No Arabic abstract
The received wisdom on how activity affects energy expenditure is that the more activity is undertaken, the more calories will have been burned by the end of the day. Yet traditional hunter-gatherers, who lead physically hard lives, burn no more calories each day than western populations living in labour-saving environments. Indeed, there is now a wealth of data, both for humans and other animals, demonstrating that long-term lifestyle changes involving increases in exercise or other physical activities do not result in commensurate increases in daily energy expenditure (DEE). This is because humans and other animals exhibit a degree of energy compensation at the organismal level, ameliorating some of the increases in DEE that would occur from the increased activity by decreasing the energy expended on other biological processes. And energy compensation can be sizable, reaching many hundreds of calories in humans. But the processes that are downregulated in the long-term to achieve energy compensation are far from clear, particularly in humans. We do not know how energy compensation is achieved. My review here of the literature on relevant exercise intervention studies, for both humans and other species, indicates conflict regarding the role that basal metabolic rate (BMR) or low level activity such as fidgeting play, if any, particularly once changes in body composition are factored out. In situations where BMR and low-level activity are not major components of energy compensation, what then drives it? I discuss how changes in mitochondrial efficiency and changes in circadian fluctuations in BMR may contribute to our understanding of energy management. Currently unexplored, these mechanisms and others may provide important insights into the mystery of how energy compensation is achieved.
Metabolic energy consumption has long been thought to play a major role in the aging process ({it 1}). Across species, a gram of tissue on average expends about the same amount of energy during life-span ({it 2}). Energy restriction has also been shown that increases maximum life-span ({it 3}) and retards age-associated changes ({it 4}). However, there are significant exceptions to a universal energy consumption during life-span, mainly coming from the inter-class comparison ({it 5, 6}). Here we present a unique relation for life-span energy consumption, valid for $sim$300 species representing all classes of living organisms, from unicellular ones to the largest mammals. The relation has an average scatter of only 0.3 dex, with 95% ($rm 2-sigma$) of the organisms having departures less than a factor of $pi$ from the relation, despite the $sim$20 orders of magnitude difference in body mass, reducing any possible inter-class variation in the relation to only a geometrical factor. This result can be interpreted as supporting evidence for the existence of an approximately constant total number $rm N_r sim 10^8$ of respiration cycles per lifetime for all organisms, effectively predetermining the extension of life by the basic energetics of respiration, being an incentive for future studies that investigate the relation of such constant $rm N_r$ cycles per lifetime with the production rates of free radicals and oxidants, which may give definite constraints on the origin of ageing.
A system-level framework of complex microbe-microbe and host-microbe chemical cross-talk would help elucidate the role of our gut microbiota in health and disease. Here we report a literature-curated interspecies network of the human gut microbiota, called NJS16. This is an extensive data resource composed of ~570 microbial species and 3 human cell types metabolically interacting through >4,400 small-molecule transport and macromolecule degradation events. Based on the contents of our network, we develop a mathematical approach to elucidate representative microbial and metabolic features of the gut microbial community in a given population, such as a disease cohort. Applying this strategy to microbiome data from type 2 diabetes patients reveals a context-specific infrastructure of the gut microbial ecosystem, core microbial entities with large metabolic influence, and frequently-produced metabolic compounds that might indicate relevant community metabolic processes. Our network presents a foundation towards integrative investigations of community-scale microbial activities within the human gut.
Circadian clocks ubiquitous in life forms ranging bacteria to multi-cellular organisms, often exhibit intrinsic temperature compensation; the period of circadian oscillators is maintained constant over a range of physiological temperatures, despite the expected Arrhenius form for the reaction coefficient. Observations have shown that the amplitude of the oscillation depends on the temperature but the period does not---this suggests that although not every reaction step is temperature independent, the total system comprising several reactions still exhibits compensation. We present a general mechanism for such temperature compensation. Consider a system with multiple activation energy barriers for reactions, with a common enzyme shared across several reaction steps with a higher activation energy. These reaction steps rate-limit the cycle if the temperature is not high. If the total abundance of the enzyme is limited, the amount of free enzyme available to catalyze a specific reaction decreases as more substrates bind to common enzyme. We show that this change in free enzyme abundance compensate for the Arrhenius-type temperature dependence of the reaction coefficient. Taking the example of circadian clocks with cyanobacterial proteins KaiABC consisting of several phosphorylation sites, we show that this temperature compensation mechanisms is indeed valid. Specifically, if the activation energy for phosphorylation is larger than that for dephosphorylation, competition for KaiA shared among the phosphorylation reactions leads to temperature compensation. Moreover, taking a simpler model, we demonstrate the generality of the proposed compensation mechanism, suggesting relevance not only to circadian clocks but to other (bio)chemical oscillators as well.
An active microbiota, reaching up to 10 E+7 cells/g, was found to inhabit a naturally occurring asphalt lake characterized by low water activity and elevated temperature. Geochemical and molecular taxonomic approaches revealed novel and deeply branching microbial assemblages mediating anaerobic hydrocarbon degradation, metal respiration and C1 utilization pathways. These results open a window into the origin and adaptive evolution of microbial life within recalcitrant hydrocarbon matrices, and establish the site as a useful analog for the liquid hydrocarbon environments on Saturns moon Titan.
The phenotype of any organism on earth is, in large part, the consequence of interplay between numerous gene products encoded in the genome, and such interplay between gene products affects the evolutionary fate of the genome itself through the resulting phenotype. In this regard, contemporary genomes can be used as molecular records that reveal associations of various genes working in their natural lifestyles. By analyzing thousands of orthologs across ~600 bacterial species, we constructed a map of gene-gene co-occurrence across much of the sequenced biome. If genes preferentially co-occur in the same organisms, they were called herein correlogs; in the opposite case, called anti-correlogs. To quantify correlogy and anti-correlogy, we alleviated the contribution of indirect correlations between genes by adapting ideas developed for reverse engineering of transcriptional regulatory networks. Resultant correlogous associations are highly enriched for physically interacting proteins and for co-expressed transcripts, clearly differentiating a subgroup of functionally-obligatory protein interactions from conditional or transient interactions. Other biochemical and phylogenetic properties were also found to be reflected in correlogous and anti-correlogous relationships. Additionally, our study elucidates the global organization of the gene association map, in which various modules of correlogous genes are strikingly interconnected by anti-correlogous crosstalk between the modules. We then demonstrate the effectiveness of such associations along different domains of life and environmental microbial communities. These phylogenetic profiling approaches infer functional coupling of genes regardless of mechanistic details, and may be useful to guide exogenous gene import in synthetic biology.