Energetic Compensation Research Articles

Communication between DNA and nucleotide binding sites facilitates stepping by the RecBCD helicase.

Double-strand DNA breaks are the severest type of genomic damage, requiring rapid response to ensure survival. RecBCD helicase in prokaryotes initiates processive and rapid DNA unzipping, essential for break repair. The energetics of RecBCD during translocation along the DNA track are quantitatively not defined. Specifically, it's essential to understand the mechanism by which RecBCD switches between its binding states to enable its translocation. Here, we determine, by systematic affinity measurements, the degree of coupling between DNA and nucleotide binding to RecBCD. In the presence of ADP, RecBCD binds weakly to DNA that harbors a double overhang mimicking an unwinding intermediate. Consistently, RecBCD binds weakly to ADP in the presence of the same DNA. We did not observe coupling between DNA and nucleotide binding for DNA molecules having only a single overhang, suggesting that RecBCD subunits must both bind DNA to 'sense' the nucleotide state. On the contrary, AMPpNp shows weak coupling as RecBCD remains strongly bound to DNA in its presence. Detailed thermodynamic analysis of the RecBCD reaction mechanism suggests an 'energetic compensation' between RecB and RecD, which may be essential for rapid unwinding. Our findings provide the basis for a plausible stepping mechanism' during the processive translocation of RecBCD.

Disallowed spots in protein structures

Ramachandran (ϕ, ψ) steric map was introduced in 1963 to describe available conformation space for protein structures. Subsequently, residues were observed in high-energy disallowed regions of the map. To unequivocally identify the locations of disallowed conformations of residues, we got 36 noise-free protein structures (resolution ≤1 Å, Rwork/Rfree ≤ 0.10). These stringent criteria were applied to rule out data or model errors or any crystallographic disorders. No disallowed conformation was found in the dataset. Further, we also examined disallowed conformations in a larger dataset (resolution ≤1.5 Å, devoid of any model errors, or disorders). The observed locations of disallowed residues are referred as disallowed spots. These spots include short loops of 3–5 residues, and locations where residues participate in disulfide bonding or intramolecular interactions or inter-molecular interactions with neighboring water, metals or ligands. Conformational sampling revealed that short loops in between secondary structures hardly have any opportunity to relieve from conformational strain. Residues involved in interactions, which provide energetic compensation for high-energy conformational states, were relieved from strain once the causative interaction was removed. The present study aims to identify disallowed spots in the native state of proteins, wherein residues are forced to be trapped in high-energy disallowed conformations. Moreover, it was also observed that pre-Pro, Ser, Asp, trans-Pro, Val, Asn & Gly have higher tendency to occur in disallowed conformation, which could be attributed to factors such as conformational restrictions, residue propensity of secondary structures and compensating sidechain and mainchain interactions, stabilizing turn-mimics.

Fullerene Complexation in a Hydrogen-Bonded Porphyrin Receptor via Induced-Fit: Cooperative Action of Tautomerization and C-H···π Interactions.

A supramolecular chiral hydrogen-bonded tetrameric aggregate possessing a large cavity and tetraarylporphyrin substituents was assembled using alternating 4H- and 2H-bonds between ureidopyrimidinone and isocytosine units, respectively. The aggregation mode was rationally shifted from social to narcissistic self-sorting by changing urea substituent size only. The H-bonded tetramer forms a strong complex with C60 guest, at the same time undergoing remarkable structural changes. Namely, the cavity adjusts to the guest via keto-to-enol tautomerization of the ureidopyrimidinone unit and as a result, porphyrin substituents move apart from each other in a scissor blade-like opening fashion. The rearrangement is accompanied by C-H···π interaction between the alkyl solubilizing groups and the nearby placed porphyrin π-systems. The latter interaction was found to be crucial for the guest complexation event, providing energetic compensation for otherwise costly tautomerization. We showed that only the systems possessing sufficiently long alkyl chains capable of interacting with a porphyrin ring are able to form a complex with C60. The structural rearrangement of the tetramer was quantitatively characterized by electron paramagnetic resonance pulsed dipolar spectroscopy measurements using photogenerated triplets of porphyrin and C60 as spin probes. Further exploring the C-H···π interaction as a decisive element for the C60 recognition, we investigated the guest-induced self-sorting phenomenon using scrambled tetramer assemblies composed of two types of monomers possessing alkyl chains of different lengths. The presence of the fullerene guest has enabled the selective scavenging of monomers capable of C-H···π interaction to form homo-tetrameric aggregates.

Projected near-future ocean acidification decreases mercury toxicity in marine copepods

Here, we examined the combinational effect of ocean acidification (OA) and mercury (Hg) in the planktonic copepod Pseudodiaptomus annandalei in cross-factored response to different pCO2 (400, 800 μatm) and Hg (control, 1.0 and 2.5 μg/L) exposures for three generations (F0–F2), followed by single-generation recovery (F3) under clean condition. Several phenotypic traits and Hg accumulation were analyzed for F0–F3. Furthermore, shotgun-based quantitative proteomics was performed for F0 and F2. Our results showed that OA insignificantly influenced the traits. During F0–F2, combined exposure reduced Hg accumulation as compared with the counterpart Hg treatment, supporting the mitigating effect of OA on Hg toxicity in copepods. Proteomics analysis indicated that the copepods probably increased energy production/storage and stress response to ensure physiological resilience against OA. However, Hg induced many toxic events (e.g., energy depletion and degenerated organomorphogenesis/embryogenesis for F0; cell cycle arrest and detrimental stress-defense for F2), which were translated to the population-level adverse outcome, i.e., compromised growth/reproduction. Particularly, compensatory proteome response was identified (e.g., increased immune defense for F0; energetic compensation and enhanced embryogenesis for F2), accounting for a negative interaction between OA and Hg. Together, this study provides the molecular mechanisms behind the effects of OA and Hg pollution in marine copepods.

OGA Inhibition Alters Energetics and Nutrient Sensing in Alzheimer's Disease Cytoplasmic Hybrids.

Alzheimer's disease (AD) features reductions in key bioenergetic fluxes and perturbed mitochondrial function. Cytoplasmic hybrids (cybrids) generated through the transfer of AD subject mitochondria to mtDNA-depleted SH-SY5Y neuroblastoma cells recapitulate some of these features in an in vitro setting. For this study, we used the AD cybrid model to assess the impact of a nutrient-excess like-state via increasing O-GlcNAcylation on whole cell and mitochondrial homeostasis. We induced increased O-GlcNAc by treating AD and control cybrid cell lines with Thiamet G (TMG), an inhibitor of the O-GlcNAcase enzyme that mediates removal of the nutrient-dependent O-GlcNAc modification. Relative to control cybrid cell lines, AD cybrid lines showed a blunted response to TMG-induced O-GlcNAcylation. At baseline, AD cybrid cell line mitochondria showed partial activation of several proteins that help maintain bioenergetic homeostasis such as AMP-Regulated Kinase suggesting that AD mitochondria initiate a state of nutrient stress promoting energetic compensation; however, this compensation reduces the capacity of cells to respond to additional nutrient-related stresses such as TMG treatment. Also, TMG caused disruptions in acetylation and Sirtuin 3 expression, while lowing total energetic output of the cell. Together, these findings suggest that modulation of O-GlcNAc is essential for proper energetic function of the mitochondria, and AD mitochondrial capacity to handle nutrient-excess is limited.

Maintenance costs of male dominance and sexually antagonistic selection in the wild

Abstract Variation in dominance status determines male mating and reproductive success, but natural selection for male dominance can be detrimental or antagonistic for female performance, and ultimately their fitness. Attaining and maintaining a high dominance status in a population of competing individuals is physiologically costly for males. But how male dominance status is mediated by maintenance energetics is currently not well understood, nor are the corresponding effects of male energetics on his sisters recognized. We conducted laboratory and field experiments on rodent populations to test whether selective breeding for male dominance status (dominant vs. subordinate breeding lines) antagonistically affected basal metabolic rate (BMR) and fitness of females under wild conditions. Our results showed elevated BMR in females, but not in males, from the dominant breeding line. However, phenotypically dominant males from the subordinate breeding line had the highest BMR. Males from the dominant line with low BMR sired the most litters and offspring in the field. Similarly, females from the dominant selection line tended to have more offspring if they had lower BMR, while the opposite trend was found in females from the subordinate selection line. Females with high and low BMR reproduced most often, as indicated by a significant quadratic selection gradient. The increased female BMR resulting from selection for male dominance suggests genetic incompatibility between sexes in metabolism inheritance. Elevated BMR in behaviourally dominant males, but not in males from the dominant breeding line, suggests physiological costs in males not genetically suited for dominance. Fitness costs of elevated maintenance costs (measured as BMR) shown here support the energetic compensation hypothesis where high BMR is selected against as it would trade off energy required for other important life‐history attributes. A plain language summary is available for this article.

The effects of elevated temperature and ocean acidification on the metabolic pathways of notothenioid fish.

The adaptations used by notothenioid fish to combat extreme cold may have left these fish poorly poised to deal with a changing environment. As such, the expected environmental perturbations brought on by global climate change have the potential to significantly affect the energetic demands and subsequent cellular processes necessary for survival. Despite recent lines of evidence demonstrating that notothenioid fish retain the ability to acclimate to elevated temperatures, the underlying mechanisms responsible for temperature acclimation in these fish remain largely unknown. Furthermore, little information exists on the capacity of Antarctic fish to respond to changes in multiple environmental variables. We have examined the effects of increased temperature and pCO2 on the rate of oxygen consumption in three notothenioid species, Trematomus bernacchii, Pagothenia borchgrevinki, and Trematomus newnesi. We combined these measurements with analysis of changes in aerobic and anaerobic capacity, lipid reserves, fish condition, and growth rates to gain insight into the metabolic cost associated with acclimation to this dual stress. Our findings indicated that temperature is the major driver of the metabolic responses observed in these fish and that increased pCO2 plays a small, contributing role to the energetic costs of the acclimation response. All three species displayed varying levels of energetic compensation in response to the combination of elevated temperature and pCO2. While P. borchgrevinki showed nearly complete compensation of whole animal oxygen consumption rates and aerobic capacity, T. newnesi and T. bernacchii displayed only partial compensation in these metrics, suggesting that at least some notothenioids may require physiological trade-offs to fully offset the energetic costs of long-term acclimation to climate change related stressors.

Parametric Design for Ecological Purposes – Case Studies and Algorithm Examples

Ecological architecture, which is often confused with low energy architecture, is some kind of energetic compensation for environment which is also giving a new direction for developing of new technologies and architectural solutions. The problem of global human population growth, demand for building materials, electricity, fossil fuels and water - systematically raises environmental standards which have to be met by modern architectural objects - whose construction, operation, maintenance and disposal today consume 60% - 70% of the world's energy. This issue becomes important also on a larger scale which is the urban and spatial planning - creating a vast area of research and the profession for contemporary design thinking. Software engineers develop tools which allow designers design in accordance with the doctrine of ecology and sustainability. At the forefront of this technological race, there are parametric and generative design programs - giving designers extraordinary opportunities to shape the form of buildings based on the assumed ecological parameters. This article will talk about the Bridge Pavilion in Zaragoza (2008), 30 St Mary Axe in London (2004), Al Bahar Towers in Abu Dhabi (2012), City of Culture of Galicia in Santago De Compostela, (2000-2013), Free Railway International Competition in Posen (2015). Beyond the theoretical consideration of the specifics of the presented objects, the article defines practical algorithmic sequences for generating forms of these objects. Sequences presented in the article were created in the Grasshopper and illustrate methods of creating specific buildings, with special attention to their environmental properties.DOI: http://dx.doi.org/10.5755/j01.sace.12.3.12989

Relationship between pathological findings and enzymes of the energy metabolism in liver of rats infected by Trypanosoma evansi

The aim of this study was to investigate the activities of important enzymes involved in the energetic metabolism in the liver of rats experimentally infected by Trypanosoma evansi. Adenylate kinase (AK), pyruvate kinase (PK), and lactate dehydrogenase (LDH) in liver homogenate, as well as aspartate aminotransferase (AST), alanine aminotransferase (ALT), and clotting time in plasma were evaluated at 5 and 15days post-infection (PI). The activities of the respiratory chain complexes and of Na+, K+-ATPase were also evaluated. This study demonstrates energetic metabolism impairment in rats infected by T. evansi. A reduced energy metabolism in the liver of rats infected by T. evansi was observed, demonstrated by AK decreased and PK increased activities at 5days PI, a mechanism known as energetic compensation. However, at 15days PI a decrease of AK and PK activities were observed. In addition, an increase in the activities of respiratory chain complexes II, II–III and IV in infected rats at 15days PI, and a decrease of Na+, K+-ATPase activities in infected rats on days 5 and 15 PI were verified. In the plasma, we observed an increase in ALT and AST activities on days 5 and 15 PI, and increase in clotting time in infected rats. The changes caused by T. evansi infection on the activity of enzymes of hepatic energy metabolism can corroborate to elucidate the mechanisms that lead to liver injury and inflammatory infiltration verified in T. evansi infected rats. Therefore, these alterations are directly related to disease pathogenesis.

Energetic compensation is historically contingent and not supported for small mammals in South American or Asian deserts

Understanding the nature of faunal assembly and community structure remains central to ecology. Research in North American deserts and some tropical forests provides evidence of energetic compensation and zero‐sum dynamics, suggesting that species in some natural assemblages may be replaced with limited impact on ecosystem function. Experimental removal of a dominant small mammal (degu, Octodon degus) from replicate plots in semiarid coastal thorn‐scrub habitat in north‐central Chile revealed no evidence for energetic or functional compensation; energy consumption remained significantly lower on degu exclusions relative to control plots after 17 years of exclusion. This occurred in spite of the fact that the geographic species pools for South American sites generally are similar in size to those of most North American sites (mean and median number of species, 16.3 and 21.5 vs. 21.0 and 20, respectively). A macroecological assessment of energetically equivalent species at 394 arid sites in North America, the Gobi Desert, and South America indicated that the number of potentially equivalent species was lower than (Gobi) or similar to (South America) that found in North America, but when segregated by trophic groups, these faunas differed markedly. North American sites included large numbers of granivorous species whereas South American sites were dominated by omnivores. The more general trophic strategy in the latter sites would be expected to facilitate compensatory responses within local faunas, suggesting either that our site is anomalous or that other factors are governing local dynamics. Further research is needed to understand the generality of compensatory dynamics within natural systems, as this mechanism has direct relevance to discussions on ecological resilience in the face of ongoing environmental change.

Sparsely populated residue conformations in protein structures: Revisiting “experimental” Ramachandran maps

The Ramachandran map clearly delineates the regions of accessible conformational (φ-ψ) space for amino acid residues in proteins. Experimental distributions of φ, ψ values in high-resolution protein structures, reveal sparsely populated zones within fully allowed regions and distinct clusters in apparently disallowed regions. Conformational space has been divided into 14 distinct bins. Residues adopting these relatively rare conformations are presented and amino acid propensities for these regions are estimated. Inspection of specific examples in a completely "arid", fully allowed region in the top left quadrant establishes that side-chain and backbone interactions may provide the energetic compensation necessary for populating this region of φ-ψ space. Asn, Asp, and His residues showed the highest propensities in this region. The two distinct clusters in the bottom right quadrant which are formally disallowed on strict steric considerations correspond to the gamma turn (C7 axial) conformation (Bin 12) and the i + 1 position of Type II' β turns (Bin 13). Of the 516 non-Gly residues in Bin 13, 384 occupied the i + 1 position of Type II' β turns. Further examination of these turn segments revealed a high propensity to occur at the N-terminus of helices and as a tight turn in β hairpins. The β strand-helix motif with the Type II' β turn as a connecting element was also found in as many as 57 examples.

Complementary mechanistic properties of Fe- and Mn-doped aluminophosphates in the catalytic aerobic oxidation of hydrocarbons

A comparative computational study of the reaction mechanisms for hydrocarbon oxidations catalysed by Mn- and Fe-doped nanoporous aluminophosphates shows distinctive features for each transition metal depending on its electronic configuration. Preactivation of Mn catalysts is easier due to the higher stability of Mn(II), but its oxidation during propagation requires activation barriers. In contrast, preactivation of Fe is more difficult and avoids a direct Fe reduction because of the low stability of Fe(II). Fe(II) is only produced at the end of the propagation cycle, favoured by an energetic compensation caused by the simultaneous exothermic oxidation of an alcohol molecule. Fe-catalysed propagation is kinetically favoured since it requires lower activation barriers, and is further assisted by higher adsorption energies of the reactants and lower desorption energies of the products on the active site. The mechanistic information gained can be used for the rational design of improved oxidation catalysts.

Extreme Entropy–Enthalpy Compensation in a Drug-Resistant Variant of HIV-1 Protease

The development of HIV-1 protease inhibitors has been the historic paradigm of rational structure-based drug design, where structural and thermodynamic analyses have assisted in the discovery of novel inhibitors. While the total enthalpy and entropy change upon binding determine the affinity, often the thermodynamics are considered in terms of inhibitor properties only. In the current study, profound changes are observed in the binding thermodynamics of a drug-resistant variant compared to wild-type HIV-1 protease, irrespective of the inhibitor bound. This variant (Flap+) has a combination of flap and active site mutations and exhibits extremely large entropy-enthalpy compensation compared to wild-type protease, 5-15 kcal/mol, while losing only 1-3 kcal/mol in total binding free energy for any of six FDA-approved inhibitors. Although entropy-enthalpy compensation has been previously observed for a variety of systems, never have changes of this magnitude been reported. The co-crystal structures of Flap+ protease with four of the inhibitors were determined and compared with complexes of both the wild-type protease and another drug-resistant variant that does not exhibit this energetic compensation. Structural changes conserved across the Flap+ complexes, which are more pronounced for the flaps covering the active site, likely contribute to the thermodynamic compensation. The finding that drug-resistant mutations can profoundly modulate the relative thermodynamic properties of a therapeutic target independent of the inhibitor presents a new challenge for rational drug design.

Essential Role of the Redox-Sensitive Kinase p66shcin Determining Energetic and Oxidative Status and Cell Fate in Neuronal Preconditioning

Ischemic preconditioning is a phenomenon in which low-level stressful stimuli upregulate endogenous defensive programs, resulting in subsequent resistance to otherwise lethal injuries. We previously observed that signal transduction systems typically associated with neurodegeneration such as caspase activation are requisite events for the expression of tolerance and induction of HSP70. In this work, we sought to determine the extent and duration of oxidative and energetic dysfunction as well as the role of effector kinases on metabolic function in preconditioned cells. Using an in vitro neuronal culture model, we observed a robust increase in Raf and p66(Shc) activation within 1 h of preconditioning. Total ATP content decreased by 25% 3 h after preconditioning but returned to baseline by 24 h. Use of a free radical spin trap or p66(shc) inhibitor increased ATP content whereas a Raf inhibitor had no effect. Phosphorylated p66(shc) rapidly relocalized to the mitochondria and in the absence of activated p66(shc), autophagic processing increased. The constitutively expressed chaperone HSC70 relocalized to autophagosomes. Preconditioned cells experience significant total oxidative stress measured by F(2)-isoprostanes and neuronal stress evaluated by F(4)-neuroprostane measurement. Neuroprostane levels were enhanced in the presence of Shc inhibitors. Finally, we found that inhibiting either p66(shc) or Raf blocked neuroprotection afforded by preconditioning as well as upregulation of HSP70, suggesting both kinases are critical for preconditioning but function in fundamentally different ways. This is the first work to demonstrate the essential role of p66(shc) in mediating requisite mitochondrial and energetic compensation after preconditioning and suggests a mechanism by which protein and organelle damage mediated by ROS can increase HSP70.

Treatment of human astrocytoma U87 cells with silicon dioxide nanoparticles lowers their survival and alters their expression of mitochondrial and cell signaling proteins

Recent evidence suggests silicon dioxide micro- and nanoparticles induce cytotoxic effects on lung cells. Thus, there is an increasing concern regarding their potential health hazard. Nevertheless, the putative toxicity of nanoparticles in mammalian cells has not yet been systematically investigated. We previously noted that several metallic oxide nanoparticles exert differential cytotoxic effects on human neural and nonneural cells. Therefore, we hypothesized that silicon dioxide nanoparticles induce cytotoxicity in U87 cells by lowering their survival by decreasing cell survival signaling and disturbing mitochondrial function. To investigate this hypothesis, we determined the activities of the key mitochondrial enzymes, citrate synthase and malate dehydrogenase, in astrocytoma U87 cells treated with silicon dioxide nanoparticles. In addition, we studied the expression of the mitochondrial DNA-encoded proteins, cytochrome C oxidase II and nicotinamide adenine dinucleotide (NADPH) dehydrogenase subunit 6, and cell signaling pathway protein extracellular signal-regulated kinase (ERK) and phosphorylated ERK in treated U87 cells. The activated form of ERK controls cell growth, differentiation, and proliferation. In parallel, we determined survival of U87 cells after treating them with various concentrations of silicon dioxide nanoparticles. Our results indicated that treatment with silicon dioxide nanoparticles induced decreases in U87 cell survival in a dose-related manner. The activities of citrate synthase and malate dehydrogenase in treated U87 cells were increased, possibly due to an energetic compensation in surviving cells. However, the expression of mitochondrial DNA-encoded cytochrome C oxidase subunit II and NADH dehydrogenase subunit 6 and the cell signaling protein ERK and phosphorylated ERK were altered in the treated U87 cells, suggesting that silicon dioxide nanoparticles induced disruption of mitochondrial DNA-encoded protein expression, leading to decreased mitochondrial energy production and decreased cell survival/proliferation signaling. Thus, our results strongly suggest that the cytotoxicity of silicon dioxide nanoparticles in human neural cells implicates altered mitochondrial function and cell survival/proliferation signaling.

Pressure dissociation of integration host factor-DNA complexes reveals flexibility-dependent structural variation at the protein-DNA interface

E. coli Integration host factor (IHF) condenses the bacterial nucleoid by wrapping DNA. Previously, we showed that DNA flexibility compensates for structural characteristics of the four consensus recognition elements associated with specific binding (Aeling et al., J. Biol. Chem. 281, 39236–39248, 2006). If elements are missing, high-affinity binding occurs only if DNA deformation energy is low. In contrast, if all elements are present, net binding energy is unaffected by deformation energy. We tested two hypotheses for this observation: in complexes containing all elements, (1) stiff DNA sequences are less bent upon binding IHF than flexible ones; or (2) DNA sequences with differing flexibility have interactions with IHF that compensate for unfavorable deformation energy. Time-resolved Förster resonance energy transfer (FRET) shows that global topologies are indistinguishable for three complexes with oligonucleotides of different flexibility. However, pressure perturbation shows that the volume change upon binding is smaller with increasing flexibility. We interpret these results in the context of Record and coworker's model for IHF binding (J. Mol. Biol. 310, 379–401, 2001). We propose that the volume changes reflect differences in hydration that arise from structural variation at IHF–DNA interfaces while the resulting energetic compensation maintains the same net binding energy.

Co-adsorption of water and hydroxyl on a Pt 2Ru surface

Gradient-corrected periodic density functional theory calculations are performed to explain the mobility of surface-bonded hydroxyl on a Pt 2Ru(1 1 1) surface in the presence of co-adsorbed water, as recently observed by Desai and Neurock [S.K. Desai, M. Neurock, Phys. Rev. B 68 (2003) 075420] in ab initio molecular dynamics calculations. The effect can to a large extent be explained by an energetic compensation effect: the loss in energy associated with transferring OH from a Ru site to a Pt site is compensated by a gain in energy with the associated transfer of H 2O from the Pt to the Ru site. The calculated property of the Pt 2Ru(1 1 1) surface would support the OH spillover mechanism suggested by Davies et al. [J.C. Davies, B.E. Hayden, D.J. Pegg, M.E. Rendall, Surf. Sci. 496 (2002) 110], at least in as far as it concerns OH spillover to Pt site neighboring a Ru site, and provides new insight into the classical bifunctional mechanism of CO electro-oxidation.

Is the antipredatory response in behaviour reflected in stress measured in faecal corticosteroids in a small rodent?

Predation risk has been shown to alter various behaviours in prey. Risk alters activity, habitat use and foraging, and weight decrease might be a consequence of that. In mammals, studies on physiological measures affected by risk of predation, other than weight, are rare. We studied in two separate laboratory experiments foraging, hoarding behaviour and expression of stress measured non-invasively from the faeces in the bank vole (Clethrionomys glareolus), a common boreal rodent. Voles were exposed to predation risk using odours of the least weasels (Mustela nivalis nivalis). Distilled water served as control. In the first experiment, we found that foraging effort, measured as sunflower seeds taken from seed trays filled with sand, was significantly lower in trays scented with weasel odour. Both immediate consumption of seeds and hoarding were affected negatively by the weasel odour. Females hoarded significantly more than males in autumn. In the second experiment, the negative effect of weasel odour on foraging was consistent over a 3-day experiment, but the strongest effect was observed in the first night. Foraging increased over the time of the experiment, which might reflect either energetic compensation during a longer period of risk, predicted in the predation risk allocation hypothesis, or habituation to the odour-simulated risk. Despite decreased foraging under predation risk, stress measured as corticosteroid metabolite concentration in vole faeces was not affected by the weasel odour treatment. In conclusion, we were able to verify predation-risk-mediated changes in the foraging effort of bank voles but no physiological stress response was measured non-invasively, probably due to great individual variation in secretion of stress hormones.

Energy balance and reproductive function in active women.

Athletes engaged in rigorous training programs expend large amounts of energy and require appropriate energetic compensation to maintain or improve performance. If these exercise regimens are not fueled sufficiently, a negative energy balance will likely emerge and lead to a broad spectrum of menstrual cycle disturbances and less than optimal performance. This review examines the theory and evidence surrounding energy availability and reproductive function. Implications for performance and treatment strategies are also addressed.

Meeting the energy demands of reproduction in female koalas, Phascolarctos cinereus: evidence for energetic compensation.

Koalas are generally considered to be limited by their ability to acquire energy from their diet of Eucalyptus foliage and have the lowest mass-specific peak lactational energy output measured in any mammal to date. This study considered the energetics and sources of energy utilised for reproduction in free-ranging female koalas. Energy requirements and foliage intake were greater in both lactating and non-lactating females in winter than summer, presumably due to demands of thermoregulation. Koalas met the peak energy requirements of lactation primarily by a 36% increase in their intake of foliage. Metabolic energy expenditure (field metabolic rate, 1778 kJ.day(-1) for a 6.25-kg female at the time of peak lactation) was not elevated during lactation. This was due to compensation for part of their lactational demands by reduction of another, non-reproductive, component of their energy budget. The observed energetic compensation was probably due primarily to substitution of the waste heat from the metabolic costs of milk production and increased heat increment of feeding for thermoregulatory energy expenditure. There may also have been energetic compensation by reduction of some aspect of maintenance metabolism. Such energetic compensation, together with the strategy of spreading lactation over a long period, minimises the magnitude of lactational energy demands on koalas, and thus the increase in daily food intake required during lactation. As the nutritional requirements of females at peak lactation are the highest of any members of the population, low reproductive requirements effectively increase the types and amount of habitat able to support koala populations.