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1
Bowden, Pye. "Including the body in psychotherapy." Ata: Journal of Psychotherapy Aotearoa New Zealand 7, no. 1 (July 30, 2001): 65–71. http://dx.doi.org/10.9791/ajpanz.2001.06.
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This paper describes the development of Bioenergetic Analysis, one of the more recent psychotherapies to arrive in New Zealand. Bioenergetics opens up psychoanalytic theory and practice to include all aspects of the self: the mind, the body, emotion, energy and relationship. In doing so it provides a holistic psychotherapy for the twenty-first century. The paper describes Bioenergetic's beginnings with Wilhelm Reich, a contemporary of Freud, and its establishment by Alexander Lowen. It critiques Bioenergetic's association with the 'cathartic' approach of the 1960s and describes how Bioenergetics is integrating Reich's and Lowen's work with current thinking about the therapeutic relationship.
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Sandage, Mary J., and Audrey G. Smith. "Muscle Bioenergetic Considerations for Intrinsic Laryngeal Skeletal Muscle Physiology." Journal of Speech, Language, and Hearing Research 60, no. 5 (May 24, 2017): 1254–63. http://dx.doi.org/10.1044/2016_jslhr-s-16-0192.
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PurposeIntrinsic laryngeal skeletal muscle bioenergetics, the means by which muscles produce fuel for muscle metabolism, is an understudied aspect of laryngeal physiology with direct implications for voice habilitation and rehabilitation. The purpose of this review is to describe bioenergetic pathways identified in limb skeletal muscle and introduce bioenergetic physiology as a necessary parameter for theoretical models of laryngeal skeletal muscle function.MethodA comprehensive review of the human intrinsic laryngeal skeletal muscle physiology literature was conducted. Findings regarding intrinsic laryngeal muscle fiber complement and muscle metabolism in human models are summarized and exercise physiology methodology is applied to identify probable bioenergetic pathways used for voice function.ResultsIntrinsic laryngeal skeletal muscle fibers described in human models support the fast, high-intensity physiological requirements of these muscles for biological functions of airway protection. Inclusion of muscle bioenergetic constructs in theoretical modeling of voice training, detraining, fatigue, and voice loading have been limited.ConclusionsMuscle bioenergetics, a key component for muscle training, detraining, and fatigue models in exercise science, is a little-considered aspect of intrinsic laryngeal skeletal muscle physiology. Partnered with knowledge of occupation-specific voice requirements, application of bioenergetics may inform novel considerations for voice habilitation and rehabilitation.
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Lowen, Alexander. "Al Lowen riflette sugli aspetti teorici dell'analisi bioenergetica e sulla sua esperienza negli ultimi quarant'anni." GROUNDING, no. 2 (July 2009): 17–32. http://dx.doi.org/10.3280/gro2008-002003.
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- Alexander Lowen recounts his meeting with Reich, its therapeutic experience with him and the reasons that led him to decide to continue the work of his teacher developing the bioenergetic analysis. As in his costume, biographical and theoretical elements are closely related.Key words: Wilhelm Reich, body, vegetoteraphy, bioenergetic analysisParole chiave: Wilhelm Reich, corpo, vegetoterapia, analisi bioenergetica
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Mahapatra, Gargi, Zhengrong Gao, James Bateman, Jenny L. Gonzalez-Armenta, Allison Amick, Ramon Casanova, Suzanne Craft, and Anthony J. A. Molina. "Systemic Bioenergetic Capacity Changes with Cognitive Status and Insulin Sensitivity in Older Adults." Innovation in Aging 5, Supplement_1 (December 1, 2021): 638. http://dx.doi.org/10.1093/geroni/igab046.2423.
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Abstract Systemic mitochondrial dysfunction is reported with AD progression, suggesting that peripheral blood cells may be used to investigate systemic mitochondrial alterations related to cognitive decline. We aimed to identify bioenergetic signatures associated with AD-related dementia and differences in insulin sensitivity associated with AD risk. We analyzed mitochondrial bioenergetics in peripheral blood cells collected from 365 older adults with varying cognitive status (normal, mild cognitive impairment, and AD) and insulin sensitivity. Normoglycemic individuals exhibited lower maximal bioenergetic capacity with AD (PBMCs: 239.6 pmol·min−1, p = 0.02; Platelets: 151.7 pmol·min−1, p = 0.06) compared to normal cognition (PBMCs: 271.5 pmol·min−1; Platelets: 171.7 pmol·min−1). Individuals with impaired insulin sensitivity exhibited lower maximal bioenergetic capacity in platelets with AD (171.6 pmol·min−1, p = 0.008) compared to normal cognition (210.6 pmol.min−1). Participants with impaired insulin sensitivity also exhibited unique bioenergetic profiles exemplified by overall higher levels of mitochondrial respiration, indicating that comorbidities such as diabetes can significantly influence bioenergetic capacity. We observed strong positive associations between maximal respiration in normoglycemic individuals with cognitive function, as measured by Modified Preclinical Alzheimer’s Cognitive Composite (mPACC5) (p = 0.06), and fatty acid oxidation in individuals with impaired insulin sensitivity with cortical thickness (p = 0.05). This study demonstrates that circulating cells may provide a cost-effective and minimally invasive way to monitor systemic bioenergetic changes associated with AD risk, progression, and insulin sensitivity. These findings also suggest that blood-based bioenergetics are related to key features of AD development and progression and should be further developed as a potential biomarker.
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Coven, Arnold B. "The Bioenergetic Approach to Rehabilitation Counseling." Journal of Applied Rehabilitation Counseling 16, no. 2 (June 1, 1985): 6–10. http://dx.doi.org/10.1891/0047-2220.16.2.6.
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The current focus on assisting the severely disabled confronts rehabilitation counselors with the demand of being more effective behavioral change agents. This article suggests that counselors try out Bioenergetics, a mindbody counseling approach. An overview of Bioenergetics theory is presented with examples of how it can be applied to the impaired. Guidelines for using Bioenergetic techniques are identified along with the necessary precautions.
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Chacko, Balu K., Philip A. Kramer, Saranya Ravi, Gloria A. Benavides, Tanecia Mitchell, Brian P. Dranka, David Ferrick, et al. "The Bioenergetic Health Index: a new concept in mitochondrial translational research." Clinical Science 127, no. 6 (May 29, 2014): 367–73. http://dx.doi.org/10.1042/cs20140101.
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Bioenergetics has become central to our understanding of pathological mechanisms, the development of new therapeutic strategies and as a biomarker for disease progression in neurodegeneration, diabetes, cancer and cardiovascular disease. A key concept is that the mitochondrion can act as the ‘canary in the coal mine’ by serving as an early warning of bioenergetic crisis in patient populations. We propose that new clinical tests to monitor changes in bioenergetics in patient populations are needed to take advantage of the early and sensitive ability of bioenergetics to determine severity and progression in complex and multifactorial diseases. With the recent development of high-throughput assays to measure cellular energetic function in the small number of cells that can be isolated from human blood these clinical tests are now feasible. We have shown that the sequential addition of well-characterized inhibitors of oxidative phosphorylation allows a bioenergetic profile to be measured in cells isolated from normal or pathological samples. From these data we propose that a single value–the Bioenergetic Health Index (BHI)–can be calculated to represent the patient's composite mitochondrial profile for a selected cell type. In the present Hypothesis paper, we discuss how BHI could serve as a dynamic index of bioenergetic health and how it can be measured in platelets and leucocytes. We propose that, ultimately, BHI has the potential to be a new biomarker for assessing patient health with both prognostic and diagnostic value.
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Strope, Taylor A., Cole J. Birky, and Heather M. Wilkins. "The Role of Bioenergetics in Neurodegeneration." International Journal of Molecular Sciences 23, no. 16 (August 16, 2022): 9212. http://dx.doi.org/10.3390/ijms23169212.
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Bioenergetic and mitochondrial dysfunction are common hallmarks of neurodegenerative diseases. Decades of research describe how genetic and environmental factors initiate changes in mitochondria and bioenergetics across Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS). Mitochondria control many cellular processes, including proteostasis, inflammation, and cell survival/death. These cellular processes and pathologies are common across neurodegenerative diseases. Evidence suggests that mitochondria and bioenergetic disruption may drive pathological changes, placing mitochondria as an upstream causative factor in neurodegenerative disease onset and progression. Here, we discuss evidence of mitochondrial and bioenergetic dysfunction in neurodegenerative diseases and address how mitochondria can drive common pathological features of these diseases.
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Patón, Mauricio, and Jorge Rodríguez. "Integration of bioenergetics in the ADM1 and its impact on model predictions." Water Science and Technology 80, no. 2 (July 15, 2019): 339–46. http://dx.doi.org/10.2166/wst.2019.279.
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Abstract In this work, the integration of dynamic bioenergetic calculations in the IWA Anaerobic Digestion Model No. 1 (ADM1) is presented. The impact of bioenergetics on kinetics was addressed via two different approaches: a thermodynamic-based inhibition function and variable microbial growth yields based on dynamic Gibbs free energy calculations. The dynamic bioenergetic calculations indicate that the standard ADM1 predicts positive reaction rates under thermodynamically unfeasible conditions. The dissolved hydrogen inhibition approach used in ADM1 is, however, deemed as adequate, offering the trade-off of not requiring dynamic bioenergetics computation despite the need of hydrogen inhibition parameters. Simulations of the model with bioenergetics showed the low amount of energy available in butyrate and propionate oxidation, suggesting that microbial growth on these substrates must be very limited or occur via alternative mechanisms rather than dissolved hydrogen.
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Lehrer, H. Matthew, Lauren Chu, Martica Hall, and Kyle Murdock. "009 Self-Reported Sleep Efficiency and Duration are Associated with Systemic Bioenergetic Function in Community-Dwelling Adults." Sleep 44, Supplement_2 (May 1, 2021): A4. http://dx.doi.org/10.1093/sleep/zsab072.008.
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Abstract Introduction Sleep is important for aging, health, and disease, but its cellular role in these outcomes is poorly understood. Basic research suggests that disturbed and insufficient sleep impair mitochondrial bioenergetics, which is involved in numerous aging-related chronic conditions. However, the relationship between sleep and bioenergetics has not been examined in humans. We examined associations of self-reported sleep with systemic bioenergetic function in peripheral blood mononuclear cells (PBMCs) of community-dwelling adults. Methods N = 43 adults (79% female) ages 48–70 (M = 61.63, SD = 5.99) completed the Pittsburgh Sleep Quality Index (PSQI) from which key components of sleep (satisfaction, alertness, timing, efficiency, and duration) were calculated. Participants provided blood samples from which PBMCs were isolated and measured for bioenergetics using extracellular flux analysis. Associations of sleep components with bioenergetic parameters, including the Bioenergetic Health Index (BHI), were examined. Results In bivariate analyses, lower sleep efficiency was associated with lower maximal respiration, spare capacity, and BHI (ps < 0.05). Longer sleep duration was associated with lower BHI (p < 0.01) and later sleep timing was associated with higher basal respiration, ATP-linked respiration, maximal respiration, spare capacity, and non-mitochondrial respiration (ps < 0.05). After adjustment for age, sex, and body mass index, lower sleep efficiency (β = 0.52, p < 0.01) and longer sleep duration (β = -0.43, p < 0.01) were associated with lower BHI. Conclusion Self-reported indices of sleep efficiency and duration are related to systemic bioenergetic function in humans, suggesting a possible cellular pathway linking sleep to health. Support (if any) T32HL082610
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Hill, Bradford G., Gloria A. Benavides, Jack R. Lancaster, Scott Ballinger, Lou Dell’Italia, Jianhua Zhang, and Victor M. Darley-Usmar. "Integration of cellular bioenergetics with mitochondrial quality control and autophagy." Biological Chemistry 393, no. 12 (December 1, 2012): 1485–512. http://dx.doi.org/10.1515/hsz-2012-0198.
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Abstract Bioenergetic dysfunction is emerging as a cornerstone for establishing a framework for understanding the pathophysiology of cardiovascular disease, diabetes, cancer and neurodegeneration. Recent advances in cellular bioenergetics have shown that many cells maintain a substantial bioenergetic reserve capacity, which is a prospective index of ‘healthy’ mitochondrial populations. The bioenergetics of the cell are likely regulated by energy requirements and substrate availability. Additionally, the overall quality of the mitochondrial population and the relative abundance of mitochondria in cells and tissues also impinge on overall bioenergetic capacity and resistance to stress. Because mitochondria are susceptible to damage mediated by reactive oxygen/nitrogen and lipid species, maintaining a ‘healthy’ population of mitochondria through quality control mechanisms appears to be essential for cell survival under conditions of pathological stress. Accumulating evidence suggest that mitophagy is particularly important for preventing amplification of initial oxidative insults, which otherwise would further impair the respiratory chain or promote mutations in mitochondrial DNA (mtDNA). The processes underlying the regulation of mitophagy depend on several factors, including the integrity of mtDNA, electron transport chain activity, and the interaction and regulation of the autophagic machinery. The integration and interpretation of cellular bioenergetics in the context of mitochondrial quality control and genetics is the theme of this review.
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Cha, Yong-Mei, Petras P. Dzeja, Margaret M. Redfield, Win K. Shen, and Andre Terzic. "Bioenergetic protection of failing atrial and ventricular myocardium by vasopeptidase inhibitor omapatrilat." American Journal of Physiology-Heart and Circulatory Physiology 290, no. 4 (April 2006): H1686—H1692. http://dx.doi.org/10.1152/ajpheart.00384.2005.
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Deficient bioenergetic signaling contributes to myocardial dysfunction and electrical instability in both atrial and ventricular cardiac chambers. Yet, approaches capable to prevent metabolic distress are only partially established. Here, in a canine model of tachycardia-induced congestive heart failure, we compared atrial and ventricular bioenergetics and tested the efficacy of metabolic rescue with the vasopeptidase inhibitor omapatrilat. Despite intrinsic differences in energy metabolism, failing atria and ventricles demonstrated profound bioenergetic deficiency with reduced ATP and creatine phosphate levels and compromised adenylate kinase and creatine kinase catalysis. Depressed phosphotransfer enzyme activities correlated with reduced tissue ATP levels, whereas creatine phosphate inversely related with atrial and ventricular load. Chronic treatment with omapatrilat maintained myocardial ATP, the high-energy currency, and protected adenylate and creatine kinase phosphotransfer capacity. Omapatrilat-induced bioenergetic protection was associated with maintained atrial and ventricular structural integrity, albeit without full recovery of the creatine phosphate pool. Thus therapy with omapatrilat demonstrates the benefit in protecting phosphotransfer enzyme activities and in preventing impairment of atrial and ventricular bioenergetics in heart failure.
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Cockburn, Garry. "«Seeing what is so simply present”." Clinical Journal of the International Institute for Bioenergetic Analysis 23, no. 1 (February 2013): 75–99. http://dx.doi.org/10.30820/0743-4804-2013-23-75.
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Lowen’s ability to see the body was preternatural. His ability «to see what is so simply present” and to explain the whole personality in terms of the body has been an inspiration for all. Like Lowen, gifted first generation Bioenergetic therapists have generously passed on their knowledge to us. As time passes, so does the opportunity to learn from those who were personally influenced by Lowen. This raises issues of how new students of Bioenergetics can learn and keep the tradition alive. This article discusses these issues and provides a structured way of helping students learn some of the basic skills in becoming a Bioenergetic therapist. This approach draws on the training and therapeutic experiences of the author who was privileged to be trained by many of the first generation Bioenergetic therapists. A Workbook is attached to the article, which operationalizes some of the basic skills involved in becoming a Bioenergetic therapist and helps students «to see what is so simply present”.
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Schroeter, Vincentia. "Integrating Regulation Therapy and Bioenergetic Analysis." Clinical Journal of the International Institute for Bioenergetic Analysis 24, no. 1 (March 2014): 105–32. http://dx.doi.org/10.30820/0743-4804-2014-24-105.
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Attachment theorists have recently become more interested in how bodily-based processes and interventions can contribute to their interest in the emotional regulation of arousal levels. A review of current concepts and techniques in integrative regulation therapy, including their value for Bioenergetics, will be examined. The literature of recent writings on attachment within Bioenergetics will be provided, along with a clinical vignette utilizing both approaches. The paper proposes that the Bioenergetic community answer the call to promote a somatic-energetic approach to the larger psychotherapeutic world.
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Keane, Kevin N., Emily K. Calton, Vinicius F. Cruzat, Mario J. Soares, and Philip Newsholme. "The impact of cryopreservation on human peripheral blood leucocyte bioenergetics." Clinical Science 128, no. 10 (March 10, 2015): 723–33. http://dx.doi.org/10.1042/cs20140725.
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Circulating immune cells are considered a source for biomarkers in health and disease, since they are exposed to nutritional, metabolic and immunological stimuli in the vasculature. Cryopreservation of leucocytes is routinely used for long-term storage and determination of phenotypic/functional changes at a later date. Exploring the role of bioenergetics and mitochondrial (dys)function in leucocytes is often examined by using freshly isolated cells. The aim of the pilot study described herein was to assess leucocyte bioenergetics in cryopreserved cells. Leucocytes were isolated from whole blood, counted and frozen in liquid nitrogen (LN2) for a period of 3 months. Cells were thawed at regular intervals and bioenergetic analysis performed using the Seahorse XFe96 flux analyser. Cryogenic storage reduced cell viability by 20%, but cell bioenergetic responses were largely intact for up to 1 month storage in LN2. However, after 1 month storage, mitochondrial function was impaired as reflected by decreasing basal respiration, ATP production, maximum (MAX) respiration, reserve capacity and coupling efficiency. Conversely, glycolytic activity was increased after 1 month, most notably the enhanced glycolytic response to 25 mM glucose without any change in glycolytic capacity. Finally, calculation of bioenergetic health index (BHI) demonstrated that this potential diagnostic parameter was sensitive to cryopreservation. The present study has demonstrated for the first time that cryopreservation of primary immune cells modified their metabolism in a time-dependent fashion, indicated by attenuated aerobic respiration and enhanced glycolytic activity. Taken together, we recommend caution in the interpretation of bioenergetic responses or BHI in cryopreserved samples.
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González-Casacuberta, Ingrid, Dolores Vilas, Claustre Pont-Sunyer, Ester Tobías, Judith Cantó-Santos, Laura Valls-Roca, Francesc Josep García-García, et al. "Neuronal induction and bioenergetics characterization of human forearm adipose stem cells from Parkinson’s disease patients and healthy controls." PLOS ONE 17, no. 3 (March 15, 2022): e0265256. http://dx.doi.org/10.1371/journal.pone.0265256.
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Neurodegenerative diseases, such as Parkinson’s disease, are heterogeneous disorders with a multifactorial nature involving impaired bioenergetics. Stem-regenerative medicine and bioenergetics have been proposed as promising therapeutic targets in the neurologic field. The rationale of the present study was to assess the potential of human-derived adipose stem cells (hASCs) to transdifferentiate into neuronal-like cells (NhASCs and neurospheres) and explore the hASC bioenergetic profile. hASC neuronal transdifferentiation was performed through neurobasal media and differentiation factor exposure. High resolution respirometry was assessed. Increased MAP-2 neuronal marker protein expression upon neuronal induction (p<0.05 undifferentiated hASCs vs. 28–36 days of differentiation) and increased bIII-tubulin neuronal marker protein expression upon neuronal induction (p<0.05 undifferentiated hASCs vs. 6-28-36 days of differentiation) were found. The bioenergetic profile was detectable through high-resolution respirometry approaches in hASCs but did not lead to differential oxidative capacity rates in healthy or clinically diagnosed PD-hASCs. We confirmed the capability of transdifferentiation to the neuronal-like profile of hASCs derived from the forearms of human subjects and characterized the bioenergetic profile. Suboptimal maximal respiratory capacity trends in PD were found. Neuronal induction leading to positive neuronal protein expression markers is a relevant issue that encourages the suitability of NhASC models in neurodegeneration.
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Tyrrell, Daniel J., Manish S. Bharadwaj, Matthew J. Jorgensen, Thomas C. Register, Carol Shively, Rachel N. Andrews, Bryan Neth, et al. "Blood-Based Bioenergetic Profiling Reflects Differences in Brain Bioenergetics and Metabolism." Oxidative Medicine and Cellular Longevity 2017 (2017): 1–9. http://dx.doi.org/10.1155/2017/7317251.
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Blood-based bioenergetic profiling provides a minimally invasive assessment of mitochondrial health shown to be related to key features of aging. Previous studies show that blood cells recapitulate mitochondrial alterations in the central nervous system under pathological conditions, including the development of Alzheimer’s disease. In this study of nonhuman primates, we focus on mitochondrial function and bioenergetic capacity assessed by the respirometric profiling of monocytes, platelets, and frontal cortex mitochondria. Our data indicate that differences in the maximal respiratory capacity of brain mitochondria are reflected by CD14+ monocyte maximal respiratory capacity and platelet and monocyte bioenergetic health index. A subset of nonhuman primates also underwent [18F] fluorodeoxyglucose positron emission tomography (FDG-PET) imaging to assess brain glucose metabolism. Our results indicate that platelet respiratory capacity positively correlates to measures of glucose metabolism in multiple brain regions. Altogether, the results of this study provide early evidence that blood-based bioenergetic profiling is related to brain mitochondrial metabolism. While these measures cannot substitute for direct measures of brain metabolism, provided by measures such as FDG-PET, they may have utility as a metabolic biomarker and screening tool to identify individuals exhibiting systemic bioenergetic decline who may therefore be at risk for the development of neurodegenerative diseases.
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Nicholls, David G., and Samantha L. Budd. "Mitochondria and Neuronal Survival." Physiological Reviews 80, no. 1 (January 1, 2000): 315–60. http://dx.doi.org/10.1152/physrev.2000.80.1.315.
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Mitochondria play a central role in the survival and death of neurons. The detailed bioenergetic mechanisms by which isolated mitochondria generate ATP, sequester Ca2+, generate reactive oxygen species, and undergo Ca2+-dependent permeabilization of their inner membrane are currently being applied to the function of mitochondria in situ within neurons under physiological and pathophysiological conditions. Here we review the functional bioenergetics of isolated mitochondria, with emphasis on the chemiosmotic proton circuit and the application (and occasional misapplication) of these principles to intact neurons. Mitochondria play an integral role in both necrotic and apoptotic neuronal cell death, and the bioenergetic principles underlying current studies are reviewed.
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Grimm, Amandine. "Impairments in Brain Bioenergetics in Aging and Tau Pathology: A Chicken and Egg Situation?" Cells 10, no. 10 (September 24, 2021): 2531. http://dx.doi.org/10.3390/cells10102531.
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The brain is the most energy-consuming organ of the body and impairments in brain energy metabolism will affect neuronal functionality and viability. Brain aging is marked by defects in energetic metabolism. Abnormal tau protein is a hallmark of tauopathies, including Alzheimer’s disease (AD). Pathological tau was shown to induce bioenergetic impairments by affecting mitochondrial function. Although it is now clear that mutations in the tau-coding gene lead to tau pathology, the causes of abnormal tau phosphorylation and aggregation in non-familial tauopathies, such as sporadic AD, remain elusive. Strikingly, both tau pathology and brain hypometabolism correlate with cognitive impairments in AD. The aim of this review is to discuss the link between age-related decrease in brain metabolism and tau pathology. In particular, the following points will be discussed: (i) the common bioenergetic features observed during brain aging and tauopathies; (ii) how age-related bioenergetic defects affect tau pathology; (iii) the influence of lifestyle factors known to modulate brain bioenergetics on tau pathology. The findings compiled here suggest that age-related bioenergetic defects may trigger abnormal tau phosphorylation/aggregation and cognitive impairments after passing a pathological threshold. Understanding the effects of aging on brain metabolism may therefore help to identify disease-modifying strategies against tau-induced neurodegeneration.
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Cardenuto, Léia M. "Creativity and Grounding in a Liquid World." Clinical Journal of the International Institute for Bioenergetic Analysis 24, no. 1 (March 2014): 85–103. http://dx.doi.org/10.30820/0743-4804-2014-24-85.
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After more than 14 years dwelling with the challenges of a Social Clinic in Focused Bioenergetics we intend to share our experience with the bioenergetic therapists community. In all those years we have learned much about the difficulties of establishing a line of work suitable to use the bioenergetic approach with troubled people in troubled social environments, in particular those outside of our consumer society. We had to rely more on a progressive approach than on a regressive one in order to bring the analytical process to a successful outcome, consistent with the focused bioenergetics method we adopted. In this process we did not abandon our psychoanalytic-based approach, but humbly adapted our understanding to terms that could be agreed between therapists and clients, establishing what we call the symbolic universe sharing. We were very moved by the theme chosen for the present conference, «The grounded body as a safe place in difficult times”, and felt we should attend. This is the first time a conference addressed exactly our difficulty. The new concepts that were developed during this process will be presented.
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Acin-Perez, Rebeca, Cristiane Benincá, Byourak Shabane, Orian S. Shirihai, and Linsey Stiles. "Utilization of Human Samples for Assessment of Mitochondrial Bioenergetics: Gold Standards, Limitations, and Future Perspectives." Life 11, no. 9 (September 10, 2021): 949. http://dx.doi.org/10.3390/life11090949.
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Mitochondrial bioenergetic function is a central component of cellular metabolism in health and disease. Mitochondrial oxidative phosphorylation is critical for maintaining energetic homeostasis, and impairment of mitochondrial function underlies the development and progression of metabolic diseases and aging. However, measurement of mitochondrial bioenergetic function can be challenging in human samples due to limitations in the size of the collected sample. Furthermore, the collection of samples from human cohorts is often spread over multiple days and locations, which makes immediate sample processing and bioenergetics analysis challenging. Therefore, sample selection and choice of tests should be carefully considered. Basic research, clinical trials, and mitochondrial disease diagnosis rely primarily on skeletal muscle samples. However, obtaining skeletal muscle biopsies requires an appropriate clinical setting and specialized personnel, making skeletal muscle a less suitable tissue for certain research studies. Circulating white blood cells and platelets offer a promising primary tissue alternative to biopsies for the study of mitochondrial bioenergetics. Recent advances in frozen respirometry protocols combined with the utilization of minimally invasive and non-invasive samples may provide promise for future mitochondrial research studies in humans. Here we review the human samples commonly used for the measurement of mitochondrial bioenergetics with a focus on the advantages and limitations of each sample.
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Castillo, Rodrigo L., Emilio A. Herrera, Alejandro Gonzalez-Candia, Marjorie Reyes-Farias, Nicole de la Jara, Juan Pedro Peña, and Catalina Carrasco-Pozo. "Quercetin Prevents Diastolic Dysfunction Induced by a High-Cholesterol Diet: Role of Oxidative Stress and Bioenergetics in Hyperglycemic Rats." Oxidative Medicine and Cellular Longevity 2018 (2018): 1–14. http://dx.doi.org/10.1155/2018/7239123.
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Alterations in cardiac energy metabolism play a key role in the pathogenesis of diabetic cardiomyopathy. Hypercholesterolemia associated with bioenergetic impairment and oxidative stress has not been well characterized in the cardiac function under glycemic control deficiency conditions. This work aimed to determine the cardioprotective effects of quercetin (QUE) against the damage induced by a high-cholesterol (HC) diet in hyperglycemic rats, addressing intracellular antioxidant mechanisms and bioenergetics. Quercetin reduced HC-induced alterations in the lipid profile and glycemia in rats. In addition, QUE attenuated cardiac diastolic dysfunction (increased E:A ratio), prevented cardiac cholesterol accumulation, and reduced the increase in HC-induced myocyte density. Moreover, QUE reduced HC-induced oxidative stress by preventing the decrease in GSH/GSSG ratio, Nrf2 nuclear translocation, HO-1 expression, and antioxidant enzymatic activity. Quercetin also counteracted HC-induced bioenergetic impairment, preventing a reduction in ATP levels and alterations in PGC-1α, UCP2, and PPARγ expression. In conclusion, the mechanisms that support the cardioprotective effect of QUE in rats with HC might be mediated by the upregulation of antioxidant mechanisms and improved bioenergetics on the heart. Targeting bioenergetics with QUE can be used as a pharmacological approach to modulate structural and functional changes of the heart under hypercholesterolemic and hyperglycemic conditions.
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Pandya, Jignesh D., Matthew Valdez, Joyce E. Royland, Robert C. MacPhail, Patrick G. Sullivan, and Prasada Rao S. Kodavanti. "Age- and Organ-Specific Differences in Mitochondrial Bioenergetics in Brown Norway Rats." Journal of Aging Research 2020 (April 1, 2020): 1–11. http://dx.doi.org/10.1155/2020/7232614.
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Mitochondria play a central role in energy homeostasis and act as regulatory checkpoints for downstream metabolic responses and cell senescence processes during an entire life span. Acute or chronic environmental toxicant exposures have shown deleterious organ-specific human health issues at various life stages. Since mitochondria are a prime target for ensuing cellular bioenergetics responses and senescence, it is essential to understand mitochondrial bioenergetic responses in different organs over multiple life stages. Therefore, in the present study, we evaluated mitochondrial bioenergetic parameters in the liver, lung, and heart in four diverse age groups (young: 1 month; adult: 4 months; middle-aged: 12 months; old-aged: 24 month) using male Brown Norway rats as a model of aging (n = 5 sample size/organ/age group) and compared them with our previously published results on brain. Real-time mitochondrial bioenergetic parameters (i.e., State III, State IV, and State V) were measured using the Seahorse Extracellular Flux Analyzer. Additionally, mitochondrial enzyme pyruvate dehydrogenase complex (PDHC), Complex I, Complex II, and Complex IV activities were measured using Synergy HT plate reader. Our results indicated that nearly in all parameters, significant age- and organ-specific interactions were observed. We observed age-specific declines in State III (i.e., ATP synthesis rate) responses in both the heart and lung, where opposite was observed in the liver as age advances. Across the age, the heart has highest enzyme activities than the liver and lung. Interestingly, heart and liver mitochondrial bioenergetic rates and enzyme activities remain higher than the lung, which specifies their higher metabolic capabilities than the lung. Amongst all, bioenergetic rates and enzyme activities in the lung remain lowest suggesting the lung may display higher vulnerability and lower resilience to environmental toxicants during aging than other organs tested here. Overall, these age- and organ-specific findings may facilitate a more contextualized understanding of mitochondrial bioenergetic outcomes when considering the interactions of age-related sensitivities with exposure to chemical stressors from the environment.
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Armstrong, Jane A., Nicole J. Cash, Yulin Ouyang, Jack C. Morton, Michael Chvanov, Diane Latawiec, Muhammad Awais, Alexei V. Tepikin, Robert Sutton, and David N. Criddle. "Oxidative stress alters mitochondrial bioenergetics and modifies pancreatic cell death independently of cyclophilin D, resulting in an apoptosis-to-necrosis shift." Journal of Biological Chemistry 293, no. 21 (April 6, 2018): 8032–47. http://dx.doi.org/10.1074/jbc.ra118.003200.
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Mitochondrial dysfunction lies at the core of acute pancreatitis (AP). Diverse AP stimuli induce Ca2+-dependent formation of the mitochondrial permeability transition pore (MPTP), a solute channel modulated by cyclophilin D (CypD), the formation of which causes ATP depletion and necrosis. Oxidative stress reportedly triggers MPTP formation and is elevated in clinical AP, but how reactive oxygen species influence cell death is unclear. Here, we assessed potential MPTP involvement in oxidant-induced effects on pancreatic acinar cell bioenergetics and fate. H2O2 application promoted acinar cell apoptosis at low concentrations (1–10 μm), whereas higher levels (0.5–1 mm) elicited rapid necrosis. H2O2 also decreased the mitochondrial NADH/FAD+ redox ratio and ΔΨm in a concentration-dependent manner (10 μm to 1 mm H2O2), with maximal effects at 500 μm H2O2. H2O2 decreased the basal O2 consumption rate of acinar cells, with no alteration of ATP turnover at <50 μm H2O2. However, higher H2O2 levels (≥50 μm) diminished spare respiratory capacity and ATP turnover, and bioenergetic collapse, ATP depletion, and cell death ensued. Menadione exerted detrimental bioenergetic effects similar to those of H2O2, which were inhibited by the antioxidant N-acetylcysteine. Oxidant-induced bioenergetic changes, loss of ΔΨm, and cell death were not ameliorated by genetic deletion of CypD or by its acute inhibition with cyclosporine A. These results indicate that oxidative stress alters mitochondrial bioenergetics and modifies pancreatic acinar cell death. A shift from apoptosis to necrosis appears to be associated with decreased mitochondrial spare respiratory capacity and ATP production, effects that are independent of CypD-sensitive MPTP formation.
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Kovacevic, Bozica, Corina Mihaela Ionescu, Melissa Jones, Susbin Raj Wagle, Michael Lewkowicz, Maja Đanić, Momir Mikov, Armin Mooranian, and Hani Al-Salami. "The Effect of Deoxycholic Acid on Chitosan-Enabled Matrices for Tissue Scaffolding and Injectable Nanogels." Gels 8, no. 6 (June 7, 2022): 358. http://dx.doi.org/10.3390/gels8060358.
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The pathophysiology of a multitude of diseases is influenced by bioenergetic dysfunction. Healthy mitochondria are presented as essential for the regulation and function of multiple cell types, including the cells of relevance for this research: pancreatic beta cells, muscle cells, and liver cells. Hence, effects of hydrogels (particularly nanogels) on bioenergetics needs to be taken into account when designing optimum delivery matrices. Several polymers have been suggested for use in hydrogels and nanogels, with focus on chitosan due to its range of beneficial properties. Bile acids have emerged as beneficial excipients, including deoxycholic acid, which can increase membrane permeability of cells. Nanogels were manufactured containing various concentrations of chitosan and deoxycholic acid in addition to the staple sodium alginate. Nanogels then underwent an array of analysis including rheological studies and in vitro cell work assessing viability, hypoxia, and the bioenergetic profiles. Overall, deoxycholic acid showed enhanced gel strength although this resulted in slightly lower cell viability and impacted bioenergetic profiles. Results from this study showed the benefits of deoxycholic acid; however, this was found to be less suitable for cell delivery matrices and is perhaps more beneficial for drug-delivery systems.
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Martino Adami, Pamela V., Celia Quijano, Natalia Magnani, Pablo Galeano, Pablo Evelson, Adriana Cassina, Sonia Do Carmo, et al. "Synaptosomal bioenergetic defects are associated with cognitive impairment in a transgenic rat model of early Alzheimer's disease." Journal of Cerebral Blood Flow & Metabolism 37, no. 1 (July 22, 2016): 69–84. http://dx.doi.org/10.1177/0271678x15615132.
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Synaptic bioenergetic deficiencies may be associated with early Alzheimer's disease (AD). To explore this concept, we assessed pre-synaptic mitochondrial function in hemizygous (+/−)TgMcGill-R-Thy1-APP rats. The low burden of Aβ and the wide array of behavioral and cognitive impairments described in 6-month-old hemizygous TgMcGill-R-Thy1-APP rats (Tg(+/−)) support their use to investigate synaptic bioenergetics deficiencies described in subjects with early Alzheimer's disease (AD). In this report, we show that pre-synaptic mitochondria from Tg(+/−) rats evidence a decreased respiratory control ratio and spare respiratory capacity associated with deficits in complex I enzymatic activity. Cognitive impairments were prevented and bioenergetic deficits partially reversed when Tg(+/−) rats were fed a nutritionally complete diet from weaning to 6-month-old supplemented with pyrroloquinoline quinone, a mitochondrial biogenesis stimulator with antioxidant and neuroprotective effects. These results provide evidence that, as described in AD brain and not proven in Tg mice models with AD-like phenotype, the mitochondrial bioenergetic capacity of synaptosomes is not conserved in the Tg(+/−) rats. This animal model may be suitable for understanding the basic biochemical mechanisms involved in early AD.
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Davies, Karen M., and Bertram Daum. "Role of cryo-ET in membrane bioenergetics research." Biochemical Society Transactions 41, no. 5 (September 23, 2013): 1227–34. http://dx.doi.org/10.1042/bst20130029.
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To truly understand bioenergetic processes such as ATP synthesis, membrane-bound substrate transport or flagellar rotation, systems need to be analysed in a cellular context. Cryo-ET (cryo-electron tomography) is an essential part of this process, as it is currently the only technique which can directly determine the spatial organization of proteins at the level of both the cell and the individual protein complexes. The need to assess bioenergetic processes at a cellular level is becoming more and more apparent with the increasing interest in mitochondrial diseases. In recent years, cryo-ET has contributed significantly to our understanding of the molecular organization of mitochondria and chloroplasts. The present mini-review first describes the technique of cryo-ET and then discusses its role in membrane bioenergetics specifically in chloroplasts and mitochondrial research.
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Swerdlow, Russell H. "Bioenergetic medicine." British Journal of Pharmacology 171, no. 8 (March 28, 2014): 1854–69. http://dx.doi.org/10.1111/bph.12394.
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Munroe, Alex. "The Role of Bioenergetic Supervision in Bioenergetic Training." Clinical Journal of the International Institute for Bioenergetic Analysis 19, no. 1 (March 2009): 101–12. http://dx.doi.org/10.30820/0743-4804-2009-19-101.
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Supervision plays a key role in a trainee’s movement towards certification as a Bioenergetic Therapist. It is therefore important to clearly understand and discuss the components of Bioenergetic supervision. Some commonalities for supervision in psychology, social work and Bioenergetic Analysis are set out. Aspects of supervision that are unique to Bioenergetic Analysis are identified. The paper concludes with an exercise to help the reader experience some of the Bioenergetic concepts presented. The paper is a beginning attempt to contribute to this discussion.
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Schroeter, Vincentia. "Borderline Character Structure Revisited." Clinical Journal of the International Institute for Bioenergetic Analysis 19, no. 1 (March 2009): 31–51. http://dx.doi.org/10.30820/0743-4804-2009-19-31.
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Review and revision of borderline character type etiology and dynamics from bioenergetic point of view. Exploring revisions and offering new theories related to body-type, age, major blocks, and continuum on developmental phases chart from object relations schema. Included are views from prevailing theories in psychology and within bioenergetics as well as from a current scientific study. Treatment aspects are discussed and relational interventions included.
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Valenti, Daniela, Fiorenza Stagni, Marco Emili, Sandra Guidi, Renata Bartesaghi, and Rosa Anna Vacca. "Impaired Brain Mitochondrial Bioenergetics in the Ts65Dn Mouse Model of Down Syndrome Is Restored by Neonatal Treatment with the Polyphenol 7,8-Dihydroxyflavone." Antioxidants 11, no. 1 (December 28, 2021): 62. http://dx.doi.org/10.3390/antiox11010062.
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Down syndrome (DS), a major genetic cause of intellectual disability, is characterized by numerous neurodevelopmental defects. Previous in vitro studies highlighted a relationship between bioenergetic dysfunction and reduced neurogenesis in progenitor cells from the Ts65Dn mouse model of DS, suggesting a critical role of mitochondrial dysfunction in neurodevelopmental alterations in DS. Recent in vivo studies in Ts65Dn mice showed that neonatal supplementation (Days P3–P15) with the polyphenol 7,8-dihydroxyflavone (7,8-DHF) fully restored hippocampal neurogenesis. The current study was aimed to establish whether brain mitochondrial bioenergetic defects are already present in Ts65Dn pups and whether early treatment with 7,8-DHF positively impacts on mitochondrial function. In the brain and cerebellum of P3 and P15 Ts65Dn pups we found a strong impairment in the oxidative phosphorylation apparatus, resulting in a deficit in mitochondrial ATP production and ATP content. Administration of 7,8-DHF (dose: 5 mg/kg/day) during Days P3–P15 fully restored bioenergetic dysfunction in Ts65Dn mice, reduced the levels of oxygen radicals and reinstated the hippocampal levels of PGC-1α. No pharmacotherapy is available for DS. From current findings, 7,8-DHF emerges as a treatment with a good translational potential for improving mitochondrial bioenergetics and, thus, mitochondria-linked neurodevelopmental alterations in DS.
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Esparza, Orlando, Giovanny Hernandez, Rachelle Nuss, David Irwin, Marguerite Kelher, Christopher C. Silliman, Kathryn L. Hassell, and Pavel Davizon-Castillo. "The Therapeutic Modalities of Sickle Cell Disease Reprogram the Platelet Functional-Bioenergetic Profile." Blood 138, Supplement 1 (November 5, 2021): 957. http://dx.doi.org/10.1182/blood-2021-153908.
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Abstract BACKGROUND: Sickle cell disease (SCD) is a group of inherited hemoglobinopathies that continues to be highly morbid and lethal. SCD-associated platelet hyperreactivity is a well-recognized contributor to the pathophysiology of the disease via complex interactions with the immune system and endothelium. Aberrant platelet bioenergetics have been implicated as a biological mechanism for SCD-associated platelet hyperreactivity, however, little is known about the impact current medical interventions (e.g., hydroxyurea [HU] and red blood cell [RBC] exchange transfusions) have on the platelet functional-bioenergetic profile. In this study we investigate the effects of hydroxyurea and RBC exchange transfusions on reprograming the platelet functional-bioenergetic profile and provide insight into biological pathways that may be amenable to intervention. METHODS: Platelets from sex-, race-, and aged-matched adult healthy control subjects and adult patients with homozygous SCD (HbSS), actively being treated with hydroxyurea (HU group) or RBC exchange transfusions (RBC exchange transfusion group), were isolated and washed following standard protocols. Platelet activation by flow cytometry was determined at baseline and following activation with thrombin (0.075U/ml) and ADP (1.25uM). Platelet-activated fibrinogen binding site (αIIbβIII), P-selectin, and phosphatidylserine (PS) surface marker expression (as measured by mean fluorescence intensity [MFI]) was determined with PAC-1, P-selectin, and lactadherin antibodies, respectively. The bioenergetic profile of washed platelets was determined by the 24-well format Seahorse extracellular flux analyzer. Statistical analyses were performed using the one-way ANOVA. Correlations were performed by 2-tailed nonparametric Spearman correlations and linear regression analysis with 95% confidence interval (GraphPad Software v9.1.2). Data expressed as mean plus or minus standard error of the mean (SEM). Differences were considered significant at p < 0.05. RESULTS: Platelets from patients in the HU group exhibited increased surface marker expression of αIIbβIII (p = 0.004), P-selectin (p = 0.003), and PS (p = 0.003) at resting conditions when compared to the RBC exchange transfusion group and healthy controls. Additionally, an increase in PS expression was seen in the HU group upon activation with ADP (p = 0.0003). No significant differences were seen in the platelet functional profile after activation with thrombin. The platelet bioenergetic profile in the HU group demonstrated an elevated proton leak (p = 0.03) when compared to the RBC exchange transfusion group. Elevated proton leak in SCD was found to have positive correlation with P-selectin and PS expression (Figure 1). CONCLUSION: While therapeutic interventions have improved overall outcomes in patients with SCD, adverse events continue to be a deterrent to many patients prompting the need for safer, more tolerable, and cost-effective alternatives. We have identified that while HU has little impact on the hyperreactive and procoagulant platelet phenotype in SCD, RBC exchange transfusions appear to mitigate the phenotype and reprogram the bioenergetic profile. Amongst treatment groups, a strong correlation was found between platelet activation markers (i.e., P-selectin and PS) and proton leak, suggesting an interplay between alterations in platelet bioenergetics and SCD-associated platelet hyperreactivity. Further studies are needed to elucidate the metabolic pathways that are responsible for the aberrant platelet functional-bioenergetic profile seen in SCD. These observations are important as targeting the platelet bioenergetic profile via less invasive and toxic therapeutic modalities may be equally efficacious as current interventions. Figure 1 Figure 1. Disclosures No relevant conflicts of interest to declare.
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Augsburger, Fiona, Elisa B. Randi, Mathieu Jendly, Kelly Ascencao, Nahzli Dilek, and Csaba Szabo. "Role of 3-Mercaptopyruvate Sulfurtransferase in the Regulation of Proliferation, Migration, and Bioenergetics in Murine Colon Cancer Cells." Biomolecules 10, no. 3 (March 13, 2020): 447. http://dx.doi.org/10.3390/biom10030447.
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3-mercaptopyruvate sulfurtransferase (3-MST) has emerged as one of the significant sources of biologically active sulfur species in various mammalian cells. The current study was designed to investigate the functional role of 3-MST’s catalytic activity in the murine colon cancer cell line CT26. The novel pharmacological 3-MST inhibitor HMPSNE was used to assess cancer cell proliferation, migration and bioenergetics in vitro. Methods included measurements of cell viability (MTT and LDH assays), cell proliferation and in vitro wound healing (IncuCyte) and cellular bioenergetics (Seahorse extracellular flux analysis). 3-MST expression was detected by Western blotting; H2S production was measured by the fluorescent dye AzMC. The results show that CT26 cells express 3-MST protein and mRNA, as well as several enzymes involved in H2S degradation (TST, ETHE1). Pharmacological inhibition of 3-MST concentration-dependently suppressed H2S production and, at 100 and 300 µM, attenuated CT26 proliferation and migration. HMPSNE exerted a bell-shaped effect on several cellular bioenergetic parameters related to oxidative phosphorylation, while other bioenergetic parameters were either unaffected or inhibited at the highest concentration of the inhibitor tested (300 µM). In contrast to 3-MST, the expression of CBS (another H2S producing enzyme which has been previously implicated in the regulation of various biological parameters in other tumor cells) was not detectable in CT26 cells and pharmacological inhibition of CBS exerted no significant effects on CT26 proliferation or bioenergetics. In summary, 3-MST catalytic activity significantly contributes to the regulation of cellular proliferation, migration and bioenergetics in CT26 murine colon cancer cells. The current studies identify 3-MST as the principal source of biologically active H2S in this cell line.
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Hafstad, Arild. "The Mysterious Life Energy." Clinical Journal of the International Institute for Bioenergetic Analysis 28, no. 1 (February 2018): 27–43. http://dx.doi.org/10.30820/0743-4804-2018-28-27.
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The paper explores empirical validation of the bioenergetic concept by randomized controlled research on the orgone box. To improve concept validity the author anchors the bioenergetic concept in physical principles and metabolism, combined with principles from Bioenergetic Analysis. The research lends support to the bioenergetic concept by showing that «contextual” stimulation (in the orgone box) can increase free energy in the human organism, indicating influence on a human bioenergetic system. These studies show that the human bioenergetic system is under contextual influence. The orgone theory has formal weaknesses and a sound scientific strategy gives priority to examining the equipment first.
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Kerr, S. R., and L. M. Dickie. "Bioenergetics of O+ Atlantic Herring (Clupea harengus harengus)." Canadian Journal of Fisheries and Aquatic Sciences 42, S1 (December 19, 1985): s105—s110. http://dx.doi.org/10.1139/f85-266.
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On the basis of the limited published information on herring bioenergetics, together with general considerations from other species, we propose a preliminary bioenergetic model for Atlantic herring (Clupea harengus harengus). Application of the model to published data for five larval cohorts from each of two years shows that temperature and body size interact with the apparent availability of suitable prey to result in quite different metabolic environments that support relatively uniform growth.
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Liu, Haoming, Yingying Du, Jean-Philippe St-Pierre, Mads S. Bergholt, Hélène Autefage, Jianglin Wang, Mingle Cai, Gaojie Yang, Molly M. Stevens, and Shengmin Zhang. "Bioenergetic-active materials enhance tissue regeneration by modulating cellular metabolic state." Science Advances 6, no. 13 (March 2020): eaay7608. http://dx.doi.org/10.1126/sciadv.aay7608.
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Cellular bioenergetics (CBE) plays a critical role in tissue regeneration. Physiologically, an enhanced metabolic state facilitates anabolic biosynthesis and mitosis to accelerate regeneration. However, the development of approaches to reprogram CBE, toward the treatment of substantial tissue injuries, has been limited thus far. Here, we show that induced repair in a rabbit model of weight-bearing bone defects is greatly enhanced using a bioenergetic-active material (BAM) scaffold compared to commercialized poly(lactic acid) and calcium phosphate ceramic scaffolds. This material was composed of energy-active units that can be released in a sustained degradation-mediated fashion once implanted. By establishing an intramitochondrial metabolic bypass, the internalized energy-active units significantly elevate mitochondrial membrane potential (ΔΨm) to supply increased bioenergetic levels and accelerate bone formation. The ready-to-use material developed here represents a highly efficient and easy-to-implement therapeutic approach toward tissue regeneration, with promise for bench-to-bedside translation.
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Adekunbi, Daniel, Cun Li, Peter Nathanielsz, and Adam Salmon. "SEX DIFFERENCES IN MITOCHONDRIAL RESILIENCE: EVIDENCE FROM BABOON HEPATOCYTES." Innovation in Aging 6, Supplement_1 (November 1, 2022): 813. http://dx.doi.org/10.1093/geroni/igac059.2928.
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Abstract Events that occur in utero set the trajectory for later-life diseases and longevity. Compelling data exist for interactions between developmental programming and aging, but the underlying mechanisms are not clearly defined. Fetal exposure to glucocorticoids (GC) is associated with alteration in hepatic enzymes and metabolic function in later life. We previously reported increased hepatic lipid accumulation and obese phenotype in middle-age male baboons exposed to GC as fetuses. The mitochondria play significant roles in cellular processes including stress responses and possibly a nexus between developmental programming and aging. The present study investigated the long-term effects of in utero GC exposure on mitochondrial bioenergetics using hepatocytes derived from aging baboons (16–18 years, average lifespan 21 years). Mitochondrial bioenergetics of both left and right lobe liver hepatocytes were examined as well as potential sex differences in mitochondrial function. Cell viability following isolation was similar among sexes and liver lobes but hepatocytes from males were highly energetic compared to females. Significant bioenergetic differences were observed in hepatocytes isolated from female baboons’ left and right liver lobes, with higher basal, maximal, and ATP-linked respiration in left lobe hepatocytes compared to the right lobe. These lobe-specific bioenergetic differences were absent in males. Interestingly, H2O2-induced oxidative stress significantly modified male baboon hepatocyte bioenergetics but females were unaffected, suggesting mitochondrial resilience in females compared to males. These data demonstrate that early life exposure to GC elicits a sex-specific effect on mitochondrial function. These mitochondrial differences might drive differences in cell senescence between males and females.
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Cegatti, Julia, and Leticia Polosecki. "Uses of the Sphere as a Motherfied Object in Bioenergetic Analysis." Clinical Journal of the International Institute for Bioenergetic Analysis 28, no. 1 (February 2018): 99–118. http://dx.doi.org/10.30820/0743-4804-2018-28-99.
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In this article we are going to present a «Biospheres” practice. It evolved as a result of integrating our formative experiences in Bioenergetics Analysis with the «Dynamic Sphere Postural Reorganization” (Esferodinamia Reorganización Postural, which will be referred to as «RP” technique). We describe the sphere (large rubber ball) qualities and how it can be helpful for body psychotherapy interventions. Finally, we look into two cases using this clinical tool. The sphere becomes an element that facilitates clinical and educational work in the contemporary Bioenergetic field.
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Bettinazzi, Stefano, Liliana Milani, Pierre U. Blier, and Sophie Breton. "Bioenergetic consequences of sex-specific mitochondrial DNA evolution." Proceedings of the Royal Society B: Biological Sciences 288, no. 1957 (August 18, 2021): 20211585. http://dx.doi.org/10.1098/rspb.2021.1585.
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Doubly uniparental inheritance (DUI) represents a notable exception to the general rule of strict maternal inheritance (SMI) of mitochondria in metazoans. This system entails the coexistence of two mitochondrial lineages (F- and M-type) transmitted separately through oocytes and sperm, thence providing an unprecedented opportunity for the mitochondrial genome to evolve adaptively for male functions. In this study, we explored the impact of a sex-specific mitochondrial evolution upon gamete bioenergetics of DUI and SMI bivalve species, comparing the activity of key enzymes of glycolysis, fermentation, fatty acid metabolism, tricarboxylic acid cycle, oxidative phosphorylation and antioxidant metabolism. Our findings suggest reorganized bioenergetic pathways in DUI gametes compared to SMI gametes. This generally results in a decreased enzymatic capacity in DUI sperm with respect to DUI oocytes, a limitation especially prominent at the terminus of the electron transport system. This bioenergetic remodelling fits a reproductive strategy that does not require high energy input and could potentially link with the preservation of the paternally transmitted mitochondrial genome in DUI species. Whether this phenotype may derive from positive or relaxed selection acting on DUI sperm is still uncertain.
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Affourtit, Charles, Ben Alberts, Jonathan Barlow, Jane E. Carré, and Anthony G. Wynne. "Control of pancreatic β-cell bioenergetics." Biochemical Society Transactions 46, no. 3 (April 17, 2018): 555–64. http://dx.doi.org/10.1042/bst20170505.
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The canonical model of glucose-stimulated insulin secretion (GSIS) by pancreatic β-cells predicts a glucose-induced rise in the cytosolic ATP/ADP ratio. Such bioenergetic sensitivity to metabolic fuel is unusual as it implies that ATP flux is governed, to a significant extent, by ATP supply, while it is predominantly demand-driven in other cell types. Metabolic control is generally shared between different processes, but potential control of ATP consumption over β-cell bioenergetics has been largely ignored to date. The present paper offers a brief overview of experimental evidence that demonstrates ATP flux control by glucose-fuelled oxidative phosphorylation. Based on old and new data, it is argued that ATP supply does not hold exclusive control over ATP flux, but shares it with ATP demand, and that the distribution of control is flexible. Quantification of the bioenergetic control distribution will be important from basic and clinical perspectives, but precise measurement of the cytosolic ATP/ADP ratio is complicated by adenine nucleotide compartmentalisation. Metabolic control analysis of β-cell bioenergetics will likely clarify the mechanisms by which glucose and fatty acids amplify and potentiate GSIS, respectively. Moreover, such analysis may offer hints as to how ATP flux control shifts from ATP supply to ATP demand during the development of type 2 diabetes, and why prolonged sulfonylurea treatment causes β-cell deterioration.
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Fan, Yang-Yi, Laurie A. Davidson, Evelyn S. Callaway, Gus A. Wright, Stephen Safe, and Robert S. Chapkin. "A bioassay to measure energy metabolism in mouse colonic crypts, organoids, and sorted stem cells." American Journal of Physiology-Gastrointestinal and Liver Physiology 309, no. 1 (July 1, 2015): G1—G9. http://dx.doi.org/10.1152/ajpgi.00052.2015.
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Evidence suggests that targeting cancer cell energy metabolism might be an effective therapeutic approach for selective ablation of malignancies. Using a Seahorse Extracellular Flux Analyzer, we have demonstrated that select environmental agents can alter colonic mitochondrial function by increasing respiration-induced proton leak, thereby inducing apoptosis, a marker of colon cancer risk. To further probe bioenergetics in primary intestinal cells, we developed methodology that can be modified and adapted to measure the bioenergetic profiles of colonic crypts, the basic functional unit of the colon, and colonic organoids, an ex vivo 3D culture of colonic crypts. Furthermore, in combination with the MoFlo Astrios High-Speed Cell Sorter, we were able to measure the bioenergetic profiles of colonic adult stem and daughter cells from Lgr5-EGFP-IRES-creERT2 transgenic mice. We examined the effects of 2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD), a full arylhydrocarbon receptor agonist, known to affect gastrointestinal function and cancer risk, on the bioenergetic profiles of intestinal epithelial cells. Mouse colonic crypts, organoids, or sorted single cells were seeded onto Matrigel-precoated Seahorse XF24 microplates for extracellular flux analysis. Temporal analyses revealed distinct energy metabolic profiles in crypts and organoids challenged with TCDD. Furthermore, sorted Lgr5+ stem cells exhibited a Warburg-like metabolic profile. This is noteworthy because perturbations in stem cell dynamics are generally believed to represent the earliest step toward colon tumorigenesis. We propose that our innovative methodology may facilitate future in vivo/ex vivo metabolic studies using environmental agents affecting colonocyte energy metabolism.
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Bafiti, Vivi, Sotiris Ouzounis, Eleni Siapi, Ioanna Maria Grypari, Andreas Theofanopoulos, Vasilios Panagiotopoulos, Vasiliki Zolota, Dimitrios Kardamakis, and Theodora Katsila. "Bioenergetic Profiling in Glioblastoma Multiforme Patients with Different Clinical Outcomes." Metabolites 13, no. 3 (February 28, 2023): 362. http://dx.doi.org/10.3390/metabo13030362.
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The accumulation of cell biomass is associated with dramatically increased bioenergetic and biosynthetic demand. Metabolic reprogramming, once thought as an epiphenomenon, currently relates to disease progression, also in response to extracellular fate-decisive signals. Glioblastoma multiforme patients often suffer misdiagnosis, short survival time, low quality of life, and poor disease management options. Today, tumor genetic testing and histological analysis guide diagnosis and treatment. We and others appreciate that metabolites complement translational biomarkers and molecular signatures in disease profiling and phenotyping. Herein, we coupled a mixed-methods content analysis to a mass spectrometry-based untargeted metabolomic analysis on plasma samples from glioblastoma multiforme patients to delineate the role of metabolic remodeling in biological plasticity and, hence, disease severity. Following data processing and analysis, we established a bioenergetic profile coordinated by the mitochondrial function and redox state, lipids, and energy substrates. Our findings show that epigenetic modulators are key players in glioblastoma multiforme cell metabolism, in particular when microRNAs are considered. We propose that biological plasticity in glioblastoma multiforme is a mechanism of adaptation and resistance to treatment which is eloquently revealed by bioenergetics.
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Osorio, Teresa, Ernest R. Scoma, Daniel H. Shain, Diana S. Melissaratos, Lindsey M. Riggs, Vedangi Hambardikar, and Maria E. Solesio. "The Glacier Ice Worm, Mesenchytraeus solifugus, Elevates Mitochondrial Inorganic Polyphosphate (PolyP) Levels in Response to Stress." Biology 11, no. 12 (December 6, 2022): 1771. http://dx.doi.org/10.3390/biology11121771.
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The inorganic polymer, polyphosphate (polyP), is present in all organisms examined to date with putative functions ranging from the maintenance of bioenergetics to stress resilience and protein homeostasis. Bioenergetics in the glacier-obligate, segmented worm, Mesenchytraeus solifugus, is characterized by a paradoxical increase in intracellular ATP levels as temperatures decline. We show here that steady-state, mitochondrial polyP levels vary among species of Annelida, but were elevated only in M. solifugus in response to thermal stress. In contrast, polyP levels decreased with temperature in the mesophilic worm, Enchytraeus crypticus. These results identify fundamentally different bioenergetic strategies between closely related annelid worms, and suggest that I worm mitochondria maintain ATP and polyP in a dynamic equilibrium.
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Nesbeth, Paula-Dene, Thomas Ziegler, Daiana Weiss, Li Hao, Matthew Smith, Dean Jones, M. Neale Weitzmann, and Jessica Alvarez. "Linoleic Acid Reduces Oxidative Phosphorylation and Impairs Early Differentiation of MC3T3-E1 Osteoblast Precursor Cells." Current Developments in Nutrition 6, Supplement_1 (June 2022): 452. http://dx.doi.org/10.1093/cdn/nzac057.018.
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Abstract Objectives Untargeted metabolomics analyses by our group have shown that plasma linoleic acid (LA) was inversely associated with bone mineral density Z-score and that bone formation indices were associated with energy-generating metabolic pathways, including fatty acid b-oxidation, in adult cohorts. Here, we examined the effect of increasing LA concentrations on osteoblast precursor cell bioenergetics and osteoblast differentiation to determine whether high LA is detrimental to bone formation. Methods We treated MC3T3-E1 pre-osteoblastic cells with 0 µM (control), 1 μM, and 50 μM LA cultured in osteogenic differentiation media supplemented with 50 µM L-ascorbic acid and 2 mM β-glycerophosphate. To assess the effect of LA on early commitment/differentiation, cells were stained for alkaline phosphatase activity and late differentiation using Alizarin Red S staining for mineral deposition, at 7 and 18 days, respectively. To assess cellular bioenergetics, real-time ATP production rates in LA treated (1 or 50 μM) and control MC3T3-E1 cells were measured using an extracellular flux analyzer after 24 hours (normalized for total protein content). Differences in bioenergetic values were determined using one-way ANOVA or Kruskal-Wallis test with Tukey's HSD or Dunn's post hoc tests. Results While LA had no effect on late differentiation/mineralizing activity of MC3T3 cells, LA dose-dependently decreased commitment/early differentiation. LA also significantly altered the bioenergetic profile of MC3T3-E1 cells by decreasing basal oxygen consumption rate (P < 0.001), as well as mitochondrial and total ATP production rate (P < 0.05 and P < 0.001, respectively). There were no significant changes in glycolytic ATP production rate. Conclusions Osteoblast differentiation is a highly bioenergetic process, and this study suggests excess LA may impair ATP production from oxidative phosphorylation. This, in turn, may impede commitment and early differentiation of osteoblasts. Our study supports further clinical and translational investigation into the role of LA and energy metabolism in osteoblast function, as well as bone formation. Funding Sources National Institutes of Health.
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Shapiro, Bennett. "Bioenergetic Boundary-Building." Clinical Journal of the International Institute for Bioenergetic Analysis 16, no. 1 (March 2006): 155–78. http://dx.doi.org/10.30820/0743-4804-2006-16-155.
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The purpose of this article is to stimulate you to think about your own boundary issues and explore five components for strengthening your boundaries while experiencing three exercises. There are six sections: I. Strong Boundaries vs. Weak Boundaries discusses how strong healthy boundaries are formed when, as infants/ young children, our outgoing impulses are met appropriately; conversely, weak boundaries result from our impulses being met inappropriately, and/or even hurtfully. II. Which Boundary is More Like Your Own Boundary? asks you to consider if your boundary issues are »too loose«, »too tight«, or a combination of »loose« and »tight«. III. Five Components of Bioenergetic Boundary-Building describes the energetic, muscular and psychological aspects of five major components for Boundary-Building, and each component’s usefulness in tightening boundaries that are »too loose« or loosening boundaries that are »too tight«. IV. Three Physical Exercises for Strengthening your Boundaries gives you some direct experience of the five components; doing these exercises will help strengthen your boundaries and diagnose your boundary issues. V. Utilizing Boundary Supports describes the various boundary supports, the effects of exercises involving these supports, theoretical explanations and implications for ongoing therapy. VI. Future Investigations.
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Sousa, Filipa L., Thorsten Thiergart, Giddy Landan, Shijulal Nelson-Sathi, Inês A. C. Pereira, John F. Allen, Nick Lane, and William F. Martin. "Early bioenergetic evolution." Philosophical Transactions of the Royal Society B: Biological Sciences 368, no. 1622 (July 19, 2013): 20130088. http://dx.doi.org/10.1098/rstb.2013.0088.
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Life is the harnessing of chemical energy in such a way that the energy-harnessing device makes a copy of itself. This paper outlines an energetically feasible path from a particular inorganic setting for the origin of life to the first free-living cells. The sources of energy available to early organic synthesis, early evolving systems and early cells stand in the foreground, as do the possible mechanisms of their conversion into harnessable chemical energy for synthetic reactions. With regard to the possible temporal sequence of events, we focus on: (i) alkaline hydrothermal vents as the far-from-equilibrium setting, (ii) the Wood–Ljungdahl (acetyl-CoA) pathway as the route that could have underpinned carbon assimilation for these processes, (iii) biochemical divergence, within the naturally formed inorganic compartments at a hydrothermal mound, of geochemically confined replicating entities with a complexity below that of free-living prokaryotes, and (iv) acetogenesis and methanogenesis as the ancestral forms of carbon and energy metabolism in the first free-living ancestors of the eubacteria and archaebacteria, respectively. In terms of the main evolutionary transitions in early bioenergetic evolution, we focus on: (i) thioester-dependent substrate-level phosphorylations, (ii) harnessing of naturally existing proton gradients at the vent–ocean interface via the ATP synthase, (iii) harnessing of Na + gradients generated by H + /Na + antiporters, (iv) flavin-based bifurcation-dependent gradient generation, and finally (v) quinone-based (and Q-cycle-dependent) proton gradient generation. Of those five transitions, the first four are posited to have taken place at the vent. Ultimately, all of these bioenergetic processes depend, even today, upon CO 2 reduction with low-potential ferredoxin (Fd), generated either chemosynthetically or photosynthetically, suggesting a reaction of the type ‘reduced iron → reduced carbon’ at the beginning of bioenergetic evolution.
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Tasche, Jens. "Self-Regulation and Psychodynamics in Bioenergetic Analysis." Clinical Journal of the International Institute for Bioenergetic Analysis 31, no. 1 (May 2021): 59–78. http://dx.doi.org/10.30820/0743-4804-2021-31-59.
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This article presents ten theses containing theoretical considerations for a postgraduate curriculum as currently tested by the Polish Society for Bioenergetic Analysis. The bioenergetic notion of the self, of affect regulation and of mental defense are modified in order to allow for psychodynamic conflict-, structureand trauma-pathological concepts to be integrated into Bioenergetic Analysis. Among other advantages, this approach facilitates the work with structural disorders (narcissism, borderline personality disorder) in Bioenergetic Analysis.
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Bottoni, Patrizia, Alessandro Pontoglio, Salvatore Scarà, Luisa Pieroni, Andrea Urbani, and Roberto Scatena. "Mitochondrial Respiratory Complexes as Targets of Drugs: The PPAR Agonist Example." Cells 11, no. 7 (March 30, 2022): 1169. http://dx.doi.org/10.3390/cells11071169.
Full textAbstract:
Mitochondrial bioenergetics are progressively acquiring significant pathophysiological roles. Specifically, mitochondria in general and Electron Respiratory Chain in particular are gaining importance as unintentional targets of different drugs. The so-called PPAR ligands are a class of drugs which not only link and activate Peroxisome Proliferator-Activated Receptors but also show a myriad of extrareceptorial activities as well. In particular, they were shown to inhibit NADH coenzyme Q reductase. However, the molecular picture of this intriguing bioenergetic derangement has not yet been well defined. Using high resolution respirometry, both in permeabilized and intact HepG2 cells, and a proteomic approach, the mitochondrial bioenergetic damage induced by various PPAR ligands was evaluated. Results show a derangement of mitochondrial oxidative metabolism more complex than one related to a simple perturbation of complex I. In fact, a partial inhibition of mitochondrial NADH oxidation seems to be associated not only with hampered ATP synthesis but also with a significant reduction in respiratory control ratio, spare respiratory capacity, coupling efficiency and, last but not least, serious oxidative stress and structural damage to mitochondria.
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Serbulea, Vlad, Clint M. Upchurch, Michael S. Schappe, Paxton Voigt, Dory E. DeWeese, Bimal N. Desai, Akshaya K. Meher, and Norbert Leitinger. "Macrophage phenotype and bioenergetics are controlled by oxidized phospholipids identified in lean and obese adipose tissue." Proceedings of the National Academy of Sciences 115, no. 27 (June 11, 2018): E6254—E6263. http://dx.doi.org/10.1073/pnas.1800544115.
Full textAbstract:
Adipose tissue macrophages (ATMs) adapt their metabolic phenotype either to maintain lean tissue homeostasis or drive inflammation and insulin resistance in obesity. However, the factors in the adipose tissue microenvironment that control ATM phenotypic polarization and bioenergetics remain unknown. We have recently shown that oxidized phospholipids (OxPL) uniquely regulate gene expression and cellular metabolism in Mox macrophages, but the presence of the Mox phenotype in adipose tissue has not been reported. Here we show, using extracellular flux analysis, that ATMs isolated from lean mice are metabolically inhibited. We identify a unique population of CX3CR1neg/F4/80low ATMs that resemble the Mox (Txnrd1+HO1+) phenotype to be the predominant ATM phenotype in lean adipose tissue. In contrast, ATMs isolated from obese mice had characteristics typical of the M1/M2 (CD11c+CD206+) phenotype with highly activated bioenergetics. Quantifying individual OxPL species in the stromal vascular fraction of murine adipose tissue, using targeted liquid chromatography-mass spectrometry, revealed that high fat diet-induced adipose tissue expansion led to a disproportional increase in full-length over truncated OxPL species. In vitro studies showed that macrophages respond to truncated OxPL species by suppressing bioenergetics and up-regulating antioxidant programs, mimicking the Mox phenotype of ATMs isolated from lean mice. Conversely, full-length OxPL species induce proinflammatory gene expression and an activated bioenergetic profile that mimics ATMs isolated from obese mice. Together, these data identify a redox-regulatory Mox macrophage phenotype to be predominant in lean adipose tissue and demonstrate that individual OxPL species that accumulate in adipose tissue instruct ATMs to adapt their phenotype and bioenergetic profile to either maintain redox homeostasis or to promote inflammation.
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Skulachev, Vladimir P. "Bioenergetics: the evolution of molecular mechanisms and the development of bioenergetic concepts." Antonie van Leeuwenhoek 65, no. 4 (1994): 271–84. http://dx.doi.org/10.1007/bf00872213.
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Lee, Seong-il, Janneke G. J. Hoeijmakers, Catharina G. Faber, Ingemar S. J. Merkies, Giuseppe Lauria, and Stephen G. Waxman. "The small fiber neuropathy NaV1.7 I228M mutation: impaired neurite integrity via bioenergetic and mitotoxic mechanisms, and protection by dexpramipexole." Journal of Neurophysiology 123, no. 2 (February 1, 2020): 645–57. http://dx.doi.org/10.1152/jn.00360.2019.
Full textAbstract:
Gain-of-function variants in voltage-gated sodium channel NaV1.7 that increase firing frequency and spontaneous firing of dorsal root ganglion (DRG) neurons have recently been identified in 5–10% of patients with idiopathic small fiber neuropathy (I-SFN). Our previous in vitro observations suggest that enhanced sodium channel activity can contribute to a decrease in length of peripheral sensory axons. We have hypothesized that sustained sodium influx due to the expression of SFN-associated sodium channel variants may trigger an energetic deficit in neurons that contributes to degeneration and loss of nerve fibers in SFN. Using an ATP FRET biosensor, we now demonstrate reduced steady-state levels of ATP and markedly faster ATP decay in response to membrane depolarization in cultured DRG neurons expressing an SFN-associated variant NaV1.7, I228M, compared with wild-type neurons. We also observed that I228M neurons show a significant reduction in mitochondrial density and size, indicating dysfunctional mitochondria and a reduced bioenergetic capacity. Finally, we report that exposure to dexpramipexole, a drug that improves mitochondrial energy metabolism, increases the neurite length of I228M-expressing neurons. Our data suggest that expression of gain-of-function variants of NaV1.7 can damage mitochondria and compromise cellular capacity for ATP production. The resulting bioenergetic crisis can consequently contribute to loss of axons in SFN. We suggest that, in addition to interventions that reduce ionic disturbance caused by mutant NaV1.7 channels, an alternative therapeutic strategy might target the bioenergetic burden and mitochondrial damage that occur in SFN associated with NaV1.7 gain-of-function mutations. NEW & NOTEWORTHY Sodium channel NaV1.7 mutations that increase dorsal root ganglion (DRG) neuron excitability have been identified in small fiber neuropathy (SFN). We demonstrate reduced steady-state ATP levels, faster depolarization-evoked ATP decay, and reduced mitochondrial density and size in cultured DRG neurons expressing SFN-associated variant NaV1.7 I228M. Dexpramipexole, which improves mitochondrial energy metabolism, has a protective effect. Because gain-of-function NaV1.7 variants can compromise bioenergetics, therapeutic strategies that target bioenergetic burden and mitochondrial damage merit study in SFN.