Relationship of Mitochondrial Enzymes to Fatigue Intensity in Men With Prostate Cancer Receiving External Beam Radiation Therapy

Filler, Kristin; Lyon, Debra E.; McCain, Nancy L.; Bennett, James P.; Fernández-Martínez, Juan Luis; deAndrés-Galiana, Enrique J.; Elswick, R. K.; Lukkahatai, Nada; Saligan, Leorey N.

doi:10.1177/1099800415617848

Cited by 15 publications

(18 citation statements)

References 26 publications

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“…In sum, most evidence for an association between fatigue and mitochondrial functioning comes from CFS, indicating lower levels of antioxidants and possible reductions in mitochondrial ATP production. While lower antioxidant levels were not found in cancer patients (Filler et al, 2016 ), alterations in mitochondrial gene expression do indicate a role for mitochondrial functioning in fatigue. Results from clinical and pre-clinical studies point toward possible beneficial effects of mitochondria-supporting supplements.…”

Section: Persistent Fatigue As a Results Of Reduced Energy Availabilitmentioning

confidence: 98%

“…However, a handful of observational patient studies from one research group report an association in prostate cancer patients undergoing radiation therapy. Their results point to reduced mitochondrial functioning in association with fatigue, as evidenced by reduced expression of mitochondria-related genes (Hsiao et al, 2013 , 2014 ), decreased expression of mitochondrial electron transport complex II enzymes (Filler et al, 2016 ), and increased apoliprotein A1 (ApoA1) in association with higher fatigue (Lukkahatai et al, 2014 ). ApoA1 is important for lipid scavenging, and an increase in ApoA1 is indicative of a reduced use of lipids for ATP synthesis.…”

Section: Persistent Fatigue As a Results Of Reduced Energy Availabilitmentioning

confidence: 99%

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The High Costs of Low-Grade Inflammation: Persistent Fatigue as a Consequence of Reduced Cellular-Energy Availability and Non-adaptive Energy Expenditure

Lacourt

Vichaya

Chiu

et al. 2018

Front. Behav. Neurosci.

130

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Chronic or persistent fatigue is a common, debilitating symptom of several diseases. Persistent fatigue has been associated with low-grade inflammation in several models of fatigue, including cancer-related fatigue and chronic fatigue syndrome. However, it is unclear how low-grade inflammation leads to the experience of fatigue. We here propose a model of an imbalance in energy availability and energy expenditure as a consequence of low-grade inflammation. In this narrative review, we discuss how chronic low-grade inflammation can lead to reduced cellular-energy availability. Low-grade inflammation induces a metabolic switch from energy-efficient oxidative phosphorylation to fast-acting, but less efficient, aerobic glycolytic energy production; increases reactive oxygen species; and reduces insulin sensitivity. These effects result in reduced glucose availability and, thereby, reduced cellular energy. In addition, emerging evidence suggests that chronic low-grade inflammation is associated with increased willingness to exert effort under specific circumstances. Circadian-rhythm changes and sleep disturbances might mediate the effects of inflammation on cellular-energy availability and non-adaptive energy expenditure. In the second part of the review, we present evidence for these metabolic pathways in models of persistent fatigue, focusing on chronic fatigue syndrome and cancer-related fatigue. Most evidence for reduced cellular-energy availability in relation to fatigue comes from studies on chronic fatigue syndrome. While the mechanistic evidence from the cancer-related fatigue literature is still limited, the sparse results point to reduced cellular-energy availability as well. There is also mounting evidence that behavioral-energy expenditure exceeds the reduced cellular-energy availability in patients with persistent fatigue. This suggests that an inability to adjust energy expenditure to available resources might be one mechanism underlying persistent fatigue.

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Section: Persistent Fatigue As a Results Of Reduced Energy Availabilitmentioning

confidence: 98%

Section: Persistent Fatigue As a Results Of Reduced Energy Availabilitmentioning

confidence: 99%

The High Costs of Low-Grade Inflammation: Persistent Fatigue as a Consequence of Reduced Cellular-Energy Availability and Non-adaptive Energy Expenditure

Lacourt

Vichaya

Chiu

et al. 2018

Front. Behav. Neurosci.

130

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“…Unfortunately, the scientific community has not come to a consensus on a standard definition of symptom phenotypes, which has implications for symptom assessment and management. The CRS consortium is dedicated to addressing the many challenges facing CRS science research (Filler et al, ; Gonzalez, Abbas‐Aghababazadeh, Fridley, Ghansah, & Saligan, ; Hsiao, Wang, Kaushal, Chen, & Saligan, ; Lukkahatai, Patel, Gucek, Hsiao, & Saligan, ; Lynch Kelly et al, ; Mayo et al, ; McCabe, ; Musanti & Murley, ).…”

Section: Research Exemplars and Outcomes Of The Crs Consortiummentioning

confidence: 99%

“…Using the SSM, several CRS consortium members incorporate omics approaches to generate new hypotheses that can be used for grant applications and establish a network of multidisciplinary collaborations. For example, consortium members observed the associations of cancer‐related fatigue with the differential expressions of genes associated with mitochondrial bioenergetics (Filler et al, ; Hsiao, Wang, Kaushal, & Saligan, ; Hsiao et al, ), neurotrophic process (Saligan et al, ), metabolic (Gonzalez et al, ), and inflammatory pathways using genomic and proteomic methodologies (Saligan et al, ). Recently, how cancer treatments perturb the gastrointestinal microbiome, also termed dysbiosis, has become an emerging area of investigation for some members of the CRS consortium.…”

Section: Research Exemplars and Outcomes Of The Crs Consortiummentioning

confidence: 99%

Consortium Building for Nurse Scientists Interested in Symptoms Research in the Era of Precision Health

Hsiao

Dickinson

González-Mercado

et al. 2019

J of Nursing Scholarship

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Purpose This article aims to provide perspectives on the establishment of a consortium for nurse scientists with similar career trajectories interested in cancer‐related symptoms (CRS) research. Hereby, we describe the development of and recent outcomes from the CRS consortium, the lessons learned in establishing the consortium, and future directions to advance the science of CRS. Model and Methods New and innovative strategies are needed to address the complexity of CRS research. A CRS consortium was created to allow a mechanism for oncology nurse scientists with varying expertise to collaborate to advance CRS research. The National Institutes of Health (NIH) Symptom Science Model (SSM) guides the research of the CRS Consortium. Discussion and Conclusions A need for improved CRS assessment and management has been identified. The CRS consortium was created as a collaborative think tank to begin to address this need. Guided by the NIH SSM, CRS consortium members have worked to define symptom phenotypes, enhance understanding of the biologic mechanisms that can contribute to symptom phenotypes, and develop tailored interventions to improve symptom management. Dissemination of the CRS consortium efforts involve publications and presentations. Clinical Implications Nurse scientists interested in symptom science and biobehavorial research face many challenges on how to initiate and sustain independent programs of research. Through the formation of a CRS consortium, oncology nurse scientists can work together to address identified issues in symptom measurement and management.

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“…6 Perhaps in a related mechanism, aerobic exercise has been shown to improve fatigue in men with prostate cancer undergoing radiotherapy. 2,7,8 Mitochondrial genetics 9 and enzymatic dysregulation 10 have also been associated with RIF in PCPs. The proposed association of RIF with mitochondrial function is linked to adenosine triphosphate depletion and impairment of mitochondrial bioenergetics, because of radiation-induced genetic instability and cellular damage.…”

Section: Introductionmentioning

confidence: 99%

Exploring Genetic Attributions Underlying Radiotherapy-Induced Fatigue in Prostate Cancer Patients

Hashemi

Martínez

Saligan

et al. 2017

Journal of Pain and Symptom Management

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The implications of herein presented RIF pathways are purely theoretical until specific end-point driven experiments are conducted in more congruent contexts. Nevertheless, the presented attributions are informative, directing future investigation to definitively elucidate RIF's pathoetiology. This study demonstrates an arguably comprehensive method of approaching known differential expression underlying a complex phenotype, to correlate feasible pathophysiology.

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Relationship of Mitochondrial Enzymes to Fatigue Intensity in Men With Prostate Cancer Receiving External Beam Radiation Therapy

Abstract: Distinct patterns of changes in the absorbance of MOPC enzymes delineated fatigue intensification among participants. Further investigation using a larger sample is warranted.

Cited by 15 publications

References 26 publications

The High Costs of Low-Grade Inflammation: Persistent Fatigue as a Consequence of Reduced Cellular-Energy Availability and Non-adaptive Energy Expenditure

The High Costs of Low-Grade Inflammation: Persistent Fatigue as a Consequence of Reduced Cellular-Energy Availability and Non-adaptive Energy Expenditure

Consortium Building for Nurse Scientists Interested in Symptoms Research in the Era of Precision Health

Exploring Genetic Attributions Underlying Radiotherapy-Induced Fatigue in Prostate Cancer Patients

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