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inducing mitochondrial biogenesis

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https://www.readbyqxmd.com/read/28223503/mitochondrial-energy-deficiency-leads-to-hyperproliferation-of-skeletal-muscle-mitochondria-and-enhanced-insulin-sensitivity
#1
Ryan M Morrow, Martin Picard, Olga Derbeneva, Jeremy Leipzig, Meagan J McManus, Gilles Gouspillou, Sébastien Barbat-Artigas, Carlos Dos Santos, Russell T Hepple, Deborah G Murdock, Douglas C Wallace
Diabetes is associated with impaired glucose metabolism in the presence of excess insulin. Glucose and fatty acids provide reducing equivalents to mitochondria to generate energy, and studies have reported mitochondrial dysfunction in type II diabetes patients. If mitochondrial dysfunction can cause diabetes, then we hypothesized that increased mitochondrial metabolism should render animals resistant to diabetes. This was confirmed in mice in which the heart-muscle-brain adenine nucleotide translocator isoform 1 (ANT1) was inactivated...
February 21, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/28220896/mitochondrial-dysregulation-secondary-to-endoplasmic-reticulum-stress-in-autosomal-dominant-tubulointerstitial-kidney-disease-umod-adtkd-umod
#2
Elisabeth Kemter, Thomas Fröhlich, Georg J Arnold, Eckhard Wolf, Rüdiger Wanke
'Autosomal dominant tubulointerstitial kidney disease - UMOD' (ADTKD-UMOD) is caused by impaired maturation and secretion of mutant uromodulin (UMOD) in thick ascending limb of Henle loop (TAL) cells, resulting in endoplasmic reticulum (ER) stress and unfolded protein response (UPR). To gain insight into pathophysiology, we analysed proteome profiles of TAL-enriched outer renal medulla samples from ADTKD-UMOD and control mice by quantitative LC-MS/MS. In total, 212 differentially abundant proteins were identified...
February 21, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28216426/no-control-of-mitochondrial-function-in-normal-and-transformed-cells
#3
Celia H Tengan, Carlos T Moraes
Nitric oxide (NO) is a signaling molecule with multiple facets and involved in numerous pathological process, including cancer. Among the different pathways where NO has a functionally relevant participation, is the control of mitochondrial respiration and biogenesis. NO is able to inhibit the electron transport chain, mainly at Complex IV, regulating oxygen consumption and ATP generation, but at the same time, can also induce increase in reactive oxygen and nitrogen species. The presence of reactive species can induce oxidative damage or participate in redox signaling...
February 16, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28216385/the-role-of-mitochondria-in-cardiac-development-and-protection
#4
REVIEW
Jaakko L Pohjoismäki, Steffi Goffart
Mitochondria are essential for the development as well as maintenance of the myocardium, the most energy consuming tissue in the human body. Mitochondria are not only a source of ATP energy but also generators of reactive oxygen species (ROS), that cause oxidative damage, but also regulate physiological processes such as the switch from hyperplastic to hypertrophic growth after birth. As excess ROS production and oxidative damage are associated with cardiac pathology, it is not surprising that much of the research focused on the deleterious aspects of free radicals...
February 16, 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28207937/mitochondrial-dysfunction-is-involved-in-the-aggravation-of-periodontitis-by-diabetes
#5
Xiaoyu Sun, Yixin Mao, Panpan Dai, Xumin Li, Weiyan Gu, Huining Wang, Gang Wu, Jianfeng Ma, Shengbin Huang
AIM: To elucidate whether mitochondrial dysfunction contributes to aggravated periodontitis in diabetes. MATERIALS AND METHODS: 64 wistar rats were randomly assigned into four groups: control, periodontitis, diabetes, and diabetic periodontitis. Two weeks after induction of diabetes, periodontitis was induced by silk ligation for 2 weeks and thereafter evaluated by assessing alveolar bone loss and apoptosis of periodontium cells. Mitochondrial oxidative stress was detected by MitoSOX staining...
February 16, 2017: Journal of Clinical Periodontology
https://www.readbyqxmd.com/read/28207880/skeletal-muscle-metabolic-adaptations-to-endurance-exercise-training-are-attainable-in-mice-with-simvastatin-treatment
#6
William M Southern, Anna S Nichenko, Daniel D Shill, Corey C Spencer, Nathan T Jenkins, Kevin K McCully, Jarrod A Call
We tested the hypothesis that a 6-week regimen of simvastatin would attenuate skeletal muscle adaptation to low-intensity exercise. Male C57BL/6J wildtype mice were subjected to 6-weeks of voluntary wheel running or normal cage activities with or without simvastatin treatment (20 mg/kg/d, n = 7-8 per group). Adaptations in in vivo fatigue resistance were determined by a treadmill running test, and by ankle plantarflexor contractile assessment. The tibialis anterior, gastrocnemius, and plantaris muscles were evaluated for exercised-induced mitochondrial adaptations (i...
2017: PloS One
https://www.readbyqxmd.com/read/28199195/tissue-transglutaminase-tg2-and-mitochondrial-function-and-dysfunction
#7
Thung-S Lai, Cheng-Jui Lin, Yu-Ting Wu, Chih-Jen Wu
Mitochondria are the cell's power plant to satisfy the energy demands. However, dysfunctional mitochondria can cause overproduction of reactive oxygen species (ROS), oxidative stress, and alteration of calcium homeostasis, which are the hallmarks of mitochondrial diseases. Under prolong oxidative stress, repeated cytosolic calcium elevations even only transiently, can lead to activation of some enzymes. One calcium-activated enzyme with demonstrated pathophysiological important in mitochondrial disease is tissue transglutaminase (TG2)...
March 1, 2017: Frontiers in Bioscience (Landmark Edition)
https://www.readbyqxmd.com/read/28196867/synaptic-activity-drives-a-genomic-program-that-promotes-a-neuronal-warburg-effect
#8
Carlos Bas-Orth, Yan-Wei Tan, David Lau, Hilmar Bading
Synaptic activity drives changes in gene expression to promote long-lasting adaptations of neuronal structure and function. One example of such an adaptive response is the buildup of acquired neuroprotection, a synaptic activity- and gene transcription-mediated increase in the resistance of neurons against harmful conditions. A hallmark of acquired neuroprotection is the stabilization of mitochondrial structure and function. We therefore re-examined previously identified sets of synaptic activity-regulated genes to identify genes that are directly linked to mitochondrial function...
February 14, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28193580/astaxanthin-inhibits-inflammation-and-fibrosis-in-the-liver-and-adipose-tissue-of-mouse-models-of-diet-induced-obesity-and-nonalcoholic-steatohepatitis
#9
Bohkyung Kim, Callie Farruggia, Chai Siah Ku, Tho X Pham, Yue Yang, Minkyung Bae, Casey J Wegner, Nicholas J Farrell, Ellen Harness, Young-Ki Park, Sung I Koo, Ji-Young Lee
The objective of this study was to determine if astaxanthin (ASTX), a xanthophyll carotenoid, can prevent obesity-associated metabolic abnormalities, inflammation and fibrosis in diet-induced obesity (DIO) and nonalcoholic steatohepatitis (NASH) mouse models. Male C57BL/6J mice were fed a low-fat (6% fat, w/w), a high-fat/high-sucrose control (HF/HS; 35% fat, 35% sucrose, w/w), or a HF/HS containing ASTX (AHF/HS; 0.03% ASTX, w/w) for 30 weeks. To induce NASH, another set of mice was fed a HF/HS diet containing 2% cholesterol (HF/HS/HC) a HF/HS/HC with 0...
March 2, 2016: Journal of Nutritional Biochemistry
https://www.readbyqxmd.com/read/28192097/effects-of-iron-overload-an-iron-chelator-and-a-t-type-calcium-channel-blocker-on-cardiac-mitochondrial-biogenesis-and-mitochondrial-dynamics-in-thalassemic-mice
#10
Juthamas Khamseekaew, Sirinart Kumfu, Suwakon Wongjaikam, Sasiwan Kerdphoo, Thidarat Jaiwongkam, Somdet Srichairatanakool, Suthat Fucharoen, Siriporn C Chattipakorn, Nipon Chattipakorn
Although cardiac mitochondrial dysfunction is involved in the pathophysiology of iron-overload cardiomyopathy, the precise mechanisms of iron-induced mitochondrial dysfunction, and the roles of the iron chelator deferiprone and the T-type calcium channel blocker efonidipine on cardiac mitochondrial biogenesis in thalassemic mice are still unknown. β-thalassemic (HT) mice were fed with a normal diet (ND) or a high iron-diet (FE) for 90 days. Then, the FE-fed mice were treated with deferiprone (75mg/kg/day) or efonidipine (4mg/kg/day) for 30 days...
February 10, 2017: European Journal of Pharmacology
https://www.readbyqxmd.com/read/28179648/diet-induced-weight-loss-decreases-adipose-tissue-oxygen-tension-with-parallel-changes-in-adipose-tissue-phenotype-and-insulin-sensitivity-in-overweight-humans
#11
R G Vink, N J Roumans, M Čajlaković, J P M Cleutjens, M V Boekschoten, P Fazelzadeh, M A A Vogel, E E Blaak, E C Mariman, M A van Baak, G H Goossens
BACKGROUND/OBJECTIVES: Although adipose tissue (AT) hypoxia is present in rodent models of obesity, evidence for this in humans is limited. Here, we investigated the effects of diet-induced weight loss on abdominal subcutaneous AT oxygen tension (pO2), AT blood flow (ATBF), AT capillary density, AT morphology and transcriptome, systemic inflammatory markers, and insulin sensitivity in humans. SUBJECTS/METHODS: Fifteen overweight and obese individuals underwent a dietary intervention (DI), consisting of a 5-week very-low-calorie diet (VLCD, 500 kcal/d) (WL), and a subsequent 4-week weight stable diet (WS)...
February 9, 2017: International Journal of Obesity: Journal of the International Association for the Study of Obesity
https://www.readbyqxmd.com/read/28178868/low-level-lasers-effect-on-proliferation-migration-and-anti-apoptosis-of-mesenchymal-stem-cells
#12
Kan Yin, Rongjia Zhu, Shihua Wang, Robert Chunhua Zhao
Mesenchymal stem cells (MSCs) have been found to be helpful elements in tissue regeneration. Photobiomodulation (PBM) used extremely low level lasers (LLL) to affect the behaviour of cells. The effect mechanism of LLL on MSCs remained to be discovered. Here cell viability was assessed using MTS assays and cell cycle was evaluated by FACS. The influence of LLL on mitochondrial biogenesis (fission or fusion) and function (ATP, ROS, NO) were evaluated by TEM, FACS, RT-PCR, immunocytochemistry. Cell migration and cytoskeleton alteration (actin and tubulin) were evaluated using transwell assay, immunocytochemistry, ELISA and Western blotting...
February 8, 2017: Stem Cells and Development
https://www.readbyqxmd.com/read/28177702/modulation-of-mitochondrial-biomarkers-by-intermittent-hypobaric-hypoxia-and-aerobic-exercise-after-eccentric-exercise-in-trained-rats
#13
David Rizo-Roca, Juan Gabriel Ríos-Kristjánsson, Cristian Núñez-Espinosa, Estela Santos-Alves, José Magalhães, António Ascensão, Teresa Pagès, Ginés Viscor, Joan Ramon Torrella
Unaccustomed eccentric contractions induce muscle damage, calcium homeostasis disruption and mitochondrial alterations. Since exercise and hypoxia are known to modulate mitochondrial function, we aimed to analyze the effects on eccentric exercise-induced muscle damage (EEIMD), in trained rats, of two recovery protocols based on: 1) intermittent hypobaric hypoxia (IHH) and 2) IHH followed by exercise. The expression of biomarkers related to mitochondrial biogenesis, dynamics, oxidative stress and bioenergetics was evaluated...
February 2, 2017: Applied Physiology, Nutrition, and Metabolism, Physiologie Appliquée, Nutrition et Métabolisme
https://www.readbyqxmd.com/read/28176017/hypoxia-and-aerobic-metabolism-adaptations-of-human-endothelial-cells
#14
Agnieszka Koziel, Wieslawa Jarmuszkiewicz
The goal of our study was to assess the influence of chronic exposure to hypoxia on mitochondrial oxidative metabolism in human umbilical vein endothelial cells (EA.hy926 line) cultured for 6 days at 1% O2 tension. The hypoxia-induced effects were elucidated at the cellular and isolated mitochondria levels. Hypoxia elevated fermentation but did not change mitochondrial biogenesis or the aerobic respiratory capacity of endothelial cells. In endothelial cells, hypoxia caused a general decrease in mitochondrial respiration during carbohydrate, fatty acid, and amino acid oxidation but increased exclusively ketogenic amino acid oxidation...
February 8, 2017: Pflügers Archiv: European Journal of Physiology
https://www.readbyqxmd.com/read/28174611/pterostilbene-ameliorates-intracerebroventricular-streptozotocin-induced-memory-decline-in-rats
#15
Bhagyashree Naik, Abhijit Nirwane, Anuradha Majumdar
There is strong evidence that mitochondrial dysfunction mediated oxidative stress results in aging and energy metabolism deficits thus playing a prime role in pathogenesis of Alzheimer's disease, neuronal death and cognitive dysfunction. Evidences accrued in empirical studies suggest the antioxidant, anticancer and anti-inflammatory activities of the phytochemical pterostilbene (PTS). PTS also exhibits favourable pharmacokinetic attributes compared to other stilbenes. Hence, in the present study, we explored the neuroprotective role of PTS in ameliorating the intracerebroventricular administered streptozotocin (STZ) induced memory decline in rats...
February 2017: Cognitive Neurodynamics
https://www.readbyqxmd.com/read/28174208/l-opa1-regulates-mitoflash-biogenesis-independently-from-membrane-fusion
#16
Manon Rosselin, Jaime Santo-Domingo, Flavien Bermont, Marta Giacomello, Nicolas Demaurex
Mitochondrial flashes mediated by optic atrophy 1 (OPA1) fusion protein are bioenergetic responses to stochastic drops in mitochondrial membrane potential (Δψm) whose origin is unclear. Using structurally distinct genetically encoded pH-sensitive probes, we confirm that flashes are matrix alkalinization transients, thereby establishing the pH nature of these events, which we renamed "mitopHlashes". Probes located in cristae or intermembrane space as verified by electron microscopy do not report pH changes during Δψm drops or respiratory chain inhibition...
February 7, 2017: EMBO Reports
https://www.readbyqxmd.com/read/28165849/autophagosome-formation-and-cargo-sequestration-in-the-absence-of-lc3-gabaraps
#17
Benjamin Scott Padman, Thanh Ngoc Nguyen, Michael Lazarou
It has been widely assumed that Atg8 family LC3/GABARAP proteins are essential for the formation of autophagosomes during macroautophagy/autophagy, and the sequestration of cargo during selective autophagy. However, there is little direct evidence on the functional contribution of these proteins to autophagosome biogenesis in mammalian cells. To dissect the functions of LC3/GABARAPs during starvation-induced autophagy and PINK1-PARK2/Parkin-dependent mitophagy, we utilized CRISPR/Cas9 gene editing to generate knockouts of the LC3 and GABARAP subfamilies, and all 6 Atg8 family proteins in HeLa cells...
February 6, 2017: Autophagy
https://www.readbyqxmd.com/read/28164768/protective-effect-of-aspirin-against-oligomeric-a%C3%AE-42-induced-mitochondrial-alterations-and-neurotoxicity-in-differentiated-ec-p19-neuronal-cells
#18
Hamendra Singh Parmar, Zbynek Houdek, Martin Pesta, Vaclava Cerna, Pavel Dvorak, Jiri Hatina
Amyloid-beta (Aβ) induced mitochondrial dysfunction is one of the major causes of neuronal toxicity in Alzheimer's disease. Many recent reports suggest involvement of mitochondrial alterations through intracellular accumulation of oligomeric Aβ. These mitochondrial alterations include increased reactive oxygen species (ROS), mt-DNA depletion, decreased oxidative phosphorylation and ATP production, membrane depolarization, reduced number of mitochondria etc. These all defects cumulatively caused neural toxicity and alterations in cellular energy homeostasis...
February 2, 2017: Current Alzheimer Research
https://www.readbyqxmd.com/read/28161458/effect-of-mptp-on-mrna-expression-of-pgc-1%C3%AE-in-mouse-brain
#19
Rita Torok, Andras Salamon, Evelin Sumegi, Denes Zadori, Gabor Veres, Mate Fort Molnar, Laszlo Vecsei, Peter Klivenyi
The peroxisome proliferator-activated receptor-γ (PPARγ) coactivator 1α (PGC-1α) is a key regulator of mitochondrial biogenesis, respiration and adaptive thermogenesis. Besides the full-length protein (FL-PGC-1α), several other functionally active PGC-1α isoforms were identified as a result of alternative splicing (e.g., N-truncated PGC-1α; NT-PGC-1α) or alternative promoter usage (e.g., central nervous system-specific PGC-1α isoforms; CNS-PGC-1α). Achieving neuroprotection via CNS-targeted pharmacological stimulation is limited due to poor penetration of the blood brain barrier (BBB) by the proposed pharmaceutical agents, so preconditioning emerged as another option...
February 1, 2017: Brain Research
https://www.readbyqxmd.com/read/28146060/adenosine-monophosphate-amp-activated-protein-kinase-a-new-target-for-nutraceutical-compounds
#20
REVIEW
Fabiola Marín-Aguilar, Luis E Pavillard, Francesca Giampieri, Pedro Bullón, Mario D Cordero
Adenosine monophosphate-activated protein kinase (AMPK) is an important energy sensor which is activated by increases in adenosine monophosphate (AMP)/adenosine triphosphate (ATP) ratio and/or adenosine diphosphate (ADP)/ATP ratio, and increases different metabolic pathways such as fatty acid oxidation, glucose transport and mitochondrial biogenesis. In this sense, AMPK maintains cellular energy homeostasis by induction of catabolism and inhibition of ATP-consuming biosynthetic pathways to preserve ATP levels...
January 29, 2017: International Journal of Molecular Sciences
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