Articles de revues : « Metabolic circuitsk »

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STERLING, PETER, et MICHAEL FREED. « How robust is a neural circuit ? » Visual Neuroscience 24, n^o 4 (juillet 2007) : 563–71. http://dx.doi.org/10.1017/s0952523807070526.

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Design in engineering begins with the problem of robustness—by what factor should intrinsic capacity exceed normal demand? Here we consider robustness for a neural circuit that crosses the retina from cones to ganglion cells. The circuit's task is to represent the visual scene at many successive stages, each time by modulating a stream of stochastic events: photoisomerizations, then transmitter quanta, then spikes. At early stages, the event rates are high to achieve some critical signal-to-noise ratio and temporal bandwidth, which together set the information rate. Then neural circuits concentrate the information and repackage it, so that nearly the same total information can be represented by modulating far lower event rates. This is important for spiking because of its high metabolic cost. Considering various measurements at the outer and inner retina, we conclude that the “safety factors” are about 2–10, similar to other tissues.

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Sun, Zhi, Weijia Wei, Mingyue Zhang, Wenjia Shi, Yeqing Zong, Yihua Chen, Xiaojing Yang, Bo Yu, Chao Tang et Chunbo Lou. « Synthetic robust perfect adaptation achieved by negative feedback coupling with linear weak positive feedback ». Nucleic Acids Research 50, n^o 4 (15 février 2022) : 2377–86. http://dx.doi.org/10.1093/nar/gkac066.

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Abstract Unlike their natural counterparts, synthetic genetic circuits are usually fragile in the face of environmental perturbations and genetic mutations. Several theoretical robust genetic circuits have been designed, but their performance under real-world conditions has not yet been carefully evaluated. Here, we designed and synthesized a new robust perfect adaptation circuit composed of two-node negative feedback coupling with linear positive feedback on the buffer node. As a key feature, the linear positive feedback was fine-tuned to evaluate its necessity. We found that the desired function was robustly achieved when genetic parameters were varied by systematically perturbing all interacting parts within the topology, and the necessity of the completeness of the topological structures was evaluated by destroying key circuit features. Furthermore, different environmental perturbances were imposed onto the circuit by changing growth rates, carbon metabolic strategies and even chassis cells, and the designed perfect adaptation function was still achieved under all conditions. The successful design of a robust perfect adaptation circuit indicated that the top-down design strategy is capable of predictably guiding bottom-up engineering for robust genetic circuits. This robust adaptation circuit could be integrated as a motif into more complex circuits to robustly implement more sophisticated and critical biological functions.

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Ni, Cynthia, Christina V. Dinh et Kristala L. J. Prather. « Dynamic Control of Metabolism ». Annual Review of Chemical and Biomolecular Engineering 12, n^o 1 (7 juin 2021) : 519–41. http://dx.doi.org/10.1146/annurev-chembioeng-091720-125738.

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Metabolic engineering reprograms cells to synthesize value-added products. In doing so, endogenous genes are altered and heterologous genes can be introduced to achieve the necessary enzymatic reactions. Dynamic regulation of metabolic flux is a powerful control scheme to alleviate and overcome the competing cellular objectives that arise from the introduction of these production pathways. This review explores dynamic regulation strategies that have demonstrated significant production benefits by targeting the metabolic node corresponding to a specific challenge. We summarize the stimulus-responsive control circuits employed in these strategies that determine the criterion for actuating a dynamic response and then examine the points of control that couple the stimulus-responsive circuit to a shift in metabolic flux.

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Oyarzún, Diego A., et Madalena Chaves. « Design of a bistable switch to control cellular uptake ». Journal of The Royal Society Interface 12, n^o 113 (décembre 2015) : 20150618. http://dx.doi.org/10.1098/rsif.2015.0618.

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Bistable switches are widely used in synthetic biology to trigger cellular functions in response to environmental signals. All bistable switches developed so far, however, control the expression of target genes without access to other layers of the cellular machinery. Here, we propose a bistable switch to control the rate at which cells take up a metabolite from the environment. An uptake switch provides a new interface to command metabolic activity from the extracellular space and has great potential as a building block in more complex circuits that coordinate pathway activity across cell cultures, allocate metabolic tasks among different strains or require cell-to-cell communication with metabolic signals. Inspired by uptake systems found in nature, we propose to couple metabolite import and utilization with a genetic circuit under feedback regulation. Using mathematical models and analysis, we determined the circuit architectures that produce bistability and obtained their design space for bistability in terms of experimentally tuneable parameters. We found an activation–repression architecture to be the most robust switch because it displays bistability for the largest range of design parameters and requires little fine-tuning of the promoters' response curves. Our analytic results are based on on–off approximations of promoter activity and are in excellent qualitative agreement with simulations of more realistic models. With further analysis and simulation, we established conditions to maximize the parameter design space and to produce bimodal phenotypes via hysteresis and cell-to-cell variability. Our results highlight how mathematical analysis can drive the discovery of new circuits for synthetic biology, as the proposed circuit has all the hallmarks of a toggle switch and stands as a promising design to control metabolic phenotypes across cell cultures.

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Sen, A. K. « Application of electrical analogues for control analysis of simple metabolic pathways ». Biochemical Journal 272, n^o 1 (15 novembre 1990) : 65–70. http://dx.doi.org/10.1042/bj2720065.

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I have used electrical analogues for calculating the Flux Control Coefficients of metabolic pathways. An analogue circuit consists of resistances that are connected in series (or parallel) with a voltage (or current) source. In constructing the analogues, each of the enzymes in the pathway is associated with a resistance whose magnitude depends on the Elasticity Coefficients of the enzymes. These circuits can be designed in a heuristic fashion directly from the configuration of the pathway, without the necessity of writing down the governing equations with the use of Summation and Connectivity Theorems. The Flux Control Coefficients of the enzymes are represented by voltages across (or currents through) the resistances and are determined by an application of Ohm's Law. Results are given for (a) a simple linear pathway without feedback or feedforward regulation, and (b) a linear pathway with feedback inhibition. The analogue circuits are also convenient for assessing the relative importance of the various enzymes in flux control, and for simplifying the structure of a given pathway.

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Oyarzún, Diego A., et Guy-Bart V. Stan. « Synthetic gene circuits for metabolic control : design trade-offs and constraints ». Journal of The Royal Society Interface 10, n^o 78 (6 janvier 2013) : 20120671. http://dx.doi.org/10.1098/rsif.2012.0671.

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A grand challenge in synthetic biology is to push the design of biomolecular circuits from purely genetic constructs towards systems that interface different levels of the cellular machinery, including signalling networks and metabolic pathways. In this paper, we focus on a genetic circuit for feedback regulation of unbranched metabolic pathways. The objective of this feedback system is to dampen the effect of flux perturbations caused by changes in cellular demands or by engineered pathways consuming metabolic intermediates. We consider a mathematical model for a control circuit with an operon architecture, whereby the expression of all pathway enzymes is transcriptionally repressed by the metabolic product. We address the existence and stability of the steady state, the dynamic response of the network under perturbations, and their dependence on common tuneable knobs such as the promoter characteristic and ribosome binding site (RBS) strengths. Our analysis reveals trade-offs between the steady state of the enzymes and the intermediates, together with a separation principle between promoter and RBS design. We show that enzymatic saturation imposes limits on the parameter design space, which must be satisfied to prevent metabolite accumulation and guarantee the stability of the network. The use of promoters with a broad dynamic range and a small leaky expression enlarges the design space. Simulation results with realistic parameter values also suggest that the control circuit can effectively upregulate enzyme production to compensate flux perturbations.

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Gao, Fei, Lijun Qi, Zhongzhen Yang, Tao Yang, Yan Zhang, Hui Xu et Huan Zhao. « Impaired GABA Neural Circuits Are Critical for Fragile X Syndrome ». Neural Plasticity 2018 (3 octobre 2018) : 1–7. http://dx.doi.org/10.1155/2018/8423420.

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Fragile X syndrome (FXS) is an inheritable neuropsychological disease caused by silence of the fmr1 gene and the deficiency of Fragile X mental retardation protein (FMRP). Patients present neuronal alterations that lead to severe intellectual disability and altered sleep rhythms. However, the neural circuit mechanisms underlying FXS remain unclear. Previous studies have suggested that metabolic glutamate and gamma-aminobutyric acid (GABA) receptors/circuits are two counter-balanced factors involved in FXS pathophysiology. More and more studies demonstrated that attenuated GABAergic circuits in the absence of FMRP are critical for abnormal progression of FXS. Here, we reviewed the changes of GABA neural circuits that were attributed to intellectual-deficient FXS, from several aspects including deregulated GABA metabolism, decreased expressions of GABA receptor subunits, and impaired GABAergic neural circuits. Furthermore, the activities of GABA neural circuits are modulated by circadian rhythm of FMRP metabolism and reviewed the abnormal condition of FXS mice or patients.

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Heath, Vicky. « Altered neuronal circuits control metabolic fate ». Nature Reviews Endocrinology 10, n^o 4 (11 février 2014) : 190. http://dx.doi.org/10.1038/nrendo.2014.14.

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Narayanan, Nandakumar S., Douglas J. Guarnieri et Ralph J. DiLeone. « Metabolic hormones, dopamine circuits, and feeding ». Frontiers in Neuroendocrinology 31, n^o 1 (janvier 2010) : 104–12. http://dx.doi.org/10.1016/j.yfrne.2009.10.004.

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Kim, Do-Yeon, Inmoo Rhee et Jihye Paik. « Metabolic circuits in neural stem cells ». Cellular and Molecular Life Sciences 71, n^o 21 (19 juillet 2014) : 4221–41. http://dx.doi.org/10.1007/s00018-014-1686-0.

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Taneja, Charit, Sakshi Gera, Se-Min Kim, Jameel Iqbal, Tony Yuen et Mone Zaidi. « FSH-metabolic circuitry and menopause ». Journal of Molecular Endocrinology 63, n^o 3 (octobre 2019) : R73—R80. http://dx.doi.org/10.1530/jme-19-0152.

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FSH has a primary function in procreation, wherein it induces estrogen production in females and regulates spermatogenesis in males. However, in line with our discoveries over the past decade of non-unitary functions of pituitary hormones, we and others have described hitherto uncharacterized functions of FSH. Through high-affinity receptors, some of which are variants of the ovarian FSH receptor (FSHR), FSH regulates bone mass, adipose tissue function, energy metabolism, and cholesterol production in both sexes. These newly described actions of FSH may indeed be relevant to the pathogenesis of bone loss, dysregulated energy homeostasis, and disordered lipid metabolism that accompany the menopause in females and aging in both genders. We are therefore excited about the possibility of modulating circulating FSH levels toward a therapeutic benefit for a host of age-associated diseases, including osteoporosis, obesity and dyslipidemia, among other future possibilities.

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Elson, Amanda E., et Richard B. Simerly. « Developmental specification of metabolic circuitry ». Frontiers in Neuroendocrinology 39 (octobre 2015) : 38–51. http://dx.doi.org/10.1016/j.yfrne.2015.09.003.

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Dietrich, W. Dalton, Myron D. Ginsberg et Raul Busto. « Effect of Transient Cerebral Ischemia on Metabolic Activation of a Somatosensory Circuit ». Journal of Cerebral Blood Flow & ; Metabolism 6, n^o 4 (août 1986) : 405–13. http://dx.doi.org/10.1038/jcbfm.1986.73.

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The effects of transient ischemia on the metabolic responsiveness of a well-defined brain circuit were investigated with [14C]2-deoxyglucose autoradiography. Rats underwent 30 min of severe forebrain ischemia followed by postischemic recirculation periods of 1, 2, 3, 5, and 10 days. At these times, unilateral whisker stimulation was carried out, resulting in the metabolic activation of the whisker barrel circuit. An altered pattern of glucose utilization within both stimulated and nonstimulated circuit relay stations was observed at 1, 2, and 3 days following ischemia. At 1 day, stimulus-evoked increases in metabolic activity were severely depressed within both the ventrobasal thalamus and layer IV of the cortical barrel field region. Baseline metabolic rate within nonstimulated relay areas was also severely depressed at this time. At postischemic days 2 and 3, moderate levels of increased glucose utilization were apparent overlying cortical layer IV and the superficial half of layer VI, while layers I, II, III, and V appeared less responsive to metabolic activation. By day 5, whisker stimulation resulted in normal levels of increased glucose utilization within the activated ventrobasal thalamus and layer IV of the cortical barrel field region. Glucose utilization within nonactivated relay stations, depressed at earlier time periods, had also returned to control levels by day 5. At both 5 and 10 days, an altered laminar pattern of elevated glucose utilization was apparent within the activated barrel field region, with local CMRglu being depressed in layer V compared with control values. These results demonstrate that periods of transient ischemia produce both reversible and longer-lasting effects on the ability of the CNS to respond to peripheral activation. Functional restitution occurs slowly over a period of days following ischemia and appears to be related to the postischemic baseline level of metabolic rate. Finally, the abnormal laminar pattern of cortical activation apparent at postischemic day 10 may suggest dysfunction of intracortical circuits, a result that might be expected to alter the processing of sensory information.

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Carbonell, Pablo, Pierre Parutto, Claire Baudier, Christophe Junot et Jean-Loup Faulon. « Retropath : Automated Pipeline for Embedded Metabolic Circuits ». ACS Synthetic Biology 3, n^o 8 (16 octobre 2013) : 565–77. http://dx.doi.org/10.1021/sb4001273.

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Wang, Kui, Jingwen Jiang, Yunlong Lei, Shengtao Zhou, Yuquan Wei et Canhua Huang. « Targeting Metabolic–Redox Circuits for Cancer Therapy ». Trends in Biochemical Sciences 44, n^o 5 (mai 2019) : 401–14. http://dx.doi.org/10.1016/j.tibs.2019.01.001.

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Zhang, Fuzhong. « Special Issue on Circuits in Metabolic Engineering ». ACS Synthetic Biology 4, n^o 2 (20 février 2015) : 93–94. http://dx.doi.org/10.1021/acssynbio.5b00021.

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Barger, Natalia, Phyana Litovco, Ximing Li, Mouna Habib et Ramez Daniel. « Synthetic metabolic computation in a bioluminescence-sensing system ». Nucleic Acids Research 47, n^o 19 (23 septembre 2019) : 10464–74. http://dx.doi.org/10.1093/nar/gkz807.

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Abstract Bioluminescence is visible light produced and emitted by living cells using various biological systems (e.g. luxCDABE cassette). Today, this phenomenon is widely exploited in biological research, biotechnology and medical applications as a quantitative technique for the detection of biological signals. However, this technique has mostly been used to detect a single input only. In this work, we re-engineered the complex genetic structure of luxCDABE cassette to build a biological unit that can detect multi-inputs, process the cellular information and report the computation results. We first split the luxCDABE operon into several parts to create a genetic circuit that can compute a soft minimum in living cells. Then, we used the new design to implement an AND logic function with better performance as compared to AND logic functions based on protein-protein interactions. Furthermore, by controlling the reverse reaction of the luxCDABE cassette independently from the forward reaction, we built a comparator with a programmable detection threshold. Finally, we applied the redesigned cassette to build an incoherent feedforward loop that reduced the unwanted crosstalk between stress-responsive promoters (recA, katG). This work demonstrates the construction of genetic circuits that combine regulations of gene expression with metabolic pathways, for sensing and computing in living cells.

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Smith, Jeffrey C., Ana P. L. Abdala, Ilya A. Rybak et Julian F. R. Paton. « Structural and functional architecture of respiratory networks in the mammalian brainstem ». Philosophical Transactions of the Royal Society B : Biological Sciences 364, n^o 1529 (12 septembre 2009) : 2577–87. http://dx.doi.org/10.1098/rstb.2009.0081.

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Neural circuits controlling breathing in mammals are organized within serially arrayed and functionally interacting brainstem compartments extending from the pons to the lower medulla. The core circuit components that constitute the neural machinery for generating respiratory rhythm and shaping inspiratory and expiratory motor patterns are distributed among three adjacent structural compartments in the ventrolateral medulla: the Bötzinger complex (BötC), pre-Bötzinger complex (pre-BötC) and rostral ventral respiratory group (rVRG). The respiratory rhythm and inspiratory–expiratory patterns emerge from dynamic interactions between: (i) excitatory neuron populations in the pre-BötC and rVRG active during inspiration that form inspiratory motor output; (ii) inhibitory neuron populations in the pre-BötC that provide inspiratory inhibition within the network; and (iii) inhibitory populations in the BötC active during expiration that generate expiratory inhibition. Network interactions within these compartments along with intrinsic rhythmogenic properties of pre-BötC neurons form a hierarchy of multiple oscillatory mechanisms. The functional expression of these mechanisms is controlled by multiple drives from more rostral brainstem components, including the retrotrapezoid nucleus and pons, which regulate the dynamic behaviour of the core circuitry. The emerging view is that the brainstem respiratory network has rhythmogenic capabilities at multiple hierarchical levels, which allows flexible, state-dependent expression of different rhythmogenic mechanisms under different physiological and metabolic conditions and enables a wide repertoire of respiratory behaviours.

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Glanowska, Katarzyna M., et Suzanne M. Moenter. « Endocannabinoids and prostaglandins both contribute to GnRH neuron-GABAergic afferent local feedback circuits ». Journal of Neurophysiology 106, n^o 6 (décembre 2011) : 3073–81. http://dx.doi.org/10.1152/jn.00046.2011.

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Gonadotropin-releasing hormone (GnRH) neurons form the final common pathway for central control of fertility. Regulation of GnRH neurons by long-loop gonadal steroid feedback through steroid receptor-expressing afferents such as GABAergic neurons is well studied. Recently, local central feedback circuits regulating GnRH neurons were identified. GnRH neuronal depolarization induces short-term inhibition of their GABAergic afferents via a mechanism dependent on metabotropic glutamate receptor (mGluR) activation. GnRH neurons are enveloped in astrocytes, which express mGluRs. GnRH neurons also produce endocannabinoids, which can be induced by mGluR activation. We hypothesized the local GnRH-GABA circuit utilizes glia-derived and/or cannabinoid mechanisms and is altered by steroid milieu. Whole cell voltage-clamp was used to record GABAergic postsynaptic currents (PSCs) from GnRH neurons before and after action potential-like depolarizations were mimicked. In GnRH neurons from ovariectomized (OVX) mice, this depolarization reduced PSC frequency. This suppression was blocked by inhibition of prostaglandin synthesis with indomethacin, by a prostaglandin receptor antagonist, or by a specific glial metabolic poison, together suggesting the postulate that prostaglandins, potentially glia-derived, play a role in this circuit. This circuit was also inhibited by a CB1 receptor antagonist or by blockade of endocannabinoid synthesis in GnRH neurons, suggesting an endocannabinoid element, as well. In females, local circuit inhibition persisted in androgen-treated mice but not in estradiol-treated mice or young ovary-intact mice. In contrast, local circuit inhibition was present in gonad-intact males. These data suggest GnRH neurons interact with their afferent neurons using multiple mechanisms and that these local circuits can be modified by both sex and steroid feedback.

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Padyal, Anjum. « Effects of 12 Weeks Circuit Training on Subcutaneous Body Fat %, Skeletal Muscle % and Basal Metabolic Age in Colligate Women ». International Journal of Scientific Research 3, n^o 6 (1 juin 2012) : 35. http://dx.doi.org/10.15373/22778179/june2014/178.

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Passineau, M. J., W. Zhao, R. Busto, W. D. Dietrich, O. Alonso, J. Y. Loor, H. M. Bramlett et M. D. Ginsberg. « Chronic metabolic sequelae of traumatic brain injury : prolonged suppression of somatosensory activation ». American Journal of Physiology-Heart and Circulatory Physiology 279, n^o 3 (1 septembre 2000) : H924—H931. http://dx.doi.org/10.1152/ajpheart.2000.279.3.h924.

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Injuries to the brain acutely disrupt normal metabolic function and may deactivate functional circuits. It is unknown whether these metabolic abnormalities improve over time. We used 2-deoxyglucose (2-DG) autoradiographic image-averaging to assess local cerebral glucose utilization (lCMRGlc) of the rat brain 2 mo after moderate (1.7–2.1 atm) fluid-percussion traumatic brain injury (FPI). Four animal groups ( n = 5 each) were studied: sham-injured rats with and without stimulation of the vibrissae-barrel field ipsilateral to injury; and animals with prior FPI, with or without this stimulation. In sham-injured rats, resting lCMRGlc was normal, and vibrissae stimulation produced right-sided metabolic activation of the ventrolateral thalamic and somatosensory-cortical projection areas. In rats with prior injury, lCMRGlccontralateral to injury was normal, but lCMRGlc of the ipsilateral forebrain was depressed by ∼38–45% compared with shams. Whisker stimulation in rats with prior trauma failed to induce metabolic activation of either cortex or thalamus. Image-mapping of histological material obtained in the same injury model was undertaken to assess the possible influence of injury-induced regional brain atrophy on computed lCMRGlc; an effect was found only in the lateral cortex at the trauma epicenter. Our results show that, 2 mo after trauma, resting cerebral metabolic perturbations persist, and the whisker-barrel somatosensory circuit shows no signs of functional recovery.

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Zhao, Evan M., Makoto A. Lalwani, Jhong-Min Chen, Paulina Orillac, Jared E. Toettcher et José L. Avalos. « Optogenetic Amplification Circuits for Light-Induced Metabolic Control ». ACS Synthetic Biology 10, n^o 5 (9 avril 2021) : 1143–54. http://dx.doi.org/10.1021/acssynbio.0c00642.

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Otero-Muras, Irene, Ahmad A. Mannan, Julio R. Banga et Diego A. Oyarzún. « Multiobjective optimization of gene circuits for metabolic engineering ». IFAC-PapersOnLine 52, n^o 26 (2019) : 13–16. http://dx.doi.org/10.1016/j.ifacol.2019.12.229.

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Balaji, S., et S. Lakshminarayanan. « Conceptual comparison of metabolic pathways with electronic circuits ». Journal of Bionic Engineering 1, n^o 4 (décembre 2004) : 175–82. http://dx.doi.org/10.1007/bf03399473.

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Ihunnah, Chibueze A., Mengxi Jiang et Wen Xie. « Nuclear receptor PXR, transcriptional circuits and metabolic relevance ». Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 1812, n^o 8 (août 2011) : 956–63. http://dx.doi.org/10.1016/j.bbadis.2011.01.014.

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Cho, Eunae, Nam Kim, Jun Yun, Sue Cho, Hyun Kim et Jong Yook. « Breast Cancer Subtypes Underlying EMT-Mediated Catabolic Metabolism ». Cells 9, n^o 9 (10 septembre 2020) : 2064. http://dx.doi.org/10.3390/cells9092064.

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Efficient catabolic metabolism of adenosine triphosphate (ATP) and reduced nicotinamide adenine dinucleotide phosphate (NADPH) is essentially required for cancer cell survival, especially in metastatic cancer progression. Epithelial–mesenchymal transition (EMT) plays an important role in metabolic rewiring of cancer cells as well as in phenotypic conversion and therapeutic resistance. Snail (SNAI1), a well-known inducer of cancer EMT, is critical in providing ATP and NADPH via suppression of several gatekeeper genes involving catabolic metabolism, such as phosphofructokinase 1 (PFK1), fructose-1,6-bisphosphatase 1 (FBP1), and acetyl-CoA carboxylase 2 (ACC2). Paradoxically, PFK1 and FBP1 are counter-opposing and rate-limiting reaction enzymes of glycolysis and gluconeogenesis, respectively. In this study, we report a distinct metabolic circuit of catabolic metabolism in breast cancer subtypes. Interestingly, PFKP and FBP1 are inversely correlated in clinical samples, indicating different metabolic subsets of breast cancer. The luminal types of breast cancer consist of the pentose phosphate pathway (PPP) subset by suppression of PFKP while the basal-like subtype (also known as triple negative breast cancer, TNBC) mainly utilizes glycolysis and mitochondrial fatty acid oxidation (FAO) by loss of FBP1 and ACC2. Notably, PPP remains active via upregulation of TIGAR in the FBP1-loss basal-like subset, indicating the importance of PPP in catabolic cancer metabolism. These results indicate different catabolic metabolic circuits and thus therapeutic strategies in breast cancer subsets.

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Ritz, Ludivine, Shailendra Segobin, Coralie Lannuzel, Céline Boudehent, François Vabret, Francis Eustache, Hélène Beaunieux et Anne L. Pitel. « Direct voxel-based comparisons between grey matter shrinkage and glucose hypometabolism in chronic alcoholism ». Journal of Cerebral Blood Flow & ; Metabolism 36, n^o 9 (20 juillet 2016) : 1625–40. http://dx.doi.org/10.1177/0271678x15611136.

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Alcoholism is associated with widespread brain structural abnormalities affecting mainly the frontocerebellar and the Papez’s circuits. Brain glucose metabolism has received limited attention, and few studies used regions of interest approach and showed reduced global brain metabolism predominantly in the frontal and parietal lobes. Even though these studies have examined the relationship between grey matter shrinkage and hypometabolism, none has performed a direct voxel-by-voxel comparison between the degrees of structural and metabolic abnormalities. Seventeen alcoholic patients and 16 control subjects underwent both structural magnetic resonance imaging and 18F-2-fluoro-deoxy-glucose-positron emission tomography examinations. Structural abnormalities and hypometabolism were examined in alcoholic patients compared with control subjects using two-sample t-tests. Then, these two patterns of brain damage were directly compared with a paired t-test. Compared to controls, alcoholic patients had grey matter shrinkage and hypometabolism in the fronto-cerebellar circuit and several nodes of Papez’s circuit. The direct comparison revealed greater shrinkage than hypometabolism in the cerebellum, cingulate cortex, thalamus and hippocampus and parahippocampal gyrus. Conversely, hypometabolism was more severe than shrinkage in the dorsolateral, premotor and parietal cortices. The distinct profiles of abnormalities found within the Papez’s circuit, the fronto-cerebellar circuit and the parietal gyrus in chronic alcoholism suggest the involvement of different pathological mechanisms.

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Ibrahim, Nur Syazwani, Ayu Suzailiana Muhamad, Foong Kiew Ooi, Jamaayah Meor-Osman et Chee Keong Chen. « The effects of combined probiotic ingestion and circuit training on muscular strength and power and cytokine responses in young males ». Applied Physiology, Nutrition, and Metabolism 43, n^o 2 (février 2018) : 180–86. http://dx.doi.org/10.1139/apnm-2017-0464.

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To our knowledge, the efficacy of combined probiotic supplementation with circuit training has not been evaluated. Thus, we investigated the effects of probiotic supplementation combined with circuit training on isokinetic muscular strength and power and cytokine responses in young males. Forty-eight healthy sedentary young males were recruited and randomised into 4 separate groups: sedentary placebo control, probiotics (P), circuit training with placebo (CT), and circuit training with probiotics (CTP). Participants in the CT and CTP groups performed circuit training 3 times/week with 2 circuits of exercises from weeks 1–8 followed by 3 circuits of exercises from weeks 9–12. Participants in the P and CTP groups consumed multi-strain probiotics containing 3 × 1010 colony-forming units of Lactobacillus acidophilus, L. lactis, L. casei, Bifidobacterium longum, B. bifidum and B. infantis twice daily for 12 weeks. Measurements of body height and weight, blood pressure, resting heart rate, blood samples, and isokinetic muscular strength and power were carried out at pre- and post-tests. Isokinetic knee strength and power in CT and CTP groups were significantly higher (P < 0.05) at post-test. In addition, interleukin (IL)-10 concentration was significantly increased (P < 0.0001) at post-test in P and CT but a trend toward significant increase in CTP (P = 0.09). Nevertheless, there was no significant difference in IL-6. This study suggests that 12 weeks of circuit training alone and the combination of circuit training and probiotic consumption improved muscular performance while circuit training alone and probiotics alone increased IL-10 concentration.

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Shenshin, Vasily A., Camille Lescanne, Guillaume Gines et Yannick Rondelez. « A small-molecule chemical interface for molecular programs ». Nucleic Acids Research 49, n^o 13 (5 juillet 2021) : 7765–74. http://dx.doi.org/10.1093/nar/gkab470.

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Abstract In vitro molecular circuits, based on DNA-programmable chemistries, can perform an increasing range of high-level functions, such as molecular level computation, image or chemical pattern recognition and pattern generation. Most reported demonstrations, however, can only accept nucleic acids as input signals. Real-world applications of these programmable chemistries critically depend on strategies to interface them with a variety of non-DNA inputs, in particular small biologically relevant chemicals. We introduce here a general strategy to interface DNA-based circuits with non-DNA signals, based on input-translating modules. These translating modules contain a DNA response part and an allosteric protein sensing part, and use a simple design that renders them fully tunable and modular. They can be repurposed to either transmit or invert the response associated with the presence of a given input. By combining these translating-modules with robust and leak-free amplification motifs, we build sensing circuits that provide a fluorescent quantitative time-response to the concentration of their small-molecule input, with good specificity and sensitivity. The programmability of the DNA layer can be leveraged to perform DNA based signal processing operations, which we demonstrate here with logical inversion, signal modulation and a classification task on two inputs. The DNA circuits are also compatible with standard biochemical conditions, and we show the one-pot detection of an enzyme through its native metabolic activity. We anticipate that this sensitive small-molecule-to-DNA conversion strategy will play a critical role in the future applications of molecular-level circuitry.

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Brynildsen, M. P., W. W. Wong et J. C. Liao. « Transcriptional regulation and metabolism ». Biochemical Society Transactions 33, n^o 6 (26 octobre 2005) : 1423–26. http://dx.doi.org/10.1042/bst0331423.

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Understanding organisms from a systems perspective is essential for predicting cellular behaviour as well as designing gene-metabolic circuits for novel functions. The structure, dynamics and interactions of cellular networks are all vital components of systems biology. To facilitate investigation of these aspects, we have developed an integrative technique called network component analysis, which utilizes mRNA expression and transcriptional network connectivity to determine network component dynamics, functions and interactions. This approach has been applied to elucidate transcription factor dynamics in Saccharomyces cerevisiae cell-cycle regulation, detect cross-talks in Escherichia coli two-component signalling pathways, and characterize E. coli carbon source transition. An ultimate test of system-wide understanding is the ability to design and construct novel gene-metabolic circuits. To this end, artificial feedback regulation, cell–cell communication and oscillatory circuits have been constructed, which demonstrate the design principles of gene-metabolic regulation in the cell.

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Cui, Shixiu, Xueqin Lv, Xianhao Xu, Taichi Chen, Hongzhi Zhang, Yanfeng Liu, Jianghua Li, Guocheng Du, Rodrigo Ledesma-Amaro et Long Liu. « Multilayer Genetic Circuits for Dynamic Regulation of Metabolic Pathways ». ACS Synthetic Biology 10, n^o 7 (2 juillet 2021) : 1587–97. http://dx.doi.org/10.1021/acssynbio.1c00073.

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Oyarzún, Diego A., Jean-Baptiste Lugagne et Guy-Bart V. Stan. « Noise Propagation in Synthetic Gene Circuits for Metabolic Control ». ACS Synthetic Biology 4, n^o 2 (mai 2014) : 116–25. http://dx.doi.org/10.1021/sb400126a.

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Liu, Di, et Fuzhong Zhang. « Metabolic Feedback Circuits Provide Rapid Control of Metabolite Dynamics ». ACS Synthetic Biology 7, n^o 2 (8 janvier 2018) : 347–56. http://dx.doi.org/10.1021/acssynbio.7b00342.

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Levin, Barry E. « Metabolic imprinting on genetically predisposed neural circuits perpetuates obesity ». Nutrition 16, n^o 10 (octobre 2000) : 909–15. http://dx.doi.org/10.1016/s0899-9007(00)00408-1.

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Wang, Lei, Debin Ji, Yuxue Liu, Qian Wang, Xueying Wang, Yongjin J. Zhou, Yixin Zhang, Wujun Liu et Zongbao K. Zhao. « Synthetic Cofactor-Linked Metabolic Circuits for Selective Energy Transfer ». ACS Catalysis 7, n^o 3 (13 février 2017) : 1977–83. http://dx.doi.org/10.1021/acscatal.6b03579.

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Fernandes, Philip, Graham Walsh, Stephanie Walsh, Michael O’Neil, Jill Gelinas et Michael W. A. Chu. « Whole body perfusion for hybrid aortic arch repair : evolution of selective regional perfusion with a modified extracorporeal circuit ». Perfusion 32, n^o 3 (4 novembre 2016) : 230–37. http://dx.doi.org/10.1177/0267659116673444.

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Background: Patients undergoing hybrid aortic arch reconstruction require careful protection of vital organs. We believe that whole body perfusion with tailored dual circuitry may help to achieve optimal patient outcomes. Methods: Our circuit has evolved from a secondary circuit utilizing a cardioplegia delivery device for lower body perfusion to a dual-oxygenator circuit. This allows individually controlled regional perfusion with ease of switching from secondary to primary circuit for total body flow. The re-design allows for separate flow and temperature regulation with two oxygenators in parallel. All patients underwent a single-stage operation for simultaneous treatment of arch and descending aortic pathology via a sternotomy, using a hybrid frozen elephant trunk technique. Results: We report six consecutive patients undergoing hybrid arch and frozen elephant trunk reconstruction using a dual-oxygenator circuit. Five patients underwent elective surgery and one was emergent. One patient had an acute dissection while three underwent concomitant procedures, including a Ross procedure and two valve-sparing root reconstructions. Three cases were redo sternotomies. The mean pump time was 358 ± 131 min, the aortic cross clamp time 243 ± 135 min, the cardioplegia volume of 33,208 ml ± 16,173, cerebral ischemia 0 min, lower body ischemia 76 ± 34 min and the average lower body perfusion time was 142 min. Two patients did not require any donor blood products. The median intensive care unit (ICU) and hospital lengths of stay (LOS) were two days and 10 days, respectively. The average peak serum lactate on CPB was 7.47 mmol/L and, at admission to the ICU, it was 3.37 mmol/L. Renal and respiratory failure developed in the salvage acute type A dissection patient. No other complications occurred in this series. Conclusions: Whole body perfusion as delivered through individually controlled dual-oxygenator circuitry allows maximum flexibility for hybrid aortic arch reconstruction. A modified circuit perfusion strategy may help to limit intra-operative metabolic derangements, providing improved clinical outcomes.

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Scanlon, Seth Thomas. « A metabolic circuit in T cell immunity ». Science 371, n^o 6527 (21 janvier 2021) : 358.2–358. http://dx.doi.org/10.1126/science.371.6527.358-b.

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Molnar, J. A., J. J. Cunningham, S. Miyatani, A. Vizulis, J. D. Wright et J. F. Burke. « Closed-circuit metabolic system with multiple applications ». Journal of Applied Physiology 61, n^o 4 (1 octobre 1986) : 1582–85. http://dx.doi.org/10.1152/jappl.1986.61.4.1582.

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A closed-circuit metabolic system has been designed and tested for multiple applications. Air pressure within a closed chamber is regulated electronically while allowing for respiratory gas exchange. Compared with a previously reported standard indirect calorimetry system, the new device had by virtue of longer duration of measurement improved precision (coefficient of variation 3% vs. 14%) during studies of O2 consumption both at room temperature and at 5 degrees C. In addition, a more physiological atmospheric environment is maintained. This system has also been utilized for simultaneously labeling groups of up to 20 weanling rats with 18O2 over a 2-day period and for exposure of rats to a hyperoxic (84% O2), normobaric environment for 4-day periods. Potential applications include maintenance of pressure (hypobaric through hyperbaric) and O2 (hypoxic through hyperoxic) controlled environments, exposure to toxic gases, study of diurnal variations in metabolic rate, measurement of metabolic expenditure with activity, and adaptation to other species including humans.

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Wu, Yaokang, Taichi Chen, Yanfeng Liu, Rongzhen Tian, Xueqin Lv, Jianghua Li, Guocheng Du, Jian Chen, Rodrigo Ledesma-Amaro et Long Liu. « Design of a programmable biosensor-CRISPRi genetic circuits for dynamic and autonomous dual-control of metabolic flux in Bacillus subtilis ». Nucleic Acids Research 48, n^o 2 (4 décembre 2019) : 996–1009. http://dx.doi.org/10.1093/nar/gkz1123.

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Abstract Dynamic regulation is an effective strategy for fine-tuning metabolic pathways in order to maximize target product synthesis. However, achieving dynamic and autonomous up- and down-regulation of the metabolic modules of interest simultaneously, still remains a great challenge. In this work, we created an autonomous dual-control (ADC) system, by combining CRISPRi-based NOT gates with novel biosensors of a key metabolite in the pathway of interest. By sensing the levels of the intermediate glucosamine-6-phosphate (GlcN6P) and self-adjusting the expression levels of the target genes accordingly with the GlcN6P biosensor and ADC system enabled feedback circuits, the metabolic flux towards the production of the high value nutraceutical N-acetylglucosamine (GlcNAc) could be balanced and optimized in Bacillus subtilis. As a result, the GlcNAc titer in a 15-l fed-batch bioreactor increased from 59.9 g/l to 97.1 g/l with acetoin production and 81.7 g/l to 131.6 g/l without acetoin production, indicating the robustness and stability of the synthetic circuits in a large bioreactor system. Remarkably, this self-regulatory methodology does not require any external level of control such as the use of inducer molecules or switching fermentation/environmental conditions. Moreover, the proposed programmable genetic circuits may be expanded to engineer other microbial cells and metabolic pathways.

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Léon, Stéphane, Agnès Nadjar et Carmelo Quarta. « Microglia–Neuron Crosstalk in Obesity : Melodious Interaction or Kiss of Death ? » International Journal of Molecular Sciences 22, n^o 10 (15 mai 2021) : 5243. http://dx.doi.org/10.3390/ijms22105243.

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Diet-induced obesity can originate from the dysregulated activity of hypothalamic neuronal circuits, which are critical for the regulation of body weight and food intake. The exact mechanisms underlying such neuronal defects are not yet fully understood, but a maladaptive cross-talk between neurons and surrounding microglial is likely to be a contributing factor. Functional and anatomical connections between microglia and hypothalamic neuronal cells are at the core of how the brain orchestrates changes in the body’s metabolic needs. However, such a melodious interaction may become maladaptive in response to prolonged diet-induced metabolic stress, thereby causing overfeeding, body weight gain, and systemic metabolic perturbations. From this perspective, we critically discuss emerging molecular and cellular underpinnings of microglia–neuron communication in the hypothalamic neuronal circuits implicated in energy balance regulation. We explore whether changes in this intercellular dialogue induced by metabolic stress may serve as a protective neuronal mechanism or contribute to disease establishment and progression. Our analysis provides a framework for future mechanistic studies that will facilitate progress into both the etiology and treatments of metabolic disorders.

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Saxena, Pratik, Ghislaine Charpin-El Hamri, Marc Folcher, Henryk Zulewski et Martin Fussenegger. « Synthetic gene network restoring endogenous pituitary–thyroid feedback control in experimental Graves’ disease ». Proceedings of the National Academy of Sciences 113, n^o 5 (19 janvier 2016) : 1244–49. http://dx.doi.org/10.1073/pnas.1514383113.

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Graves’ disease is an autoimmune disorder that causes hyperthyroidism because of autoantibodies that bind to the thyroid-stimulating hormone receptor (TSHR) on the thyroid gland, triggering thyroid hormone release. The physiological control of thyroid hormone homeostasis by the feedback loops involving the hypothalamus–pituitary–thyroid axis is disrupted by these stimulating autoantibodies. To reset the endogenous thyrotrophic feedback control, we designed a synthetic mammalian gene circuit that maintains thyroid hormone homeostasis by monitoring thyroid hormone levels and coordinating the expression of a thyroid-stimulating hormone receptor antagonist (TSHAntag), which competitively inhibits the binding of thyroid-stimulating hormone or the human autoantibody to TSHR. This synthetic control device consists of a synthetic thyroid-sensing receptor (TSR), a yeast Gal4 protein/human thyroid receptor-α fusion, which reversibly triggers expression of the TSHAntag gene from TSR-dependent promoters. In hyperthyroid mice, this synthetic circuit sensed pathological thyroid hormone levels and restored the thyrotrophic feedback control of the hypothalamus–pituitary–thyroid axis to euthyroid hormone levels. Therapeutic plug and play gene circuits that restore physiological feedback control in metabolic disorders foster advanced gene- and cell-based therapies.

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Levin, Barry E. « The Obesity Epidemic : Metabolic Imprinting on Genetically Susceptible Neural Circuits ». Obesity Research 8, n^o 4 (juillet 2000) : 342–47. http://dx.doi.org/10.1038/oby.2000.41.

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Lieu, Linh, Dominic Chau, Sadia Afrin, Yanbin Dong, Amber L. Alhadeff, J. Nicholas Betley et Kevin W. Williams. « Effects of metabolic state on the regulation of melanocortin circuits ». Physiology & ; Behavior 224 (octobre 2020) : 113039. http://dx.doi.org/10.1016/j.physbeh.2020.113039.

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Clarke, Iain J. « The Nexus Between Metabolic and Reproductive Circuits in the Hypothalamus. » Biology of Reproduction 83, Suppl_1 (1 novembre 2010) : 47. http://dx.doi.org/10.1093/biolreprod/83.s1.47.

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González-García, Ismael, et Cristina García-Cáceres. « Hypothalamic Astrocytes as a Specialized and Responsive Cell Population in Obesity ». International Journal of Molecular Sciences 22, n^o 12 (8 juin 2021) : 6176. http://dx.doi.org/10.3390/ijms22126176.

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Astrocytes are a type of glial cell anatomically and functionally integrated into the neuronal regulatory circuits for the neuroendocrine control of metabolism. Being functional integral compounds of synapses, astrocytes are actively involved in the physiological regulatory aspects of metabolic control, but also in the pathological processes that link neuronal dysfunction and obesity. Between brain areas, the hypothalamus harbors specialized functional circuits that seem selectively vulnerable to metabolic damage, undergoing early cellular rearrangements which are thought to be at the core of the pathogenesis of diet-induced obesity. Such changes in the hypothalamic brain region consist of a rise in proinflammatory cytokines, the presence of a reactive phenotype in astrocytes and microglia, alterations in the cytoarchitecture and synaptology of hypothalamic circuits, and angiogenesis, a phenomenon that cannot be found elsewhere in the brain. Increasing evidence points to the direct involvement of hypothalamic astrocytes in such early metabolic disturbances, thus moving the study of these glial cells to the forefront of obesity research. Here we provide a comprehensive review of the most relevant findings of molecular and pathophysiological mechanisms by which hypothalamic astrocytes might be involved in the pathogenesis of obesity.

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Brown, Darcy M., Dan B. Dwyer, Samuel J. Robertson et Paul B. Gastin. « Metabolic Power Method : Underestimation of Energy Expenditure in Field-Sport Movements Using a Global Positioning System Tracking System ». International Journal of Sports Physiology and Performance 11, n^o 8 (novembre 2016) : 1067–73. http://dx.doi.org/10.1123/ijspp.2016-0021.

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The purpose of this study was to assess the validity of a global positioning system (GPS) tracking system to estimate energy expenditure (EE) during exercise and field-sport locomotor movements. Twenty-seven participants each completed a 90-min exercise session on an outdoor synthetic futsal pitch. During the exercise session, they wore a 5-Hz GPS unit interpolated to 15 Hz and a portable gas analyzer that acted as the criterion measure of EE. The exercise session was composed of alternating 5-minute exercise bouts of randomized walking, jogging, running, or a field-sport circuit (×3) followed by 10 min of recovery. One-way analysis of variance showed significant (P < .01) and very large underestimations between GPS metabolic power– derived EE and oxygen-consumption (VO2) -derived EE for all field-sport circuits (% difference ≈ –44%). No differences in EE were observed for the jog (7.8%) and run (4.8%), whereas very large overestimations were found for the walk (43.0%). The GPS metabolic power EE over the entire 90-min session was significantly lower (P < .01) than the VO2 EE, resulting in a moderate underestimation overall (–19%). The results of this study suggest that a GPS tracking system using the metabolic power model of EE does not accurately estimate EE in field-sport movements or over an exercise session consisting of mixed locomotor activities interspersed with recovery periods; however, is it able to provide a reasonably accurate estimation of EE during continuous jogging and running.

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Argente-Arizón, Pilar, Santiago Guerra-Cantera, Luis Miguel Garcia-Segura, Jesús Argente et Julie A. Chowen. « Glial cells and energy balance ». Journal of Molecular Endocrinology 58, n^o 1 (janvier 2017) : R59—R71. http://dx.doi.org/10.1530/jme-16-0182.

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The search for new strategies and drugs to abate the current obesity epidemic has led to the intensification of research aimed at understanding the neuroendocrine control of appetite and energy expenditure. This intensified investigation of metabolic control has also included the study of how glial cells participate in this process. Glia, the most abundant cell type in the central nervous system, perform a wide spectrum of functions and are vital for the correct functioning of neurons and neuronal circuits. Current evidence indicates that hypothalamic glia, in particular astrocytes, tanycytes and microglia, are involved in both physiological and pathophysiological mechanisms of appetite and metabolic control, at least in part by regulating the signals reaching metabolic neuronal circuits. Glia transport nutrients, hormones and neurotransmitters; they secrete growth factors, hormones, cytokines and gliotransmitters and are a source of neuroprogenitor cells. These functions are regulated, as glia also respond to numerous hormones and nutrients, with the lack of specific hormonal signaling in hypothalamic astrocytes disrupting metabolic homeostasis. Here, we review some of the more recent advances in the role of glial cells in metabolic control, with a special emphasis on the differences between glial cell responses in males and females.

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Dimski, Thomas, Timo Brandenburger, Torsten Slowinski et Detlef Kindgen-Milles. « Feasibility and safety of combined cytokine adsorption and continuous veno-venous hemodialysis with regional citrate anticoagulation in patients with septic shock ». International Journal of Artificial Organs 43, n^o 1 (3 août 2019) : 10–16. http://dx.doi.org/10.1177/0391398819866459.

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Introduction: Septic shock is characterized by severe metabolic and hemodynamic alterations. It is often accompanied by acute kidney injury. A new adjunct treatment is hemoadsorption using a cytokine adsorber in line with continuous veno-venous renal replacement therapy. We studied the feasibility, efficacy, and safety of cytokine adsorption with citrate-anticoagulated continuous veno-venous hemodialysis (regional citrate anticoagulation–continuous veno-venous hemodialysis). Methods: In 11 patients with septic shock and acute kidney injury stage 3, we studied 12 cycles of cytokine adsorption and regional citrate anticoagulation–continuous veno-venous hemodialysis. We monitored parameters of citrate anticoagulation, circuit lifetime, laboratory parameters, hemodynamics, and vasopressor demand. Results: Ten out of 12 adsorber/continuous veno-venous hemodialysis circuits reached the target lifetime of 24 h for the adsorber. One system clotted and one was stopped for non-device-related reasons. Nine of the remaining continuous renal replacement therapy circuits reached 72 h lifetime. With default settings for regional citrate anticoagulation, serum ionized calcium and pH were in the normal range. Urea and creatinine were reduced significantly, and norepinephrine dose decreased from 0.47 (±0.09) to 0.16 (±0.04) µg/kg/min ( p = 0.016) after 24 h. Discussion: We show that combined cytokine adsorption/continuous veno-venous hemodialysis is effective to control pH, to reduce urea and creatinine, and to improve hemodynamics by reducing norepinephrine doses in patients with septic shock. It can be applied safely with standard settings of regional citrate anticoagulation rendering sufficiently long filter lifetimes for the adsorber and the continuous veno-venous hemodialysis circuit. Further studies are on the way to investigate whether these effects translate into improved outcomes in septic shock patients.

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Melcher, Christoph, Ruediger Bader et Michael J. Pankratz. « Amino acids, taste circuits, and feeding behavior in Drosophila : towards understanding the psychology of feeding in flies and man ». Journal of Endocrinology 192, n^o 3 (mars 2007) : 467–72. http://dx.doi.org/10.1677/joe-06-0066.

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Feeding can be regulated by a variety of external sensory stimuli such as olfaction and gustation, as well as by systemic internal signals of feeding status and metabolic needs. Faced with a major health epidemic in eating-related conditions, such as obesity and diabetes, there is an ever increasing need to dissect and understand the complex regulatory network underlying the multiple aspects of feeding behavior. In this minireview, we highlight the use of Drosophila in studying the neural circuits that control the feeding behavior in response to external and internal signals. In particular, we outline the work on the neuroanatomical and functional characterization of the newly identified hugin neuronal circuit. We focus on the pivotal role of the central nervous system in integrating external and internal feeding-relevant information, thus enabling the organism to make one of the most basic decisions – to eat or not to eat.

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Beckham, S. G. « THE METABOLIC COST OF FREE WEIGHT CIRCUIT TRAINING ». Medicine & ; Science in Sports & ; Exercise 31, Supplement (mai 1999) : S109. http://dx.doi.org/10.1097/00005768-199905001-00399.

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