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https://www.readbyqxmd.com/read/28912256/mitochondrial-capacity-oxidative-damage-and-hypoxia-gene-expression-are-associated-with-age-related-division-of-labor-in-honey-bee-apis-mellifera-l-workers
#1
Mário S Cervoni, Carlos A M Cardoso-Júnior, Giovana Craveiro, Anderson de O Souza, Luciane C Alberici, Klaus Hartfelder
During adult life, honeybee workers undergo a succession of behavioral states. Nurses bees perform tasks inside the nest, and when they are about 2-3 weeks old they initiate foraging. This switch is associated with alterations in diet, and with the levels of juvenile hormone and vitellogenin circulating in hemolymph. Less clear is whether this behavioral maturation involves major changes at the cellular level, such as mitochondrial activity and the redox environment in the head, thorax and abdomen. Using high-resolution respirometry, biochemical assays and RT-qPCR, we evaluated the association of these parameters with this behavioral change...
September 14, 2017: Journal of Experimental Biology
https://www.readbyqxmd.com/read/28906460/a-critical-assessment-of-the-therapeutic-potential-of-resveratrol-supplements-for-treating-mitochondrial-disorders
#2
REVIEW
Boel De Paepe, Rudy Van Coster
In human cells, mitochondria provide the largest part of cellular energy in the form of adenosine triphosphate generated by the process of oxidative phosphorylation (OXPHOS). Impaired OXPHOS activity leads to a heterogeneous group of inherited diseases for which therapeutic options today remain very limited. Potential innovative strategies aim to ameliorate mitochondrial function by increasing the total mitochondrial load of tissues and/or to scavenge the excess of reactive oxygen species generated by OXPHOS malfunctioning...
September 14, 2017: Nutrients
https://www.readbyqxmd.com/read/28905387/management-of-leigh-syndrome-current-status-and-new-insights
#3
REVIEW
Ling Chen, Yu Cui, Dan Jiang, Chui Yan Ma, Hung-Fat Tse, Wuh-Liang Hwu, Qizhou Lian
Leigh syndrome (LS) is an inherited mitochondrial encephalopathy associated with gene mutations of oxidative phosphorylation(OXPHOS) pathway that result in early disability and death in affected young children. Currently, LS is incurable and unresponsive to many treatments, although some case reports indicate that supplements can improve the condition. Many novel therapies are being continuously tested in preclinical studies. In this review, we summarize the genetic basis of LS, current treatment, preclinical studies in animal models and the management of other mitochondrial diseases...
September 14, 2017: Clinical Genetics
https://www.readbyqxmd.com/read/28903946/ppara-agonist-fenofibrate-enhances-fatty-acid-%C3%AE-oxidation-and-attenuates-polycystic-kidney-and-liver-disease-in-mice
#4
Ronak Lakhia, Matanel Yheskel, Andrea Flaten, Ezekiel B Quittner-Strom, William L Holland, Vishal Patel
PPARA is nuclear hormone receptor that promotes fatty acid β-oxidation (FAO) and oxidative phosphorylation (OXPHOS). We and others have recently shown that PPARA and its target genes are downregulated, and FAO and OXPHOS are impaired in autosomal dominant polycystic kidney disease (ADPKD). However, whether PPARA and FAO/OXPHOS are causally linked to ADPKD progression is not entirely clear. We report that expression of PPARA and FAO/OXPHOS genes is downregulated and in-vivo β-oxidation rate of 3H-labelled triolein is reduced in Pkd1RC/RC mice, a slowly-progressing orthologous model of ADPKD that closely mimics the human ADPKD phenotype...
September 13, 2017: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/28899812/the-starving-brain-overfed-meets-undernourished-in-the-pathology-of-mild-cognitive-impairment-mci-and-alzheimer-s-disease-ad
#5
REVIEW
Kelly J Gibas
Type II Diabetes affects 400 million people worldwide (IDF, 2013). The pathology is paradoxical: internal starvation activated by overfeeding. Hyperinsulinemic impairments of glucose homeostasis are treated with anti-hyperglycemics exacerbating cell starvation, inducing hypoglycemia and raising respiratory quotient. Reductions in hyperglycemia are achieved at the expense of glucose dependency and metabolic inflexibility (Gibas & Gibas, 2017). The brain is not immune from these cycles of starvation. The bioenergetic model characterizes propagation of late-onset, sporadic Alzheimer's disease as loss of molecular fidelity and compromised energy originating in brain networks with highest metabolic demand...
September 9, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28899396/transcriptomic-meta-analysis-identifies-gene-expression-characteristics-in-various-samples-of-hiv-infected-patients-with-nonprogressive-disease
#6
Le-Le Zhang, Zi-Ning Zhang, Xian Wu, Yong-Jun Jiang, Ya-Jing Fu, Hong Shang
BACKGROUND: A small proportion of HIV-infected patients remain clinically and/or immunologically stable for years, including elite controllers (ECs) who have undetectable viremia (<50 copies/ml) and long-term nonprogressors (LTNPs) who maintain normal CD4(+) T cell counts for prolonged periods (>10 years). However, the mechanism of nonprogression needs to be further resolved. In this study, a transcriptome meta-analysis was performed on nonprogressor and progressor microarray data to identify differential transcriptome pathways and potential biomarkers...
September 12, 2017: Journal of Translational Medicine
https://www.readbyqxmd.com/read/28888986/pde-5-inhibitor-improves-insulin-sensitivity-by-enhancing-mitochondrial-function-in-adipocytes
#7
Hea Min Yu, Hyo Kyun Chung, Koon Soon Kim, Jae Min Lee, Jun Hwa Hong, Kang Seo Park
Adipocytes are involved in many metabolic disorders. It was recently reported that phosphodiesterase type 5 (PDE5) is expressed in human adipose tissue. In addition, PDE5 inhibitors have been shown to improve insulin sensitivity in humans. However, the mechanism underlying the role of PDE5 inhibitors as an insulin sensitizer remains largely unknown. The present study was undertaken to investigate the role of the PDE5 inhibitor udenafil in insulin signaling in adipocytes and whether this is mediated through the regulation of mitochondrial function...
September 6, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28888069/a-novel-missense-mutation-in-aifm1-results-in-axonal-polyneuropathy-and-misassembly-of-oxphos-complexes
#8
Bo Hu, Michael Wang, Ryan Castoro, Megan Simmons, Richard Dortch, Robin Yawn, Jun Li
BACKGROUND AND PURPOSE: AIFM1 (apoptosis-inducing factor, mitochondrion-associated-1) in mitochondria has captured a great attention due to its well-described function in apoptosis. Mutations in AIFM1 have resulted in multiple clinical phenotypes, including CMTX4. These syndromes usually involve multiple locations within the nervous system and/or multiple organs. This study describes a novel missense mutation in AIFM1 and its associated peripheral nerve disease. METHODS: Patients with AIFM1 mutation were characterized clinically, electrophysiologically, genetically and by MRI imaging...
September 9, 2017: European Journal of Neurology: the Official Journal of the European Federation of Neurological Societies
https://www.readbyqxmd.com/read/28883046/case-studies-in-physiology-skeletal-muscle-mitochondrial-protein-synthesis-and-respiration-in-response-to-the-energetic-stress-of-an-ultra-endurance-race
#9
Adam R Konopka, William M Castor, Christopher A Wolff, Robert V Musci, Justin J Reid, Jaime L Laurin, Zackary J Valenti, Karyn L Hamilton, Benjamin F Miller
The 2016 Colorado Trail Race (CTR) was an ultra-endurance mountain bike race where competitors cycled for up to 24 hrs/day between altitudes of 1675 to 4025 meters to complete 800 kilometers and 21,000 meters of elevation gain. In one athlete, we had the unique opportunity to characterize skeletal muscle protein synthesis and mitochondrial respiration in response to a normal activity control period (CON) and the CTR. We hypothesized that mitochondrial protein synthesis would be elevated and mitochondrial respiration would be maintained during the extreme stresses of the CTR...
September 7, 2017: Journal of Applied Physiology
https://www.readbyqxmd.com/read/28883002/genetic-dissociation-of-glycolysis-and-the-tca-cycle-affects-neither-normal-nor-neoplastic-proliferation
#10
Laura E Jackson, Sucheta Kulkarni, Huabo Wang, Jie Lu, James M Dolezal, Sivakama S Bharathi, Sarangarajan Ranganathan, Mulchand S Patel, Rahul Deshpande, Frances Alencastro, Stacy G Wendell, Eric S Goetzman, Andrew W Duncan, Edward V Prochownik
Rapidly proliferating cells increase glycolysis at the expense of oxidative phosphorylation (oxphos) to generate sufficient levels of glycolytic intermediates for use as anabolic substrates. The pyruvate dehydrogenase complex (PDC) is a critical mitochondrial enzyme that catalyzes pyruvate's conversion to acetyl coenzyme A (AcCoA), thereby connecting these two pathways in response to complex energetic, enzymatic and metabolic cues. Here we utilized a mouse model of hepatocyte-specific PDC inactivation to determine the need for this metabolic link during normal hepatocyte regeneration and malignant transformation...
September 7, 2017: Cancer Research
https://www.readbyqxmd.com/read/28881758/suppression-of-pyruvate-dehydrogenase-kinase-2-re-sensitizes-paclitaxel-resistant-human-lung-cancer-cells-to-paclitaxel
#11
Hong Sun, Anyou Zhu, Xiang Zhou, Fengchao Wang
Despite impressive initial clinical responses, the majority of lung cancer patients treated with paclitaxel eventually develop resistance to the drug. Pyruvate dehydrogenase kinase-2 (PDK2) is a key regulator of glycolysis and oxidative phosphorylation, and its expression is increased in a variety of tumors. In this study, the role of PDK2 in mediating paclitaxel resistance in lung cancer cells was investigated using biochemical and isotopic tracing methods. Increased expression of PDK2 was observed in paclitaxel-resistant cells ascompared totheir parental cells...
August 8, 2017: Oncotarget
https://www.readbyqxmd.com/read/28878225/the-pdk1-inhibitor-dichloroacetate-controls-cholesterol-homeostasis-through-the-erk5-mef2-pathway
#12
Abrar Ul Haq Khan, Nerea Allende-Vega, Delphine Gitenay, Sabine Gerbal-Chaloin, Claire Gondeau, Dang-Nghiem Vo, Sana Belkahla, Stefania Orecchioni, Giovanna Talarico, Francesco Bertolini, Milica Bozic, Jose M Valdivielso, Fabienne Bejjani, Isabelle Jariel, Isabel C Lopez-Mejia, Lluis Fajas, Charles-Henri Lecellier, Javier Hernandez, Martine Daujat, Martin Villalba
Controlling cholesterol levels is a major challenge in human health, since hypercholesterolemia can lead to serious cardiovascular disease. Drugs that target carbohydrate metabolism can also modify lipid metabolism and hence cholesterol plasma levels. In this sense, dichloroacetate (DCA), a pyruvate dehydrogenase kinase (PDK) inhibitor, augments usage of the glycolysis-produced pyruvate in the mitochondria increasing oxidative phosphorylation (OXPHOS). In several animal models, DCA decreases plasma cholesterol and triglycerides...
September 6, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28874953/pleiotropic-effects-of-biguanides-on-mitochondrial-reactive-oxygen-species-production
#13
Alena Pecinova, Zdenek Drahota, Jana Kovalcikova, Nikola Kovarova, Petr Pecina, Lukas Alan, Michal Zima, Josef Houstek, Tomas Mracek
Metformin is widely prescribed as a first-choice antihyperglycemic drug for treatment of type 2 diabetes mellitus, and recent epidemiological studies showed its utility also in cancer therapy. Although it is in use since the 1970s, its molecular target, either for antihyperglycemic or antineoplastic action, remains elusive. However, the body of the research on metformin effect oscillates around mitochondrial metabolism, including the function of oxidative phosphorylation (OXPHOS) apparatus. In this study, we focused on direct inhibitory mechanism of biguanides (metformin and phenformin) on OXPHOS complexes and its functional impact, using the model of isolated brown adipose tissue mitochondria...
2017: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/28874842/investigation-of-mitochondrial-metabolic-response-to-doxorubicin-in-prostate-cancer-cells-an-nadh-fad-and-tryptophan-flim-assay
#14
Shagufta Rehman Alam, Horst Wallrabe, Zdenek Svindrych, Ajay K Chaudhary, Kathryn G Christopher, Dhyan Chandra, Ammasi Periasamy
Prostate cancer (PCa) is one of the leading cancers in men in the USA. Lack of experimental tools that predict therapy response is one of the limitations of current therapeutic regimens. Mitochondrial dysfunctions including defective oxidative phosphorylation (OXPHOS) in cancer inhibit apoptosis by modulating ROS production and cellular signaling. Thus, correction of mitochondrial dysfunction and induction of apoptosis are promising strategies in cancer treatment. We have used Fluorescence Lifetime Imaging Microscopy (FLIM) to quantify mitochondrial metabolic response in PCa cells by tracking auto-fluorescent NAD(P)H, FAD and tryptophan (Trp) lifetimes and their enzyme-bound fractions as markers, before and after treatment with anti-cancer drug doxorubicin...
September 5, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28874356/impact-of-%C3%AE-adrenergic-signaling-in-pgc-1%C3%AE-mediated-adaptations-in-mouse-skeletal-muscle
#15
Nina Brandt, Lene Nielsen, Bjørg Thiellesen Buch, Anders Gudiksen, Stine Ringholm, Ylva Hellsten, Jens Bangsbo, Henriette Pilegaard
PGC-1α has been suggested to regulate exercise training-induced metabolic adaptations and autophagy in skeletal muscle. The factors regulating PGC-1α are however not fully resolved. The aim was to investigate the impact of β-adrenergic signaling in PGC-1α mediated metabolic adaptations in skeletal muscle with exercise training. Muscle was obtained from muscle specific PGC-1α knockout (MKO) mice and LOX/LOX 1) 3h after a single exercise bout with or without prior injection of propranolol or 3h after a single injection of clenbuterol and 2) after 5 weeks of wheel running exercise training with or without propranolol treatment or after 5 weeks of clenbuterol treatment...
September 5, 2017: American Journal of Physiology. Endocrinology and Metabolism
https://www.readbyqxmd.com/read/28870729/tigecylcine-induced-inhibition-of-mitochondrial-mtdna-translation-may-cause-a-lethal-mitochondrial-dysfunction-in-human
#16
S J Vandecasteele, S Seneca, J Smet, M Reynders, J De Ceulaer, A V Vanlander, R Van Coster
OBJECTIVES: A 65-year old patient developed an unexplained and ultimately lethal metabolic acidosis under prolonged treatment with tigecycline. Tigecycline is known to have a selective inhibitory effect on eukaryotic mitochondrial translation. The underlying molecular mechanisms of the metabolic acidosis in this patient were explored. METHODS: OXPHOS analysis, blue native PAGE followed by in-gel activity staining in mitochondria, molecular analysis of mtDNA for genomic rearrangements and sequencing of the rRNA genes was performed on the proband's skeletal muscle...
September 1, 2017: Clinical Microbiology and Infection
https://www.readbyqxmd.com/read/28864766/distinct-intracellular-sac-camp-domains-regulate-er-calcium-signaling-and-oxphos-function
#17
Federica Valsecchi, Csaba Konrad, Marilena D'Aurelio, Lavoisier S Ramos-Espiritu, Anna Stepanova, Suzanne R Burstein, Alexander Galkin, Jordi Magranè, Anatoly Starkov, Jochen Buck, Lonny R Levin, Giovanni Manfredi
cAMP regulates a wide variety of physiological functions in mammals. This single second messenger can regulate multiple, seemingly disparate functions within independently regulated cell compartments. We previously identified one such compartment inside the matrix of the mitochondria, where soluble adenylyl cyclase (sAC) regulates oxidative phosphorylation (OXPHOS). We now show that sAC KO fibroblasts have a defect in OXPHOS activity and attempt to compensate for this defect by increasing OXPHOS proteins. Importantly, sAC KO cells also exhibit decreased probability of endoplasmic reticulum (ER) Ca(2+) release associated with diminished phosphorylation of the inositol 3-phosphate receptor...
September 1, 2017: Journal of Cell Science
https://www.readbyqxmd.com/read/28863998/changes-in-mitochondrial-respiration-in-the-human-placenta-over-gestation
#18
Olivia J Holland, Anthony J R Hickey, Anna Alvsaker, Stephanie Moran, Christopher Hedges, Lawrence W Chamley, Anthony V Perkins
INTRODUCTION: Placental mitochondria are subjected to micro-environmental changes throughout gestation, in particular large variations in oxygen. How placental mitochondrial respiration adapts to changing oxygen concentrations remains unexplored. Additionally, placental tissue is often studied in culture; however, the effect of culture on placental mitochondria is unclear. MATERIAL AND METHODS: Placental tissue was obtained from first trimester and term (laboured and non-laboured) pregnancies, and selectively permeabilized to access mitochondria...
September 2017: Placenta
https://www.readbyqxmd.com/read/28863345/the-stromal-microenvironment-modulates-mitochondrial-oxidative-phosphorylation-in-chronic-lymphocytic-leukemia-cells
#19
Hima V Vangapandu, Mary L Ayres, Christopher A Bristow, William G Wierda, Michael J Keating, Kumudha Balakrishnan, Christine M Stellrecht, Varsha Gandhi
Peripheral blood chronic lymphocytic leukemia (CLL) cells are replicationally quiescent mature B-cells. In short-term cultures, supporting stromal cells provide a survival advantage to CLL cells by inducing transcription and translation without promoting proliferation. We hypothesized that the stromal microenvironment augments malignant B cells' metabolism to enable the cells to cope with their energy demands for transcription and translation. We used extracellular flux analysis to assess the two major energy-generating pathways, mitochondrial oxidative phosphorylation (OxPhos) and glycolysis, in primary CLL cells in the presence of three different stromal cell lines...
August 29, 2017: Neoplasia: An International Journal for Oncology Research
https://www.readbyqxmd.com/read/28862604/-high-resolution-respirometry-in-diagnostic-of-mitochondrial-disorders-caused-by-mitochondrial-complex-i-deficiency
#20
T D Krylova, P G Tsygankova, Yu S Itkis, N L Sheremet, T A Nevinitsyna, S V Mikhaylova, E Yu Zakharova
Complex I (CI) deficiency is one of the most common defects in the OXPHOS system; it represents more than 30% cases of mitochondrial diseases. The group is characterized by clinical and genetic heterogeneity and comprise several nosological forms. The most prevalent phenotypes for CI are LHON and Leigh syndrome. In this study we have analyzed skin fibroblasts from 11 patients with mutations in mtDNA, which cause LHON or Leigh-like phenotypes: m.11778 G>A (n=3), m.3460 A>G (n=2), m.3635 G>A (n=1), m...
July 2017: Biomedit︠s︡inskai︠a︡ Khimii︠a︡
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