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255 results for “metabolic dependency”
Mechanisms of the Nicotine Metabolism Effect on Tobacco Dependence
ClinicalTrials.gov study NCT01627392. IPD Sharing: Not stated. Countries: 1. Publications: 2.
Endotoxin & Cytokines. Do Protein Loss and Metabolic Effects Depend on Central Nervous System (CNS) Activation of Stress Hormones or on Local Mechanisms in Muscle and Fat?
ClinicalTrials.gov study NCT01452958. IPD Sharing: Not stated. Countries: 1. Publications: 1.
CARNIVAL Study: Gut Flora Dependent Metabolism of Dietary CARNItine and Phosphatidylcholine and cardioVAscuLar Disease
ClinicalTrials.gov study NCT01731236. IPD Sharing: NO. Countries: 1. Publications: 1.
L-arginine Therapy on Endothelium-dependent Vasodilation & Mitochondrial Metabolism in MELAS Syndrome
ClinicalTrials.gov study NCT01603446. IPD Sharing: Not stated. Countries: 1. Publications: 2.
Data from: The metabolic costs of sexual signalling in the chirping katydid Plangia graminea (Serville) (Orthoptera: Tettigoniidae) are context dependent: cumulative costs add up fast
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Data from: Energy demand and the context-dependent effects of genetic interactions underlying metabolism
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Metabolic rate, context-dependent selection, and the competition-colonization trade-off
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Data from: Habitat, latitude, and body mass influence the temperature dependence of metabolic rate
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Data from: Identification of glucose kinase dependent and independent pathways for carbon control of primary metabolism, development and antibiotic production in Streptomyces coelicolor by quantitative proteomics
Members of the soil-dwelling prokaryotic genus Streptomyces are indispensable for the recycling of complex polysaccharides, and produce a wide range of natural products. Nutrient availability is a major determinant for the switch to development and antibiotic production in streptomycetes. Carbon catabolite repression (CCR), a main signaling pathway underlying this phenomenon, was so far considered fully dependent on the glycolytic enzyme glucose kinase (Glk). Here we provide evidence of a novel Glk-independent pathway in Streptomyces coelicolor, using advanced proteomics that allowed the comparison of the expression of some 2,000 proteins, including virtually all enzymes for central metabolism. While CCR and inducer exclusion of enzymes for primary and secondary metabolism and precursor supply for natural products is mostly mediated via Glk, enzymes for the urea cycle, as well as for biosynthesis of the γ-butyrolactone Scb1 and the responsive cryptic polyketide Cpk are subject to Glk-independent CCR. Deletion of glkA led to strong downregulation of biosynthetic proteins for prodigionin and calcium-dependent antibiotic (CDA) in mannitol-grown cultures. Repression of bldB, bldN, and its target bldM explains the poor development of S. coelicolor on solid-grown cultures containing glucose. A new model for carbon catabolite repression in streptomycetes is presented.
Data from: Can variation in standard metabolic rate explain context-dependent performance of farmed salmon offspring?
Escaped farmed Atlantic salmon interbreed with wild Atlantic salmon, leaving offspring that often have lower success in nature than pure wild salmon. On top of this, presence of farmed salmon descendants can impair production of wild type recruits. We hypothesize that both these effects connect with farmed salmon having acquired higher standard metabolic rates (SMR, the energetic cost of self-maintenance) during domestication. Furthermore, fitness related advantages of phenotypic traits associated with both high SMR and farmed salmon (e.g. social dominance) depend on environmental conditions, such as food availability. We hypothesize that farmed offspring have an advantage at high food availability due to e.g. dominance behavior but suffer increased risks of starvation when food is scarce because this behavior is energy-demanding. To test these hypotheses, we first compare embryo SMR of pure farmed, farmed-wild hybrids and pure wild offspring. Next, we test early life performance (in terms of survival and growth) of hybrids relative to that of their wild half-siblings, as well as their competitive abilities, in semi-natural conditions of high and low food availability. Finally, we test how SMR affects early life performance at high and low food availability. We find inconclusive support for the hypothesis that domestication has induced increased SMR. Further, wild and hybrid juveniles had similar survival and growth in the semi-natural streams. Yet, the presence of hybrids led to decreased survival of their wild half-siblings. Contrary to our hypothesis about context-dependency, these effects were not modified by food availability. However, wild juveniles with high SMR had decreased survival when food was scarce, but there was no such effect at high food availability. This study provides further proof that farmed salmon introgression may compromise the viability of wild salmon populations. We cannot, however, conclude that this is connected to alterations in the metabolic phenotype of farmed salmon.
Data from: Experimental evolution of metabolic dependency in bacteria
Bacteria frequently lose biosynthetic genes, thus making them dependent on an environmental uptake of the corresponding metabolite. Despite the ubiquity of this 'genome streamlining', it is generally unclear whether the concomitant loss of biosynthetic functions is favored by natural selection or rather caused by random genetic drift. Here we demonstrate experimentally that a loss of metabolic functions is strongly selected for when the corresponding metabolites can be derived from the environment. Serially propagating replicate populations of the bacterium Escherichia coli in amino acid-containing environments revealed that auxotrophic genotypes rapidly evolved in less than 2,000 generations in almost all replicate populations. Moreover, auxotrophs also evolved in environments lacking amino acids - yet to a much lesser extent. Loss of these biosynthetic functions was due to mutations in both structural and regulatory genes. In competition experiments performed in the presence of amino acids, auxotrophic mutants gained a significant fitness advantage over the evolutionary ancestor, suggesting their emergence was selectively favored. Interestingly, auxotrophic mutants derived amino acids not only via an environmental uptake, but also by cross-feeding from coexisting strains. Our results show that adaptive fitness benefits can favor biosynthetic loss-of-function mutants and drive the establishment of intricate metabolic interactions within microbial communities.
Data from: Evolution of size-dependent intraspecific competition predicts body size scaling of metabolic rate
1. Growth in body size is accompanied by changes in foraging capacity and metabolic costs, which lead to changes in competitive ability during ontogeny. The resulting size-dependent competitive asymmetry influences population dynamics and community structure, but it is not clear whether natural selection leads to asymmetry in intraspecific competition. 2. We address this question by using a size-structured consumer-resource model, in which the strength and direction of competitive asymmetry between different consumer individuals depends on the scaling of maximum ingestion and maintenance metabolism with consumer body size. We use adaptive dynamics to study selection on the scaling exponents of these processes. 3. Selection leads to an identical scaling of maximum ingestion and maintenance metabolism with consumer body size. Equal scaling exponents neutralise strong competitive differences within the consumer population, because all consumer individuals require the same amount of resources to cover maintenance requirements. Furthermore, the scaling exponents respond adaptively to changes in mortality such that biomass production through growth or reproduction increases in the life stage that is subject to increased mortality. Also, decreasing size at birth leads to increased investment in juvenile growth, while increasing maximum size leads to increased investment in post-maturation growth and reproduction. 4. These results provide an explanation for observed variation in the ontogenetic scaling of metabolic rate with body size. Data of teleost fish are presented that support these predictions. However, selection towards equal scaling exponents is contradicted by empirical findings, which suggests that additional ecological complexity beyond this basic consumer-resource interaction is required to understand the evolution of size-dependent asymmetry in intraspecific competition.
Deep learning reveals the metabolic dependency of hypoxic tumor cells and the critical function of FLAD1 mediated mitochondrial metabolic reprogramming
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Data from: Can variation in standard metabolic rate explain context-dependent performance of farmed salmon offspring?
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Data from: Evolution of size-dependent intraspecific competition predicts body size scaling of metabolic rate
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Data from: Identification of glucose kinase dependent and independent pathways for carbon control of primary metabolism, development and antibiotic production in Streptomyces coelicolor by quantitative proteomics
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Data from: Predicting the thermal and allometric dependencies of disease transmission via the metabolic theory of ecology
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Data from: Experimental evolution of metabolic dependency in bacteria
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Data from: Metabolic theory and the temperature-size rule explain the temperature dependence of population carrying capacity
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Redox state and altered pyruvate metabolism contribute to a dose-dependent metformin-induced lactate production of human myotubes
GEO Series GSE229658. Homo sapiens. 60 samples. Type: Expression profiling by high throughput sequencing.
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