Effect of hypocaloric normoprotein or trophic feeding versus target full enteral feeding on patient outcomes in critically ill adults: a systematic review.

Uncertainty surrounds the optimal approach to feeding the critically ill, with increasing interest in the concept of intentional underfeeding to reduce metabolic stress while maintaining gut integrity. Conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines, this systematic review evaluates clinical outcomes reported in studies comparing hypocaloric normonitrogenous or trophic feeding (collectively 'intentional underfeeding') targeted full energy feeding administered via enteral nutrition to adult critically ill patients. Electronic databases including PubMed, CINAHL, EMBASE and CENTRAL were searched up to September 2017 for trials evaluating intentional underfeeding versus targeted energy feeding interventions on clinical outcomes (mortality, length of stay, duration of ventilation, infective complications, feeding intolerance and glycaemic control) among critically ill adult patients. Bias of included studies was assessed using the Cochrane risk of bias tool. Of the 595 articles identified, seven studies (six randomised controlled trials, one non-randomised trial) met the inclusion criteria, representing 2,684 patients (hypocaloric normonitrogenous n=668; trophic n=681; full energy feeding n=1335). Across the studies, there was considerable heterogeneity in study methodology, population, feeding strategy and outcomes and their timepoints. We observed no evidence that intentional underfeeding, when compared to targeting full energy feeding, reduced mortality or duration of ventilation or length of stay. However, limited trial evidence is available on the impact of intentional underfeeding on post-discharge functional and quality of life outcomes.

Energy dependence of lipopolysaccharide translocation in Salmonella typhimurium.

Energy inhibitors block translocation of pulse-labeled core lipopolysaccharide to outer membrane under conditions which allow maintenance of constant specific radioactivity of intracellular precursor pools throughout the chase period. Under the conditions used, approximately 75% of the total cellular label was membrane-bound at initiation of chase. Translocation of core lipopolysaccharide from inner to outer membrane showed apparent first order kinetics (t1/2 = 1.2 min, 32 degrees C). Translocation was blocked by arsenate (5-10 mM) under conditions where proton motive force was unchanged, while the uncouplers 2,4-dinitrophenol (0.1 mM to 0.8 mM) and carbonyl cyanide-m-chlorophenyl hydrazone (12-30 microM) inhibited translocation with no apparent effect on the ATP pool. Therefore, core lipopolysaccharide translocation appears to require maintenance of both proton motive force and high energy phosphate pools. Electron microscopic experiments show no gross disruption of zones of adhesion, the putative sites of lipopolysaccharide translocation, in the presence of arsenate or 2,4-dinitrophenol suggesting that energy is not required simply for maintenance of these structures.