.- 9.3.1. Methods for Measuring Lipid Content.- 9.3.2. Lipid Composition and Bioaccumulation.- 9.4. Mimicking Bioconcentration with Semipermeable Membrane Devices.- 9.5. Toxicity and the Role of Lipid.- 9.5.1. Release of Sequestered Contaminant During Metabolism.- 9.5.2. Lipids and Membrane Narcosis.- 9.5.3. Effect of Toxins on Lipid Metabolism and Function.- 9.6. Relevance of Food Chain Transfer to Bioaccumulation.- 9.6.1. Relevance of Trophic Transfer to Bioaccumulation...- 9.6.2. Role of Lipids in Food Chain Accumulation.- 9.6.2.1. Fugacity Model.- 9.6.2.2. Mechanism for Trophic Transfer.- 9.6.3. Factors Affecting Trophic Transfer.- 9.6.3.1. Assimilation Efficiency.- 9.6.3.2. Miscellaneous Factors Affecting Assimilation.- 9.7. Biomagnification and Organism Lipids.- 9.7.1. Is Biomagnification Real?.- 9.7.2. A Lipid-Based Model for Biomagnification.- 9.7.3. Current Issues in Biomagnification and Relationship to Lipids.- 9.8. Lipids and Transgenerational Transfer of Contaminants.- 9.9. Conclusions.- References.- 10. Lipids in Water-Surface Microlayers and Foams.- 10.1. Introduction.- 10.2. Basic Physicochemistry of Surface Microlayers.- 10.3. Basic Structure of Foams.- 10.4. Sampling Techniques.- 10.5. Physicochemical Processes at the Surface Microlayers.- 10.6. Lipids in the Water-Surface Microlayers and Foams.- 10.6.1. Total Lipids and Major Lipid Classes.- 10.6.2. Fatty Acids.- 10.7. Research Needs.- 10.8. Final Remarks.- References.- 11. Comparison of Lipids in Marine and Freshwater Organisms.- 11.1. Introduction.- 11.2. Discussion.- 11.2.1. Lipid Classes.- 11.2.2. Sterols and Cholesterol.- 11.2.3. Wax Esters and Triacylglycerols.- 11.2.4. Fatty Acids.- 11.2.5. Furan and Some Other Unusual Fatty Acids.- 11.2.6. Ether Lipids.- 11.2.7. Prostanoids.- 11.3. Conclusions.- References.

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Lipids in freshwater ecosystems

The effects of different types of dietary lipids were tested in burned guinea pigs. All diets were identical except for the type of lipid, with total energy intake from lipids equaling 10%. All animals received a 30% total body surface area (TBSA) flame burn and were fed identically by pump-controlled gastrostomy feedings for 14 days. When compared to safflower oil (74% linoleic acid) as well as linoleic acid alone, fish oil (18% eicosapentaenoic acid or EPA) administration resulted in less weight loss, better skeletal muscle mass, lower resting metabolic expenditure, better cell mediated immune responses, better opsonic indices, higher splenic weight, lower adrenal weight, higher serum transferrin, and lower serum C3 levels. With the exception of better cell mediated immune responses in the animals fed linoleic acid, the administration of indomethacin made little difference. These findings can be explained by a reduction in the synthesis of the dienoic prostaglandins that are derived from the omega 6 series of fatty acids, some of which are significantly immunosuppressive. Regulation of dietary lipids may be an important therapeutic advance in nutritional support after burn injury, and controlled trials should be considered.

The importance of lipid type in the diet after burn injury.

Dietary fatty acids and the immune system.

Weanling rats were fed on high-fat (178 g/kg) diets which contained 4.4 g α-linolenic (ALA), γ-linolenic, arachidonic (ARA), eicosapentaenoic (EPA), or docosahexaenoic acid (DHA)/100 g total fatty acids. The proportions of all other fatty acids, apart from linoleic acid, and the proportion of total polyunsaturated fatty acids (PUFA) (approximately 35 g/100 g total fatty acids) were constant, and the n−6 to n−3 PUFA ratio was maintained as close to 7 as possible. The fatty acid compositions of the serum and of spleen leukocytes were markedly influenced by that of the diet. Prostaglandin E2 production was enhanced from leukocytes from rats fed the ARA-rich diet and was decreased from leukocytes from the EPA- or DHA-fed rats. Replacing dietary ALA with EPA resulted in diminished ex vivo lymphocyte proliferation and natural killer (NK) cell activity and a reduced cell-mediated immune response in vivo. In contrast, replacing ALA with DHA reduced ex vivo lymphocyte proliferation but did not affect ex vivo NK cell activity or the cell-mediated immune response in vivo. Replacement of a proportion of linoleic acid with either γ-linolenic acid or ARA did not affect lymphocyte proliferation, NK cell activity, or the cell-mediated immune response. Thus, this study shows that different n−3 PUFA exert different immunomodulatory actions, that EPA exerts more widespread and/or stronger immunomodulatory effects than DHA, that a low level of EPA is sufficient to influence the immune response, and that the immunomodulatory effects of fish oil may be mainly due to EPA.

Eicosapentaenoic and docosahexaenoic acids alter rat spleen leukocyte fatty acid composition and prostaglandin E2 production but have different effects on lymphocyte functions and cell-mediated immunity

M.I. Gurr

Papers

The role of lipids in the regulation of the immune system