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https://www.readbyqxmd.com/read/29054807/ontogeny-of-skeletal-and-cardiac-muscle-mitochondria-oxygen-fluxes-in-two-breeds-of-chicken
#1
Sarah K G Sirsat, Edward M Dzialowski
From its earliest days of domestication, the domestic chicken (Gallus gallus domesticus) has been selectively bred for specific traits. Decades of genetic selection have resulted in significant dissimilarities in metabolism and growth between breeds, in particular fast-growing broilers and highly productive layers. A chicken develops the capacity to elevate metabolism in response to decreases in ambient temperature upon hatching, including well-developed methods of regulating thermogenesis. However, a differential timing between incipient endothermic capacities of broiler and layer strains exists...
October 17, 2017: Comparative Biochemistry and Physiology. Part A, Molecular & Integrative Physiology
https://www.readbyqxmd.com/read/29050400/metformin-reverses-trap1-mutation-associated-alterations-in-mitochondrial-function-in-parkinson-s-disease
#2
Julia C Fitzgerald, Alexander Zimprich, Daniel A Carvajal Berrio, Kevin M Schindler, Brigitte Maurer, Claudia Schulte, Christine Bus, Anne-Kathrin Hauser, Manuela Kübler, Rahel Lewin, Dheeraj Reddy Bobbili, Lisa M Schwarz, Evangelia Vartholomaiou, Kathrin Brockmann, Richard Wüst, Johannes Madlung, Alfred Nordheim, Olaf Riess, L Miguel Martins, Enrico Glaab, Patrick May, Katja Schenke-Layland, Didier Picard, Manu Sharma, Thomas Gasser, Rejko Krüger
The mitochondrial proteins TRAP1 and HTRA2 have previously been shown to be phosphorylated in the presence of the Parkinson's disease kinase PINK1 but the downstream signalling is unknown. HTRA2 and PINK1 loss of function causes parkinsonism in humans and animals. Here, we identified TRAP1 as an interactor of HTRA2 using an unbiased mass spectrometry approach. In our human cell models, TRAP1 overexpression is protective, rescuing HTRA2 and PINK1-associated mitochondrial dysfunction and suggesting that TRAP1 acts downstream of HTRA2 and PINK1...
September 1, 2017: Brain: a Journal of Neurology
https://www.readbyqxmd.com/read/29042548/human-mesenchymal-stromal-cells-transplanted-into-mice-stimulate-renal-tubular-cells-and-enhance-mitochondrial-function
#3
Luca Perico, Marina Morigi, Cinzia Rota, Matteo Breno, Caterina Mele, Marina Noris, Martino Introna, Chiara Capelli, Lorena Longaretti, Daniela Rottoli, Sara Conti, Daniela Corna, Giuseppe Remuzzi, Ariela Benigni
Mesenchymal stromal cells (MSCs) are renoprotective and drive regeneration following injury, although cellular targets of such an effect are still ill-defined. Here, we show that human umbilical cord (UC)-MSCs transplanted into mice stimulate tubular cells to regain mitochondrial mass and function, associated with enhanced microtubule-rich projections that appear to mediate mitochondrial trafficking to create a reparative dialogue among adjacent tubular cells. Treatment with UC-MSCs in mice with cisplatin-induced acute kidney injury (AKI) regulates mitochondrial biogenesis in proximal tubuli by enhancing PGC1α expression, NAD(+) biosynthesis and Sirtuin 3 (SIRT3) activity, thus fostering antioxidant defenses and ATP production...
October 17, 2017: Nature Communications
https://www.readbyqxmd.com/read/29042306/cigarette-smoke-induces-mitochondrial-metabolic-reprogramming-in-lung-cells
#4
Hitendra S Solanki, Niraj Babu, Ankit Jain, Mohd Younis Bhat, Vinuth N Puttamallesh, Jayshree Advani, Remya Raja, Kiran K Mangalaparthi, Mahesh M Kumar, T S Keshava Prasad, Premendu Prakash Mathur, David Sidransky, Harsha Gowda, Aditi Chatterjee
Cellular transformation owing to cigarette smoking is due to chronic exposure and not acute. However, systematic studies to understand the molecular alterations in lung cells due to cigarette smoke are lacking. To understand these molecular alterations induced by chronic cigarette smoke exposure, we carried out tandem mass tag (TMT) based temporal proteomic profiling of lung cells exposed to cigarette smoke upto 12months. We identified 2620 proteins in total, of which 671 proteins were differentially expressed (1...
October 14, 2017: Mitochondrion
https://www.readbyqxmd.com/read/29040448/male-brown-fat-specific-double-knockout-of-igfir-ir-atrophy-mitochondrial-fission-failure-impaired-thermogenesis-and-obesity
#5
Vanesa Viana-Huete, Carlos Guillén, Gema García, Silvia Fernández, Ana García-Aguilar, C R Kahn, Manuel Benito
It is unknown how the lack of IR (insulin receptor)/ IGFIR (insulin like growth factor receptor) in a tissue-specific manner does affect brown fat development and mitochondrial integrity and function and its impact on the redistribution of the adipose organ and the metabolic status. To address this important issue, we have developed the IR/IGFIR double knockout in brown adipose tissue-specific manner (DKO). Lack of those receptors caused a severe brown fat atrophy, an enhanced beige cell clusters in inguinal fat, loss of mitochondrial mass, mitochondrial damage related to cristae disruption, and the loss of proteins involved in autophagosome formation, mitophagy, mitochondrial quality control and dynamics and thermogenesis...
October 10, 2017: Endocrinology
https://www.readbyqxmd.com/read/29037962/mild-palmitate-treatment-increases-mitochondrial-mass-but-does-not-affect-ea-hy926-endothelial-cells-viability
#6
Dorota Dymkowska, Maria Kawalec, Tomasz Wyszomirski, Krzysztof Zabłocki
A dyslipidaemia-related increase of the concentration of long-chain fatty acids in the plasma is an important pathological factor substantially increasing risk of serious consequences in vascular endothelium. Inflammatory response, atherosclerosis and insulin resistance seem the most severe. Palmitate at excessive concentrations has been shown to have a harmful effect on endothelial cells impairing NO generation, stimulating reactive oxygen species (ROS) formation and affecting their viability. On the other hand we found that palmitate applied for 48 h at 100 μM concentration which is sufficient to induce inflammatory response, increase ROS generation and reduce insulin sensitivity of EA...
October 13, 2017: Archives of Biochemistry and Biophysics
https://www.readbyqxmd.com/read/29035693/mms19-localizes-to-mitochondria-and-protects-the-mitochondrial-genome-from-oxidative-damage
#7
Rui Wu, Qunsong Tan, Kaifeng Niu, Yuqi Zhu, Di Wei, Yongliang Zhao, Hongbo Fang
MMS19 localizes to cytoplasmic and nuclear compartments involving in transcription and nucleotide excision repair (NER). However, whether or not MMS19 localizes to mitochondria where it plays a role in maintaining mitochondrial genome stability remains elusive. In this study, we provide the first evidence that MMS19 is localized in the inner membrane of mitochondria and participates in mtDNA oxidative damage repair. MMS19 knockdown led to mitochondrial dysfunctions including decreased mtDNA copy number, diminished mtDNA repair capacity and elevated level of mtDNA common deletion after oxidative stress...
October 16, 2017: Biochemistry and Cell Biology, Biochimie et Biologie Cellulaire
https://www.readbyqxmd.com/read/29031721/cdkal1-a-type-2-diabetes-susceptibility-gene-regulates-mitochondrial-function-in-adipose-tissue
#8
Colin J Palmer, Raphael J Bruckner, Joao A Paulo, Lawrence Kazak, Jonathan Z Long, Amir I Mina, Zhaoming Deng, Katherine B LeClair, Jessica A Hall, Shangyu Hong, Peter-James H Zushin, Kyle L Smith, Steven P Gygi, Susan Hagen, David E Cohen, Alexander S Banks
OBJECTIVES: Understanding how loci identified by genome wide association studies (GWAS) contribute to pathogenesis requires new mechanistic insights. Variants within CDKAL1 are strongly linked to an increased risk of developing type 2 diabetes and obesity. Investigations in mouse models have focused on the function of Cdkal1 as a tRNA(Lys) modifier and downstream effects of Cdkal1 loss on pro-insulin translational fidelity in pancreatic β-cells. However, Cdkal1 is broadly expressed in other metabolically relevant tissues, including adipose tissue...
October 2017: Molecular Metabolism
https://www.readbyqxmd.com/read/28986697/targeting-mitochondrial-function-and-proteostasis-to-mitigate-dynapenia
#9
REVIEW
Robert V Musci, Karyn L Hamilton, Benjamin F Miller
Traditionally, interventions to treat skeletal muscle aging have largely targeted sarcopenia-the age-related loss of skeletal muscle mass. Dynapenia refers to the age-related loss in skeletal muscle function due to factors outside of muscle mass, which helps to inform treatment strategies for aging skeletal muscle. There is evidence that mechanisms to maintain protein homeostasis and proteostasis, deteriorate with age. One key mechanism to maintain proteostasis is protein turnover, which is an energetically costly process...
October 6, 2017: European Journal of Applied Physiology
https://www.readbyqxmd.com/read/28986525/non-invasive-assessment-of-hepatic-mitochondrial-metabolism-by-positional-isotopomer-nmr-tracer-analysis-pinta
#10
Rachel J Perry, Liang Peng, Gary W Cline, Gina M Butrico, Yongliang Wang, Xian-Man Zhang, Douglas L Rothman, Kitt Falk Petersen, Gerald I Shulman
Hepatic mitochondria play a central role in the regulation of intermediary metabolism and maintenance of normoglycemia, and there is great interest in assessing rates of hepatic mitochondrial citrate synthase flux (V CS) and pyruvate carboxylase flux (V PC) in vivo. Here, we show that a positional isotopomer NMR tracer analysis (PINTA) method can be used to non-invasively assess rates of V CS and V PC fluxes using a combined NMR/gas chromatography-mass spectrometry analysis of plasma following infusion of [3-(13)C]lactate and glucose tracer...
October 6, 2017: Nature Communications
https://www.readbyqxmd.com/read/28978546/subcutaneous-inguinal-white-adipose-tissue-is-responsive-to-but-dispensable-for-the-metabolic-health-benefits-of-exercise
#11
Willem T Peppler, Logan K Townsend, Carly M Knuth, Michelle T Foster, David C Wright
Exercise training has robust effects on subcutaneous inguinal white adipose tissue (iWAT), characterized by a shift to a brown adipose tissue (BAT) like phenotype. Consistent with this, transplantation of exercise-trained iWAT into sedentary rodents activates thermogenesis and improves glucose homeostasis, suggesting that iWAT metabolism may contribute to the beneficial effects of exercise. However, it is yet to be determined if adaptations in iWAT are necessary for the beneficial systemic effects of exercise...
October 3, 2017: American Journal of Physiology. Endocrinology and Metabolism
https://www.readbyqxmd.com/read/28973648/the-nad-dependent-deacetylase-sirt2-attenuates-oxidative-stress-and-mitochondrial-dysfunction-and-improves-insulin-sensitivity-in-hepatocytes
#12
Vera Lemos, Rita M Oliveira, Luana Naia, Eva Szego, Elisabete Ramos, Sónia Pinho, Fernando Magro, Cláudia Cavadas, A Cristina Rego, Vítor Costa, Tiago F Outeiro, Pedro Gomes
Insulin resistance is a major predictor of the development of metabolic disorders. Sirtuins (SIRTs) have emerged as potential targets that can be manipulated to counteract age-related diseases, including type 2 diabetes. SIRT2 has been recently shown to exert important metabolic effects, but whether SIRT2 regulates insulin sensitivity in hepatocytes is currently unknown. The aim of this study is to investigate this possibility and to elucidate underlying molecular mechanisms. Here we show that SIRT2 is downregulated in insulin-resistant hepatocytes and livers and this was accompanied by increased generation of reactive oxygen species (ROS), activation of stress-sensitive ERK1/2 kinase, and mitochondrial dysfunction...
July 26, 2017: Human Molecular Genetics
https://www.readbyqxmd.com/read/28972173/identification-of-the-signals-for-glucose-induced-insulin-secretion-in-ins1-832-13-%C3%AE-cells-using-metformin-induced-metabolic-deceleration-as-a-model
#13
Julien Lamontagne, Anfal Al-Mass, Christopher J Nolan, Barbara E Corkey, S R Murthy Madiraju, Erik Joly, Marc Prentki
Metabolic deceleration in pancreatic β-cells is associated with inhibition of glucose-induced insulin secretion (GIIS), but only in the presence of intermediate/sub-maximal glucose concentrations. Here, we used acute metformin treatment as a tool to induce metabolic deceleration in INS1 (832/13) β-cells, with the goal of identifying key pathways and metabolites involved in GIIS. Metabolites and pathways previously implicated as signals for GIIS were measured in the cells at 2-25 mM glucose, with or without 5 mM metformin...
October 2, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28972001/the-metabolic-and-proliferative-state-of-vascular-adventitial-fibroblasts-in-pulmonary-hypertension-is-regulated-through-a-mir-124-ptbp1-pkm-axis
#14
Hui Zhang, Daren Wang, Min Li, Lydie Plecitá-Hlavatá, Angelo D'Alessandro, Jan Tauber, Suzette Riddle, Sushil Kumar, Amanda R Flockton, B Alexandre McKeon, Maria G Frid, Julie A Reisz, Paola Caruso, Karim C El Kasmi, Petr Ježek, Nicholas W Morrell, Cheng-Jun Hu, Kurt R Stenmark
Background -An emerging "metabolic theory" of pulmonary hypertension (PH) suggests that cellular and mitochondrial metabolic dysfunction underlies the pathology of this disease. We and others have previously demonstrated the existence of hyper-proliferative, apoptosis-resistant, pro-inflammatory adventitial fibroblasts from human and bovine hypertensive pulmonary arterial walls (PH-Fibs) exhibit constitutive reprogramming of glycolytic and mitochondrial metabolism, accompanied by an increased ratio of glucose catabolism through glycolysis versus the TCA cycle...
September 26, 2017: Circulation
https://www.readbyqxmd.com/read/28962872/ucp2-inhibition-induces-ros-akt-mtor-axis-role-of-gapdh-nuclear-translocation-in-genipin-everolimus-anticancer-synergism
#15
Ilaria Dando, Raffaella Pacchiana, Elisa Dalla Pozza, Ivana Cataldo, Stefano Bruno, Paola Conti, Marco Cordani, Anna Grimaldi, Giovanna Butera, Michele Caraglia, Aldo Scarpa, Marta Palmieri, Massimo Donadelli
Several studies indicate that mitochondrial uncoupling protein 2 (UCP2) plays a pivotal role in cancer development by decreasing reactive oxygen species (ROS) produced by mitochondrial metabolism and by sustaining chemoresistance to a plethora of anticancer drugs. Here, we demonstrate that inhibition of UCP2 triggers Akt/mTOR pathway in a ROS-dependent mechanism in pancreatic adenocarcinoma cells. This event reduces the antiproliferative outcome of UCP2 inhibition by genipin, creating the conditions for the synergistic counteraction of cancer cell growth with the mTOR inhibitor everolimus...
September 27, 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28956034/metabolomics-reveal-mitochondrial-and-fatty-acid-metabolism-disorders-that-contribute-to-the-development-of-dkd-in-t2dm-patients
#16
Ling Li, Chengshi Wang, Hongliu Yang, Shuyun Liu, Yanrong Lu, Ping Fu, Jingping Liu
Diabetic kidney disease (DKD) is the leading cause of ESRD; however, early intervention can greatly prevent the progression of DKD; thus, sensitive biomarkers for DKD are still required. This study was aimed at the identification of potential biomarkers and revelation of underlying pathways in DKD patients by non-targeted metabolomics. Gas chromatography-mass spectrometry was used to analyze urine obtained from the control and type 2 diabetes mellitus (T2DM) and DKD patients, and the renal histological changes in DKD patients were assessed...
September 28, 2017: Molecular BioSystems
https://www.readbyqxmd.com/read/28954307/in-vitro-effects-of-the-specific-mitochondrial-tspo-ligand-ro5-4864-in-cultured-human-osteoblasts
#17
Rosenberg Nahum, Rosenberg Orit, Weizman Abraham, Veenman Leo, Gavish Moshe
The 18 kDa mitochondrial translocator protein (TSPO) ligands (10 µM), e. g., protoporphyrin IX, PK 11195 and FGIN-1-27, have different effects on metabolism and protein expression in human osteoblasts. In this study, we investigated the archetypical TSPO specific ligand Ro5-4864 (10 µM) effect in primary osteoblasts in culture aiming to further understand the TSPO role in these mature metabolically active cells.We found that following exposure to Ro5-4864, cellular [(18)F]-FDG incorporation and ATP content were reduced by 48% (p<0...
September 27, 2017: Experimental and Clinical Endocrinology & Diabetes
https://www.readbyqxmd.com/read/28951839/lower-cellular-metabolic-power-can-be-an-explanation-for-obesity-trend-in-tae-eum-type-hypothesis-and-clinical-observation
#18
Eun Bo Shim, Chae Hun Leem, Joong Jae Kim, Jong Yeol Kim
BACKGROUND: Those classified as Tae-Eum (TE)-type people in Sasang constitutional medicine (SCM) are prone to obesity. Although extensive clinical observations have confirmed this tendency, the underlying physiological mechanisms are unknown. Here, we propose a novel hypothesis using integrative physiology to explain this phenomenon. METHODS: Hypoactive lung function in the TE type indicates that respiration is attenuated at the cellular level-specifically, mitochondrial oxygen consumption...
September 2017: Integrative medicine research
https://www.readbyqxmd.com/read/28951827/transcribing-%C3%AE-cell-mitochondria-in-health-and-disease
#19
REVIEW
Hindrik Mulder
BACKGROUND: The recent genome-wide association studies (GWAS) of Type 2 Diabetes (T2D) have identified the pancreatic β-cell as the culprit in the pathogenesis of the disease. Mitochondrial metabolism plays a crucial role in the processes controlling release of insulin and β-cell mass. This notion implies that mechanisms controlling mitochondrial function have the potential to play a decisive pathogenetic role in T2D. SCOPE OF THE REVIEW: This article reviews studies demonstrating that there is indeed mitochondrial dysfunction in islets in T2D, and that GWAS have identified a variant in the gene encoding transcription factor B1 mitochondrial (TFB1M), predisposing to T2D due to mitochondrial dysfunction and impaired insulin secretion...
September 2017: Molecular Metabolism
https://www.readbyqxmd.com/read/28948792/in-vitro-anticancer-activity-and-in-vivo-biodistribution-of-rhenium-i-tricarbonyl-aqua-complexes
#20
Kevin M Knopf, Brendan L Murphy, Samantha N MacMillan, Jeremy M Baskin, Martin P Barr, Eszter Boros, Justin J Wilson
Seven rhenium(I) complexes of the general formula fac-[Re(CO)3(NN)(OH2)](+) where NN = 2,2'-bipyridine (8), 4,4'-dimethyl-2,2'-bipyridine (9), 4,4'-dimethoxy-2,2'-bipyridine (10), dimethyl 2,2'-bipyridine-4,4'-dicarboxylate (11), 1,10-phenanthroline (12), 2,9-dimethyl-1,10-phenanthroline (13), or 4,7-diphenyl-1,10-phenanthroline (14), were synthesized and characterized by (1)H NMR spectroscopy, IR spectroscopy, mass spectrometry, and X-ray crystallography. With the exception of 11, all complexes exhibited 50% growth inhibitory concentration (IC50) values that were less than 20 μM in HeLa cells, indicating that these compounds represent a new potential class of anticancer agents...
October 11, 2017: Journal of the American Chemical Society
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