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https://www.readbyqxmd.com/read/28811294/dihydrocapsiate-improved-age-associated-impairments-in-mice-by-increasing-energy-expenditure
#1
Kana Ohyama, Katsuya Suzuki
Metabolic dysfunction is associated with aging and results in age-associated chronic diseases, including type 2 diabetes mellitus, cardiovascular disease, and stroke. Hence, there has been a focus on increasing energy expenditure in aged populations to protect them from age-associated diseases. Dihydrocapsiate (DCT) is a compound that belongs to the capsinoid family. Capsinoids are capsaicin analogs that are found in non-pungent peppers and increase whole-body energy expenditure. However, their effect on energy expenditure has been reported only in young populations, and to date the effectiveness of DCT in increasing energy expenditure in aged populations has not been investigated...
August 15, 2017: American Journal of Physiology. Endocrinology and Metabolism
https://www.readbyqxmd.com/read/28807815/bcl-xl-knockout-attenuates-mitochondrial-respiration-and-causes-oxidative-stress-that-is-compensated-by-pentose-phosphate-pathway-activity
#2
Annika Pfeiffer, Julia Schneider, Diones Bueno, Amalia Dolga, Timo-Daniel Voss, Jan Lewerenz, Verena Wüllner, Axel Methner
Bcl-xL is an anti-apoptotic protein that localizes to the outer mitochondrial membrane and influences mitochondrial bioenergetics by controlling Ca(2+) influx into mitochondria. Here, we analyzed the effect of mitochondrial Bcl-xL on mitochondrial shape and function in knockout (KO), wildtype and rescued mouse embryonic fibroblast cell lines. Mitochondria of KO cells were more fragmented, exhibited a reduced ATP concentration, and reduced oxidative phosphorylation (OXPHOS) suggesting an increased importance of ATP generation by other means...
August 11, 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28797070/methyl-pyruvate-protects-a-normal-lung-fibroblast-cell-line-from-irinotecan-induced-cell-death-potential-use-as-adjunctive-to-chemotherapy
#3
Bernice Monchusi, Monde Ntwasa
The Warburg Effect, characterized by increased rate of glycolysis even under normoxic conditions, is one of the hallmarks of cancer. Relatively lower oxidative phosphorylation (OXPHOS) is also a characteristic feature in cancer cells. We hypothesized that interference with this phenomenon, by introducing exogenous pyruvate, would upset this cancer phenotype and boost the energy requirements of normal cells. We find that methyl pyruvate protects irinotecan-treated normal lung fibroblast cell line (MRC-5) probably by turning off the p53/p21 axis of the apoptotic pathways...
2017: PloS One
https://www.readbyqxmd.com/read/28795454/the-tcf7l2-pgc1%C3%AE-axis-connects-mitochondrial-biogenesis-and-metabolic-shift-with-stem-cell-commitment-to-hepatic-differentiation
#4
Anaïs Wanet, Marino Caruso, Jean-Baka Domelevo Entfellner, Mehdi Najar, Antoine Fattaccioli, Catherine Demazy, Jonathan Evraerts, Hoda El-Kehdy, Guillaume Pourcher, Etienne Sokal, Thierry Arnould, Nicki Tiffin, Mustapha Najimi, Patricia Renard
Increasing evidence supports that modifications in the mitochondrial content, oxidative phosphorylation (OXPHOS) activity, and cell metabolism influence the fate of stem cells. However, the regulators involved in the crosstalk between mitochondria and stem cell fate remain poorly characterized. Here, we identified a transcriptional regulatory axis, composed of TCF7L2 (transcription factor 7 like 2, a downstream effector of the Wnt/β-catenin pathway, repressed during differentiation) and PGC-1α (peroxisome proliferator-activated receptor gamma coactivator 1 alpha, the master regulator of mitochondrial biogenesis, induced during differentiation), coupling the loss of pluripotency and early commitment to differentiation, to the initiation of mitochondrial biogenesis and metabolic shift toward OXPHOS...
August 10, 2017: Stem Cells
https://www.readbyqxmd.com/read/28793231/association-of-mitochondrial-dna-10398-a-g-polymorphism-with-attention-deficit-and-hyperactivity-disorder-in-korean-children
#5
In Wook Hwang, Jun Ho Hong, Bit Na Kwon, Hyung Jun Kim, Nu Ri Lee, Myung Ho Lim, Ho Jang Kwon, Han Jun Jin
Mitochondria are subcellular organelles that contribute to aerobic ATP generation by oxidative phosphorylation (OXPHOS). Previous studies reported that mitochondrial dysfunction and deficiency caused by mitochondrial DNA polymorphisms is associated with various diseases. Especially, mitochondrial DNA 10398 A/G polymorphism is known to affect the regulation of mitochondrial calcium levels related to energy production, and its association with psychiatric disorders such as schizophrenia and bipolar disorder has been reported...
August 6, 2017: Gene
https://www.readbyqxmd.com/read/28777931/biallelic-mutations-in-mrps34-lead-to-instability-of-the-small-mitoribosomal-subunit-and-leigh-syndrome
#6
Nicole J Lake, Bryn D Webb, David A Stroud, Tara R Richman, Benedetta Ruzzenente, Alison G Compton, Hayley S Mountford, Juliette Pulman, Coralie Zangarelli, Marlene Rio, Nathalie Bodaert, Zahra Assouline, Mingma D Sherpa, Eric E Schadt, Sander M Houten, James Byrnes, Elizabeth M McCormick, Zarazuela Zolkipli-Cunningham, Katrina Haude, Zhancheng Zhang, Kyle Retterer, Renkui Bai, Sarah E Calvo, Vamsi K Mootha, John Christodoulou, Agnes Rötig, Aleksandra Filipovska, Ingrid Cristian, Marni J Falk, Metodi D Metodiev, David R Thorburn
The synthesis of all 13 mitochondrial DNA (mtDNA)-encoded protein subunits of the human oxidative phosphorylation (OXPHOS) system is carried out by mitochondrial ribosomes (mitoribosomes). Defects in the stability of mitoribosomal proteins or mitoribosome assembly impair mitochondrial protein translation, causing combined OXPHOS enzyme deficiency and clinical disease. Here we report four autosomal-recessive pathogenic mutations in the gene encoding the small mitoribosomal subunit protein, MRPS34, in six subjects from four unrelated families with Leigh syndrome and combined OXPHOS defects...
August 3, 2017: American Journal of Human Genetics
https://www.readbyqxmd.com/read/28769029/loss-of-succinyl-coa-synthase-adp-forming-%C3%AE-subunit-disrupts-mtdna-stability-and-mitochondrial-dynamics-in-neurons
#7
Yujun Zhao, Jing Tian, Shaomei Sui, Xiaodong Yuan, Hao Chen, Chuanqiang Qu, Yifeng Du, Lan Guo, Heng Du
Succinyl Coenzyme A synthetase (SCS) is a key mitochondrial enzyme. Defected SCS ADP-forming β subunit (SCS A-β) is linked to lethal infantile Leigh or leigh-like syndrome. However, the impacts of SCS A-β deficiency on mitochondria specifically in neurons have not yet been comprehensively investigated. Here, by down-regulating the expression levels of SCS A-β in cultured mouse neurons, we have found that SCS A-β deficiency induces severe mitochondrial dysfunction including lowered oxidative phosphorylation (OXPHOS) efficiency, increased mitochondrial superoxide production, and mtDNA depletion as well as aberrations of mitochondrial fusion and fission proteins, which eventually leads to neuronal stress...
August 2, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28768180/increased-total-mtdna-copy-number-cures-male-infertility-despite-unaltered-mtdna-mutation-load
#8
Min Jiang, Timo Eino Sakari Kauppila, Elisa Motori, Xinping Li, Ilian Atanassov, Kat Folz-Donahue, Nina Anna Bonekamp, Sara Albarran-Gutierrez, James Bruce Stewart, Nils-Göran Larsson
Mutations of mtDNA cause mitochondrial diseases and are implicated in age-associated diseases and aging. Pathogenic mtDNA mutations are often present in a fraction of all mtDNA copies, and it has been widely debated whether the proportion of mutant genomes or the absolute number of wild-type molecules determines if oxidative phosphorylation (OXPHOS) will be impaired. Here, we have studied the male infertility phenotype of mtDNA mutator mice and demonstrate that decreasing mtDNA copy number worsens mitochondrial aberrations of spermatocytes and spermatids in testes, whereas an increase in mtDNA copy number rescues the fertility phenotype and normalizes testes morphology as well as spermatocyte proteome changes...
August 1, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28767386/mitochondrial-markers-predict-survival-and-progression-in-non-small-cell-lung-cancer-nsclc-patients-use-as-companion-diagnostics
#9
Federica Sotgia, Michael P Lisanti
Here, we used an informatics-based approach to identify novel biomarkers of overall survival and tumor progression in non-small cell lung cancer (NSCLC) patients. We determined whether nuclear-encoded genes associated with mitochondrial biogenesis and function can be used to effectively predict clinical outcome in lung cancer. This strategy allowed us to directly provide in silico validation of the prognostic value of these mitochondrial components in large, clinically-relevant, lung cancer patient populations...
July 28, 2017: Oncotarget
https://www.readbyqxmd.com/read/28767134/the-differential-impact-of-amino-acids-on-oxphos-system-activity-following-carbohydrate-starvation-in-arabidopsis-cell-suspensions
#10
João Henrique F Cavalcanti, Carla G S Quinhones, Peter Schertl, Danielle S Brito, Holger Eubel, Tatjana Hildebrandt, Adriano Nunes-Nesi, Hans-Peter Braun, Wagner L Araújo
Plant respiration mostly depends on the activity of glycolysis and the oxidation of organic acids in the tricarboxylic acid (TCA) cycle to synthesize ATP. However, during stress situations plant cells also use amino acids as alternative substrates to donate electrons via the ETF/ETFQO complex to the mitochondrial electron transport chain (mETC). Given to this, here we investigated changes of the oxidative phosphorylation (OXPHOS) system in Arabidopsis thaliana cell culture under carbohydrate starvation supplied with a range of amino acids...
August 2, 2017: Physiologia Plantarum
https://www.readbyqxmd.com/read/28757909/metabolic-reprogramming-autophagy-and-reactive-oxygen-species-are-necessary-for-primordial-germ-cell-reprogramming-into-pluripotency
#11
D Sainz de la Maza, A Moratilla, V Aparicio, C Lorca, Y Alcaina, D Martín, M P De Miguel
Cellular reprogramming is accompanied by a metabolic shift from oxidative phosphorylation (OXPHOS) toward glycolysis. Previous results from our laboratory showed that hypoxia alone is able to reprogram primordial germ cells (PGCs) into pluripotency and that this action is mediated by hypoxia-inducible factor 1 (HIF1). As HIF1 exerts a myriad of actions by upregulating several hundred genes, to ascertain whether the metabolic switch toward glycolysis is solely responsible for reprogramming, PGCs were cultured in the presence of a pyruvate kinase M2 isoform (PKM2) activator, or glycolysis was promoted by manipulating PPARγ...
2017: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/28754844/mitochondrial-markers-predict-recurrence-metastasis-and-tamoxifen-resistance-in-breast-cancer-patients-early-detection-of-treatment-failure-with-companion-diagnostics
#12
Federica Sotgia, Marco Fiorillo, Michael P Lisanti
Here, we used a data-mining and informatics approach to discover new biomarkers of resistance to hormonal therapy in breast cancer. More specifically, we investigated whether nuclear-encoded genes associated with mitochondrial biogenesis can be used to predict tumor recurrence, distant metastasis and treatment failure in high-risk breast cancer patients. Overall, this strategy allowed us to directly provide in silico validation of the prognostic value of these mitochondrial components in large and clinically relevant patient populations, with >15 years of follow-up data...
July 27, 2017: Oncotarget
https://www.readbyqxmd.com/read/28748471/evaluation-of-mitochondrial-respiration-in-cultured-rat-hepatocytes
#13
Jean-Pierre Marchandeau, Gilles Labbe
Mitochondrial dysfunction is a major mechanism whereby drugs can induce liver injury and other serious side effects, such as lactic acidosis and rhabdomyolysis, in some patients. Several in vitro and in vivo investigations can be performed in order to determine if drugs can disturb mitochondrial fatty acid oxidation (FAO) and the oxidative phosphorylation (OXPHOS) process, deplete hepatic mitochondrial DNA (mtDNA), or trigger the opening of the mitochondrial permeability transition pore (MPT). Among these investigations, mitochondrial respiration is a relatively easy test to measure the potential toxicity of a drug...
2017: Methods in Molecular Biology
https://www.readbyqxmd.com/read/28744336/oxidative-phosphorylation-system-in-gastric-carcinomas-and-gastritis
#14
René G Feichtinger, Daniel Neureiter, Tom Skaria, Silja Wessler, Timothy L Cover, Johannes A Mayr, Franz A Zimmermann, Gernot Posselt, Wolfgang Sperl, Barbara Kofler
Switching of cellular energy production from oxidative phosphorylation (OXPHOS) by mitochondria to aerobic glycolysis occurs in many types of tumors. However, the significance of this switching for the development of gastric carcinoma and what connection it may have to Helicobacter pylori infection of the gut, a primary cause of gastric cancer, are poorly understood. Therefore, we investigated the expression of OXPHOS complexes in two types of human gastric carcinomas ("intestinal" and "diffuse"), bacterial gastritis with and without metaplasia, and chemically induced gastritis by using immunohistochemistry...
2017: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/28740091/microrna-mediated-differential-expression-of-trmu-gtpbp3-and-mto1-in-cell-models-of-mitochondrial-dna-diseases
#15
Salvador Meseguer, Olga Boix, Carmen Navarro-González, Magda Villarroya, Rachid Boutoual, Sonia Emperador, Elena García-Arumí, Julio Montoya, M-Eugenia Armengod
Mitochondrial diseases due to mutations in the mitochondrial (mt) DNA are heterogeneous in clinical manifestations but usually include OXPHOS dysfunction. Mechanisms by which OXPHOS dysfunction contributes to the disease phenotype invoke, apart from cell energy deficit, maladaptive responses to mitochondria-to-nucleus retrograde signaling. Here we used five different cybrid models of mtDNA diseases to demonstrate that the expression of the nuclear-encoded mt-tRNA modification enzymes TRMU, GTPBP3 and MTO1 varies in response to specific pathological mtDNA mutations, thus altering the modification status of mt-tRNAs...
July 24, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28732077/mutations-in-the-caenorhabditis-elegans-orthologs-of-human-genes-required-for-mitochondrial-trna-modification-cause-similar-electron-transport-chain-defects-but-different-nuclear-responses
#16
Carmen Navarro-González, Ismaïl Moukadiri, Magda Villarroya, Ernesto López-Pascual, Simon Tuck, M-Eugenia Armengod
Several oxidative phosphorylation (OXPHOS) diseases are caused by defects in the post-transcriptional modification of mitochondrial tRNAs (mt-tRNAs). Mutations in MTO1 or GTPBP3 impair the modification of the wobble uridine at position 5 of the pyrimidine ring and cause heart failure. Mutations in TRMU affect modification at position 2 and cause liver disease. Presently, the molecular basis of the diseases and why mutations in the different genes lead to such different clinical symptoms is poorly understood...
July 2017: PLoS Genetics
https://www.readbyqxmd.com/read/28724580/il-7-restores-t-lymphocyte-immunometabolic-failure-in-septic-shock-patients-through-mtor-activation
#17
Fabienne Venet, Julie Demaret, Benjamin J Blaise, Christelle Rouget, Thibaut Girardot, Estellie Idealisoa, Thomas Rimmelé, François Mallet, Alain Lepape, Julien Textoris, Guillaume Monneret
T lymphocyte alterations are central to sepsis pathophysiology, whereas related mechanisms remain poorly understood. We hypothesized that metabolic alterations could play a role in sepsis-induced T lymphocyte dysfunction. Samples from septic shock patients were obtained at day 3 and compared with those from healthy donors. T cell metabolic status was evaluated in the basal condition and after T cell stimulation. We observed that basal metabolic content measured in lymphocytes by nuclear magnetic resonance spectroscopy was altered in septic patients...
July 19, 2017: Journal of Immunology: Official Journal of the American Association of Immunologists
https://www.readbyqxmd.com/read/28716939/distinct-requirements-for-energy-metabolism-in-mouse-primordial-germ-cells-and-their-reprogramming-to-embryonic-germ-cells
#18
Yohei Hayashi, Kei Otsuka, Masayuki Ebina, Kaori Igarashi, Asuka Takehara, Mitsuyo Matsumoto, Akio Kanai, Kazuhiko Igarashi, Tomoyoshi Soga, Yasuhisa Matsui
Primordial germ cells (PGCs), undifferentiated embryonic germ cells, are the only cells that have the ability to become gametes and to reacquire totipotency upon fertilization. It is generally understood that the development of PGCs proceeds through the expression of germ cell-specific transcription factors and characteristic epigenomic changes. However, little is known about the properties of PGCs at the metabolite and protein levels, which are directly responsible for the control of cell function. Here, we report the distinct energy metabolism of PGCs compared with that of embryonic stem cells...
August 1, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/28716914/metabolic-profiles-of-exercise-in-patients-with-mcardle-disease-or-mitochondrial-myopathy
#19
Nigel F Delaney, Rohit Sharma, Laura Tadvalkar, Clary B Clish, Ronald G Haller, Vamsi K Mootha
McArdle disease and mitochondrial myopathy impair muscle oxidative phosphorylation (OXPHOS) by distinct mechanisms: the former by restricting oxidative substrate availability caused by blocked glycogen breakdown, the latter because of intrinsic respiratory chain defects. We applied metabolic profiling to systematically interrogate these disorders at rest, when muscle symptoms are typically minimal, and with exercise, when symptoms of premature fatigue and potential muscle injury are unmasked. At rest, patients with mitochondrial disease exhibit elevated lactate and reduced uridine; in McArdle disease purine nucleotide metabolites, including xanthine, hypoxanthine, and inosine are elevated...
August 1, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/28715403/improving-strength-power-muscle-aerobic-capacity-and-glucose-tolerance-through-short-term-progressive-strength-training-among-elderly-people
#20
Eva A Andersson, Per Frank, Marjan Pontén, Björn Ekblom, Maria Ekblom, Marcus Moberg, Kent Sahlin
This protocol describes the simultaneous use of a broad span of methods to examine muscle aerobic capacity, glucose tolerance, strength, and power in elderly people performing short-term resistance training (RET). Supervised progressive resistance training for 1 h three times a week over 8 weeks was performed by RET participants (71±1 years, range 65-80). Compared to a control group without training, the RET showed improvements on the measures used to indicate strength, power, glucose tolerance, and several parameters of muscle aerobic capacity...
July 5, 2017: Journal of Visualized Experiments: JoVE
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