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inducing mitochondrial biogenesis

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https://www.readbyqxmd.com/read/28528294/isoliquiritigenin-reduces-oxidative-damage-and-alleviates-mitochondrial-impairment-by-sirt1-activation-in-experimental-diabetic-neuropathy
#1
Veera Ganesh Yerra, Anil Kumar Kalvala, Ashutosh Kumar
Sirtuin (SIRT1) inactivation underlies the pathogenesis of insulin resistance and hyperglycaemia-associated vascular complications, but its role in diabetic neuropathy (DN) has not been yet explored. We have evaluated hyperglycaemia-induced alteration of SIRT1 signalling and the effect of isoliquiritigenin (ILQ) on SIRT1-directed AMP kinase (AMPK) and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) signalling in peripheral nerves of streptozotocin (STZ) (55 mg/kg, ip)-induced diabetic rats and in high glucose (30 mM)-exposed neuro2a (N2A) cells...
May 11, 2017: Journal of Nutritional Biochemistry
https://www.readbyqxmd.com/read/28524859/mesenchymal-stem-cells-sense-mitochondria-released-from-damaged-cells-as-danger-signals-to-activate-their-rescue-properties
#2
Meriem Mahrouf-Yorgov, Lionel Augeul, Claire Crola Da Silva, Maud Jourdan, Muriel Rigolet, Sylvie Manin, René Ferrera, Michel Ovize, Adeline Henry, Aurélie Guguin, Jean-Paul Meningaud, Jean-Luc Dubois-Randé, Roberto Motterlini, Roberta Foresti, Anne-Marie Rodriguez
Mesenchymal stem cells (MSCs) protect tissues against cell death induced by ischemia/reperfusion insults. This therapeutic effect seems to be controlled by physiological cues released by the local microenvironment following injury. Recent lines of evidence indicate that MSC can communicate with their microenvironment through bidirectional exchanges of mitochondria. In particular, in vitro and in vivo studies report that MSCs rescue injured cells through delivery of their own mitochondria. However, the role of mitochondria conveyed from somatic cells to MSC remains unknown...
May 19, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28514599/a-bioenergetics-systems-evaluation-of-ketogenic-diet-liver-effects
#3
Lewis J Hutfles, Heather M Wilkins, Scott J Koppel, Ian W Weidling, J Eva Selfridge, Eephie Tan, John P Thyfault, Chad Slawson, Aron W Fenton, Hao Zhu, Russell H Swerdlow
Ketogenic diets induce hepatocyte fatty acid oxidation and ketone body production. To further evaluate how ketogenic diets affect hepatocyte bioenergetic infrastructure, we analyzed livers from C57Bl/6J male mice maintained for one month on a ketogenic or standard chow diet. Compared to the standard diet, the ketogenic diet increased cytosolic and mitochondrial protein acetylation and also altered protein succinylation patterns. SIRT3 protein decreased while SIRT5 protein increased, and gluconeogenesis, oxidative phosphorylation, and mitochondrial biogenesis pathway proteins were variably and likely strategically altered...
May 17, 2017: Applied Physiology, Nutrition, and Metabolism, Physiologie Appliquée, Nutrition et Métabolisme
https://www.readbyqxmd.com/read/28507194/molecular-basis-of-exercise-induced-skeletal-muscle-mitochondrial-biogenesis-historical-advances-current-knowledge-and-future-challenges
#4
Christopher G R Perry, John A Hawley
We provide an overview of groundbreaking studies that laid the foundation for our current understanding of exercise-induced mitochondrial biogenesis and its contribution to human skeletal muscle fitness. We highlight the mechanisms by which skeletal muscle responds to the acute perturbations in cellular energy homeostasis evoked by a single bout of endurance-based exercise and the adaptations resulting from the repeated demands of exercise training that ultimately promote mitochondrial biogenesis through hormetic feedback loops...
May 15, 2017: Cold Spring Harbor Perspectives in Medicine
https://www.readbyqxmd.com/read/28507060/alogliptin-a-dipeptidyl-peptidase-4-inhibitor-alleviates-atrial-remodeling-and-improves-mitochondrial-function-and-biogenesis-in-diabetic-rabbits
#5
Xiaowei Zhang, Zhiwei Zhang, Yungang Zhao, Ning Jiang, Jiuchun Qiu, Yajuan Yang, Jian Li, Xue Liang, Xinghua Wang, Gary Tse, Guangping Li, Tong Liu
BACKGROUND: There is increasing evidence implicating atrial mitochondrial dysfunction in the pathogenesis of atrial fibrillation. In this study, we explored whether alogliptin, a dipeptidyl peptidase-4 inhibitor, can prevent mitochondrial dysfunction and atrial remodeling in a diabetic rabbit model. METHODS AND RESULTS: A total of 90 rabbits were randomized into 3 groups as follows: control group (n=30), alloxan-induced diabetes mellitus group (n=30), and alogliptin-treated (12...
May 15, 2017: Journal of the American Heart Association
https://www.readbyqxmd.com/read/28506826/an-x-chromosome-linked-mouse-model-ndufa1-s55a-for-systemic-partial-complex-i-deficiency-for-studying-predisposition-to-neurodegeneration-and-other-diseases
#6
Chul Kim, Prasanth Potluri, Ahmed Khalil, Daria Gaut, Meagan McManus, Shannon Compton, Douglas C Wallace, Nagendra Yadava
The respiratory chain Complex I deficiencies are the most common cause of mitochondrial diseases. Complex I biogenesis is controlled by 58 genes and at least 47 of these cause mitochondrial disease in humans. Two of these are X-chromosome linked nuclear (nDNA) genes (NDUFA1 and NDUFB11), and 7 are mitochondrial (mtDNA, MT-ND1-6, 4L) genes, which may be responsible for sex-dependent variation in the presentation of mitochondrial diseases. In this study, we describe an X-chromosome linked mouse model (Ndufa1(S55A)) for systemic partial Complex I deficiency...
May 12, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28504722/thyroid-hormone-protects-hepatocytes-from-hbx-induced-carcinogenesis-by-enhancing-mitochondrial-turnover
#7
H-C Chi, S-L Chen, S-L Lin, C-Y Tsai, W-Y Chuang, Y-H Lin, Y-H Huang, M-M Tsai, C-T Yeh, K-H Lin
Infection by hepatitis B virus (HBV) accounts for 50-80% of hepatocellular carcinoma (HCC) development worldwide, in which the HBV-encoded X protein (HBx) has critical role in the induction of carcinogenesis. Several studies have shown that thyroid hormone (TH) suppresses HCC development and protects hepatocytes from HBx-induced damage, thus it is of interest to examine whether TH can protect hepatocytes from HBx-induced carcinogenesis. By treating HBx- transgenic mice with or without TH, we confirmed the protective effects of TH on HBx-induced hepatocarcinogenesis, which was achieved via reduction of reactive oxygen species (ROS) inflicted DNA damage...
May 15, 2017: Oncogene
https://www.readbyqxmd.com/read/28501483/reversal-of-bioenergetics-dysfunction-by-diphenyl-diselenide-is-critical-to-protection-against-the-acetaminophen-induced-acute-liver-failure
#8
Nélson R Carvalho, Cintia C Tassi, Fernando Dobraschinski, Guilherme P Amaral, Ana P Zemolin, Ronaldo M Golombieski, Cristiane L Dalla Corte, Jeferson L Franco, José L Mauriz, Javier González-Gallego, Félix A Soares
Physiopathological conditions such as acute liver failure (ALF) induced by acetaminophen (APAP) can often impair the mitochondrial bioenergetics. Diphenyl diselenide [(PhSe)2] has been shown protects against APAP-induced ALF. The present study aimed to clarify the signaling mechanism involved in the protection of bioenergetics dysfunction associated with ALF-induced by APAP overdose. Mice received APAP (600mg/kg) or (PhSe)2 (15.6mg/kg) alone, or APAP+(PhSe)2, all the solutions were administered by the intraperitoneal (i...
May 10, 2017: Life Sciences
https://www.readbyqxmd.com/read/28497127/evidence-of-glycolysis-up-regulation-and-pyruvate-mitochondrial-oxidation-mismatch-during-mechanical-unloading-of-the-failing-human-heart-implications-for-cardiac-reloading-and-conditioning
#9
Nikolaos A Diakos, Sutip Navankasattusas, E Dale Abel, Jared Rutter, Lauren McCreath, Peter Ferrin, Stephen H McKellar, Dylan V Miller, Song Y Park, Russell S Richardson, Ralph Deberardinis, James E Cox, Abdallah G Kfoury, Craig H Selzman, Josef Stehlik, James C Fang, Dean Y Li, Stavros G Drakos
This study sought to investigate the effects of mechanical unloading on myocardial energetics and the metabolic perturbation of heart failure (HF) in an effort to identify potential new therapeutic targets that could enhance the unloading-induced cardiac recovery. The authors prospectively examined paired human myocardial tissue procured from 31 advanced HF patients at left ventricular assist device (LVAD) implant and at heart transplant plus tissue from 11 normal donors. They identified increased post-LVAD glycolytic metabolites without a coordinate increase in early, tricarboxylic acid (TCA) cycle intermediates...
October 2016: JACC. Basic to Translational Science
https://www.readbyqxmd.com/read/28495843/treating-fructose-induced-metabolic-changes-in-mice-with-high-intensity-interval-training-insights-in-the-liver-white-adipose-tissue-and-skeletal-muscle
#10
Victor Faria Motta, Thereza Lonzetti Bargut, Marcia Barbosa Aguila, Carlos Alberto Mandarim-de-Lacerda
Fructose-rich caloric sweeteners induce adverse changes in the population metabolism. The study evaluated the effects of high-intensity interval training (HIIT) on a fructose feeding model, focusing on the liver, white adipose tissue (WAT), skeletal muscle, and their interplay. Male C57BL/6 mice were fed for 18 weeks one of the following diets: control (C; 5 % of total energy from fructose), or fructose (F; 55 % of total energy from fructose). In the 10th week, for an additional eight-week period the groups were divided into non-trained (NT) or HIIT groups, totaling four groups: C-NT, C-HIIT, F-NT, and F-HIIT...
May 11, 2017: Journal of Applied Physiology
https://www.readbyqxmd.com/read/28493443/natural-alkaloid-bouchardatine-ameliorates-metabolic-disorders-in-high-fat-diet-fed-mice-via-stimulating-the-sirt1-lkb1-ampk-axis
#11
Yong Rao, Hong Yu, Lin Gao, Yu-Ting Lu, Zhao Xu, Hong Liu, Lian-Quan Gu, Ji-Ming Ye, Zhi-Shu Huang
BACKGROUND AND PURPOSE: Promoting energy metabolism is known to provide therapeutic effects for obesity and associated metabolic disorders. The present study evaluated the therapeutic effects of the newly-identified bouchardatine (Bou) on obesity associated metabolic disorders and the molechular mechanisms for these effects. EXPERIMENTAL APPROACH: The molecular mode of action of Bou for its effects on lipid metabolism was first examined in 3T3-L1 adipocytes and HepG2 cells...
May 10, 2017: British Journal of Pharmacology
https://www.readbyqxmd.com/read/28492551/haploinsufficiency-in-the-mitochondrial-protein-chchd4-reduces-brain-injury-in-a-mouse-model-of-neonatal-hypoxia-ischemia
#12
Yanyan Sun, Tao Li, Cuicui Xie, Yiran Xu, Kai Zhou, Juan Rodriguez, Wei Han, Xiaoyang Wang, Guido Kroemer, Nazanine Modjtahedi, Klas Blomgren, Changlian Zhu
Mitochondria contribute to neonatal hypoxic-ischemic brain injury by releasing potentially toxic proteins into the cytosol. CHCHD4 is a mitochondrial intermembrane space protein that plays a major role in the import of intermembrane proteins and physically interacts with apoptosis-inducing factor (AIF). The purpose of this study was to investigate the impact of CHCHD4 haploinsufficiency on mitochondrial function and brain injury after cerebral hypoxia-ischemia (HI) in neonatal mice. CHCHD4(+/-) and wild-type littermate mouse pups were subjected to unilateral cerebral HI on postnatal day 9...
May 11, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28486920/mitochondria-a-novel-therapeutic-target-in-diabetic-nephropathy
#13
Shikun Yang, Yachun Han, Jun Liu, Panai Song, Xiaoxuan Xu, Li Zhao, Chun Hu, Li Xiao, Fuyou Liu, Hao Zhang, Lin Sun
Diabetic nephropathy (DN) is an important diabetic microvascular complication, and it is becoming the leading cause of end-stage renal disease worldwide. Unfortunately, there are no effective therapies to treat established DN. Therefore, new therapeutic targets are urgently required. Accumulating studies indicate that mitochondrial dysfunction is central to the pathogenesis of DN, such as elevated oxidative stress induced by disorders of the mitochondrial respiratory chain complex and mitochondrial dynamic disorders...
May 9, 2017: Current Medicinal Chemistry
https://www.readbyqxmd.com/read/28485388/charting-organellar-importomes-by-quantitative-mass-spectrometry
#14
Christian D Peikert, Jan Mani, Marcel Morgenstern, Sandro Käser, Bettina Knapp, Christoph Wenger, Anke Harsman, Silke Oeljeklaus, André Schneider, Bettina Warscheid
Protein import into organelles is essential for all eukaryotes and facilitated by multi-protein translocation machineries. Analysing whether a protein is transported into an organelle is largely restricted to single constituents. This renders knowledge about imported proteins incomplete, limiting our understanding of organellar biogenesis and function. Here we introduce a method that enables charting an organelle's importome. The approach relies on inducible RNAi-mediated knockdown of an essential subunit of a translocase to impair import and quantitative mass spectrometry...
May 9, 2017: Nature Communications
https://www.readbyqxmd.com/read/28482072/endoplasmic-reticulum-stress-induced-chop-inhibits-pgc-1%C3%AE-and-causes-mitochondrial-dysfunction-in-diabetic-embryopathy
#15
Xi Chen, Jianxiang Zhong, Daoyin Dong, Gentao Liu, Peixin Yang
Endoplasmic reticulum (ER) stress has been implicated in the development of maternal diabetes-induced neural tube defects (NTDs). ER stress-induced C/EBP homologous protein (CHOP) plays an important role in the pro-apoptotic execution pathways. However, the molecular mechanism underlying ER stress- and CHOP-induced neuroepithelium cell apoptosis in diabetic embryopathy are still unclear. Deletion of the Chop gene significantly reduced maternal diabetes-induced NTDs. CHOP deficiency abrogated maternal diabetes-induced mitochondrial dysfunction and neuroepithelium cell apoptosis...
May 8, 2017: Toxicological Sciences: An Official Journal of the Society of Toxicology
https://www.readbyqxmd.com/read/28473878/ho-1-is-essential-for-tetrahydroxystilbene-glucoside-mediated-mitochondrial-biogenesis-and-anti-inflammation-process-in-lps-treated-raw264-7-macrophages
#16
Weihua Yu, Xiaodi Zhang, Hao Wu, Qingbiao Zhou, Zhao Wang, Rui Liu, Jiangzheng Liu, Xin Wang, Chunxu Hai
2,3,5,4'-Tetrahydroxystilbene-2-O-β-D-glucoside (TSG), an important monomer extracted from Polygonum multiflorum, can prevent a number of inflammation associated chronic diseases. However, the mechanism involved in TSG inducing anti-inflammatory role remains unclear. As an inducible antioxidant enzyme, Heme oxygenase-1 (HO-1), is crucial for protecting the mammalian cells against adverse stimuli. Here, we found that the TSG treatment strongly induces the expression of HO-1 in an NRF2-depended manner. Meanwhile, TSG increased the mitochondrial mass through upregulation of the mitochondrial biogenesis activators (PGC-1α, NRF1, and TFAM) as well as the mitochondrial complex IV...
2017: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/28473603/increased-hepatic-mitochondrial-fa-oxidation-leads-to-lower-tg-levels-in-rat-liver-and-plasma-and-is-associated-with-upregulation-of-uncoupling-proteins-and-downregulation-of-apolipoprotein-c-iii
#17
Carine Lindquist, Bodil Bjørndal, Christine Renate Rossmann, Deusdedit Tusubira, Asbjørn Svardal, Gro Vatne Røsland, Karl Johan Tronstad, Seth Hallström, Rolf Kristian Berge
Hepatic mitochondrial function, APOC-III and LPL are potential targets for TG lowering drugs. After three weeks of dietary treatment with the compound 2-(tridec-12 -yn-1-ylthio) acetic acid (1-triple TTA), the hepatic mitochondrial FA oxidation increased more than 5-fold in male Wistar rats. Gene expression analysis in liver showed significant downregulation of APOC-III, and upregulation of LPL and the VLDL receptor. This led to lower hepatic (53 %) and plasma (73 %) TG levels. Concomitantly liver-specific biomarkers related to mitochondrial biogenesis and function (mitochondrial DNA, citrate synthase activity and cytochrome c and Tfam gene expression) were elevated...
May 4, 2017: Journal of Lipid Research
https://www.readbyqxmd.com/read/28467933/ppar%C3%AE-is-essential-for-maintaining-normal-levels-of-pgc-1%C3%AE-and-mitochondria-and-for-the-increase-in-muscle-mitochondria-induced-by-exercise
#18
Jin-Ho Koh, Chad R Hancock, Shin Terada, Kazuhiko Higashida, John O Holloszy, Dong-Ho Han
The objective of this study was to evaluate the specific mechanism(s) by which PPARβ regulates mitochondrial content in skeletal muscle. We discovered that PPARβ increases PGC-1α by protecting it from degradation by binding to PGC-1α and limiting ubiquitination. PPARβ also induces an increase in nuclear respiratory factor 1 (NRF-1) expression, resulting in increases in mitochondrial respiratory chain proteins and MEF2A, for which NRF-1 is a transcription factor. There was also an increase in AMP kinase phosphorylation mediated by an NRF-1-induced increase in CAM kinase kinase-β (CaMKKβ)...
May 2, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28462117/function-of-specialized-regulatory-proteins-and-signaling-pathways-in-exercise-induced-muscle-mitochondrial-biogenesis
#19
REVIEW
Avigail T Erlich, Liam D Tryon, Matthew J Crilly, Jonathan M Memme, Zahra S Mesbah Moosavi, Ashley N Oliveira, Kaitlyn Beyfuss, David A Hood
Skeletal muscle mitochondrial content and function are regulated by a number of specialized molecular pathways that remain to be fully defined. Although a number of proteins have been identified to be important for the maintenance of mitochondria in quiescent muscle, the requirement for these appears to decrease with the activation of multiple overlapping signaling events that are triggered by exercise. This makes exercise a valuable therapeutic tool for the treatment of mitochondrially based metabolic disorders...
September 2016: Integr Med Res
https://www.readbyqxmd.com/read/28460056/dimethyl-fumarate-mediates-nrf2-dependent-mitochondrial-biogenesis-in-mice-and-humans
#20
Genki Hayashi, Mittal Jasoliya, Francesco Saccà, Chiara Pane, Alessandro Filla, Angela Marsili, Giorgia Puorro, Roberta Lanzillo, Vincenzo Brescia Morra, Gino Cortopassi
The induction of mitochondrial biogenesis could potentially alleviate mitochondrial and muscle disease. We show here that dimethyl fumarate (DMF) dose-dependently induces mitochondrial biogenesis and function dosed to cells in in vitro, and also dosed in vivo to mice and humans. The induction of mitochondrial gene expression is more dependent on its target Nrf2 than hydroxycarboxylic acid receptor 2 (HCAR2). Thus, DMF induces mitochondrial biogenesis primarily through its action on Nrf2, and is the first drug demonstrated to increase mitochondrial biogenesis with in vivo human dosing...
April 28, 2017: Human Molecular Genetics
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