Iron-Sulfur (Fe/S) Protein Biogenesis: Phylogenomic and Genetic Studies of A-Type Carriers

OPEN ACCESS

Source: PLoS-GENETICS, http://www.plosgenetics.org/article/info%3Adoi%2F10.1371%2Fjournal.pgen.1000497 (full text)

Iron-Sulfur (Fe/S) Protein Biogenesis: Phylogenomic and Genetic Studies of A-Type Carriers

Daniel Vinella1,2, Céline Brochier-Armanet1,2, Laurent Loiseau1,2, Emmanuel Talla1,2, Frédéric Barras1,2*
1 Laboratoire de Chimie Bactérienne, Institut Fédératif de Recherche 88 - Institut de Microbiologie de la Méditerranée, Centre National de la Recherche Scientifique, Marseille, France, 2 Aix-Marseille Université, Marseille, France

Abstract Top
Iron sulfur (Fe/S) proteins are ubiquitous and participate in multiple biological processes, from photosynthesis to DNA repair. Iron and sulfur are highly reactive chemical species, and the mechanisms allowing the multiprotein systems ISC and SUF to assist Fe/S cluster formation in vivo have attracted considerable attention. Here, A-Type components of these systems (ATCs for A-Type Carriers) are studied by phylogenomic and genetic analyses. ATCs that have emerged in the last common ancestor of bacteria were conserved in most bacteria and were acquired by eukaryotes and few archaea via horizontal gene transfers. Many bacteria contain multiple ATCs, as a result of gene duplication and/or horizontal gene transfer events. Based on evolutionary considerations, we could define three subfamilies: ATC-I, -II and -III. Escherichia coli, which has one ATC-I (ErpA) and two ATC-IIs (IscA and SufA), was used as a model to investigate functional redundancy between ATCs in vivo. Genetic analyses revealed that, under aerobiosis, E. coli IscA and SufA are functionally redundant carriers, as both are potentially able to receive an Fe/S cluster from IscU or the SufBCD complex and transfer it to ErpA. In contrast, under anaerobiosis, redundancy occurs between ErpA and IscA, which are both potentially able to receive Fe/S clusters from IscU and transfer them to an apotarget. Our combined phylogenomic and genetic study indicates that ATCs play a crucial role in conveying ready-made Fe/S clusters from components of the biogenesis systems to apotargets. We propose a model wherein the conserved biochemical function of ATCs provides multiple paths for supplying Fe/S clusters to apotargets. This model predicts the occurrence of a dynamic network, the structure and composition of which vary with the growth conditions. As an illustration, we depict three ways for a given protein to be matured, which appears to be dependent on the demand for Fe/S biogenesis.

Author Summary Top
Iron sulfur (Fe/S) proteins are found in all living organisms where they participate in a wide array of biological processes. Accordingly, genetic defects in Fe/S biogenesis yield pleiotropic phenotypes in bacteria and several syndromes in humans. Multiprotein systems that assist Fe/S cluster formation and insertion into apoproteins have been identified. Most systems include so-called A-type proteins (which we refer to as ATC proteins hereafter), which have an undefined role in Fe/S biogenesis. Phylogenomic analyses presented, here, reveal that the ATC gene is ancient, that it was already present in the last common ancestor of bacteria, and that it subsequently spread to eukaryotes via mitochondria or chloroplastic endosymbioses and to a few archaea via horizontal gene transfers. Proteobacteria are unusual in having multiple ATCs. We show by a genetic approach that the three ATC proteins of E. coli are potentially interchangeable, but that redundancy is limited in vivo, either because of gene expression control or because of inefficient Fe/S transfers between ATCs and other components within the Fe/S biogenesis pathway. The combined phylogenomic and genetic approaches allow us to propose that multiple ATCs enable E. coli to diversify the ways for conveying ready-made Fe/S clusters from components of the biogenesis systems to apotargets, and that environmental conditions influence which pathway is used.
Citation: Vinella D, Brochier-Armanet C, Loiseau L, Talla E, Barras F (2009) Iron-Sulfur (Fe/S) Protein Biogenesis: Phylogenomic and Genetic Studies of A-Type Carriers. PLoS Genet 5(5): e1000497. doi:10.1371/journal.pgen.1000497
Editor: William F. Burkholder, Stanford University, United States of America
Received: December 1, 2008; Accepted: April 28, 2009; Published: May 29, 2009
Copyright: © 2009 Vinella et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Funding: This study was supported by Centre National de la Recherche Scientifique, Université de la Méditerranée, Agence Nationale de la Recherche, Programme Blanc CSD 8 and a CNRS ATIP grant to CB-A. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Competing interests: The authors have declared that no competing interests exist.
* E-mail: barras@ifr88.cnrs-mrs.fr

Multiple Sclerosis Patients Benefit From Diabetes Drug

A drug currently FDA-approved for use in diabetes shows some protective effects in the brains of patients with relapsing remitting multiple sclerosis, researchers at the University of Illinois at Chicago College of Medicine report in a study currently available online in the Journal of Neuroimmunology.

Keywords: University of Illinois, pioglitazone, Actos, neuronal survival, clinical trial.

Source Medical News Today
Full text Link: http://www.medicalnewstoday.com/articles/151448.php

Note: Currently in France is running a clinical trial with Pioglitazone for patients with FA.
( http://www.clinicaltrials.gov/ct2/show/NCT00811681?term=friedreich )

New Therapy Substitutes Missing Protein In Those With Muscular Dystrophy

New Therapy Substitutes Missing Protein In Those With Muscular Dystrophy

ScienceDaily (May 27, 2009) — Researchers at the University of Minnesota Medical School have discovered a new therapy that shows potential to treat people with Duchenne muscular dystrophy, a fatal disease and the most common form of muscular dystrophy in children.

Source / Full text: http://www.sciencedaily.com/releases/2009/05/090526152713.htm

Keyword: TAT, Duchenne muscular dystrophy, dystrophin, TAT-utrophin, protein replacement

Antioxidants prevent health-promoting effects of physical exercise in humans

OPEN ACCESS ARTICLE

Antioxidants prevent health-promoting effects of physical exercise in humans

Michael Ristowa,b,1,2, Kim Zarsea,2, Andreas Oberbachc,2, Nora Klötingc, Marc Birringera, Michael Kiehntopfd, Michael Stumvollc, C. Ronald Kahne and Matthias Blüherc,2
+Author Affiliations

aDepartment of Human Nutrition, Institute of Nutrition, University of Jena, Jena D-07743, Germany;

bGerman Institute of Human Nutrition, Potsdam-Rehbrücke D-14558, Germany;

cDepartment of Medicine, University of Leipzig, Leipzig D-04103, Germany;

dInstitute of Clinical Chemistry and Laboratory Medicine, University of Jena, Jena D-07743, Germany; and

eResearch Division, Joslin Diabetes Center, Harvard Medical School, Boston, MA 02215

↵2M.R., K.Z., A.O., and M. Blüher contributed equally to this work.

Contributed by C. Ronald Kahn, March 31, 2009 (sent for review March 14, 2009)

Abstract
Exercise promotes longevity and ameliorates type 2 diabetes mellitus and insulin resistance. However, exercise also increases mitochondrial formation of presumably harmful reactive oxygen species (ROS). Antioxidants are widely used as supplements but whether they affect the health-promoting effects of exercise is unknown. We evaluated the effects of a combination of vitamin C (1000 mg/day) and vitamin E (400 IU/day) on insulin sensitivity as measured by glucose infusion rates (GIR) during a hyperinsulinemic, euglycemic clamp in previously untrained (n = 19) and pretrained (n = 20) healthy young men. Before and after a 4 week intervention of physical exercise, GIR was determined, and muscle biopsies for gene expression analyses as well as plasma samples were obtained to compare changes over baseline and potential influences of vitamins on exercise effects. Exercise increased parameters of insulin sensitivity (GIR and plasma adiponectin) only in the absence of antioxidants in both previously untrained (P < 0.001) and pretrained (P < 0.001) individuals. This was paralleled by increased expression of ROS-sensitive transcriptional regulators of insulin sensitivity and ROS defense capacity, peroxisome-proliferator-activated receptor gamma (PPARγ), and PPARγ coactivators PGC1α and PGC1β only in the absence of antioxidants (P < 0.001 for all). Molecular mediators of endogenous ROS defense (superoxide dismutases 1 and 2; glutathione peroxidase) were also induced by exercise, and this effect too was blocked by antioxidant supplementation. Consistent with the concept of mitohormesis, exercise-induced oxidative stress ameliorates insulin resistance and causes an adaptive response promoting endogenous antioxidant defense capacity. Supplementation with antioxidants may preclude these health-promoting effects of exercise in humans.

1To whom correspondence should be addressed. E-mail: mristow@mristow.org
Author contributions: M.R., M. Birringer, M.S., C.R.K., and M. Blüher designed research; M.R., K.Z., A.O., N.K., M. Birringer, M.K., M.S., and M. Blüher performed research; K.Z. and M.S. analyzed data; and M.R., M.S., C.R.K., and M. Blüher wrote the paper.
The authors declare no conflict of interest.
Freely available online through the PNAS open access option

Full text link: http://www.pnas.org/content/early/2009/05/11/0903485106.full.pdf+html

http://health.groups.yahoo.com/group/FA_babelFAmily/message/2974

Novel antibody-based strategies for the rapid diagnosis of mitochondrial disease and dysfunction.

Int J Biochem Cell Biol. 2009 May 18. [Epub ahead of print]

Related Articles

Novel antibody-based strategies for the rapid diagnosis of mitochondrial disease and dysfunction.

Marusich MF, Murray J, Xie J, Capaldi RA.

MitoSciences, Inc, 1850 Millrace Dr. Eugene, OR 97403.

.../... we recently reported that Friedreich's Ataxia (FA) patients and carriers can be identified on the basis of a simple dipstick test to measure levels of a single protein, frataxin .../...

Identification of potential neuromotor mechanisms of manual therapy in patients with musculoskeletal disablement

Study protocol

Identification of potential neuromotor mechanisms of manual therapy in patients with musculoskeletal disablement: rationale and description of a clinical trial

Beth E Fisher , Todd E Davenport , Kornelia Kulig and Allan D Wu

BMC Neurology 2009, 9:20 doi:10.1186/1471-2377-9-20
Published: 21 May 2009

Abstract (provisional)

Background

Many health care practitioners use a variety of hands-on treatments to improve symptoms and disablement in patients with musculoskeletal pathology. Research to date indirectly suggests a potentially broad effect of manual therapy on the neuromotor processing of functional behavior within the supraspinal central nervous system (CNS) in a manner that may be independent of modification at the level of local spinal circuits. However, the effect of treatment speed, as well as the specific mechanism and locus of CNS changes, remain unclear.

Results

We developed a placebo-controlled, randomized study to test the hypothesis that manual therapy procedures directed to the talocrural joint in individuals with post-acute ankle sprain induce a change in corticospinal excitability that is relevant to improve the performance of lower extremity functional behavior.

Conclusion

This study is designed to identify potential neuromotor changes associated with manual therapy procedures directed to the appendicular skeleton, compare the relative effect of treatment speed on potential neuromotor effects of manual therapy procedures, and determine the behavioral relevance of potential neuromotor effects of manual therapy procedures.

The complete article is available as a provisional PDF.

Proteins Underlying Devastating Brain Diseases Uncovered

ScienceDaily (May 19, 2009) — Scientists at the Wellcome Trust Sanger Institute have discovered a set of brain proteins responsible for some of the most common and devastating brain diseases. The proteins underlie epilepsy, depression, schizophrenia, bipolar disease, mental retardation and neurodegenerative diseases including Alzheimer's and Huntington's diseases.

PPARγ stimulation promotes mitochondrial biogenesis and prevents glucose deprivation-induced neuronal cell loss

Neurochem Int. 2009 May 11. [Epub ahead of print]

PPARgamma stimulation promotes mitochondrial biogenesis and prevents glucose deprivation-induced neuronal cell loss.

Miglio G, Rosa AC, Rattazzi L, Collino M, Lombardi G, Fantozzi R.Department of Anatomy, Pharmacology and Forensic Medicine, University of Turin, Turin, Italy.

Pro-oxidant mitochondrial matrix-targeted ubiquinone MitoQ10 acts as anti-oxidant at retarded electron transport or proton pumping within Complex I.

Pro-oxidant mitochondrial matrix-targeted ubiquinone MitoQ10 acts as anti-oxidant at retarded electron transport or proton pumping within Complex I.


Plecitá-Hlavatá L, Jezek J, Jezek P. Department No 75, Institute of Physiology, Academy of Sciences, Vídenská 1083, Prague, Czech Republic. plecita@...

Source: Int J Biochem Cell Biol. 2009 Aug-Sep;41(8-9):1697-707. Epub 2009 Mar 3.
Link to this abstract: http://www.ncbi.nlm.nih.gov/pubmed/19433311

The bioenergetic and antioxidant status of neurons is controlled by continuous degradation of a key glycolytic enzyme by APC/C–Cdh1

Nature Cell Biology Published online: 17 May 2009 doi:10.1038/ncb1881

The bioenergetic and antioxidant status of neurons is controlled by continuous degradation of a key glycolytic enzyme by APC/C–Cdh1

Angel Herrero-Mendez1, Angeles Almeida1,2, Emilio Fernández1, Carolina Maestre1,2, Salvador Moncada3 & Juan P. Bolaños1

Departamento de Bioquimica y Biologia Molecular, Universidad de Salamanca, Instituto de Neurociencias de Castilla y Leon, 37007 Salamanca, Spain.
Unidad de Investigacion, Hospital Universitario de Salamanca, Instituto de Estudios de Ciencias de la Salud de Castilla y Leon, 37007 Salamanca, Spain.
Wolfson Institute for Biomedical Research, University College London, Gower Street, London WC1E 6BT, UK.
Correspondence to: Juan P. Bolaños1 e-mail: jbolanos@usal.es
Correspondence to: Salvador Moncada3 e-mail: s.moncada@ucl.ac.uk

Autosomal recessive cerebellar ataxias.

Presse Med. 2009 May 11. [Epub ahead of print]

Autosomal recessive cerebellar ataxias.

[Article in French]
Tranchant C, Anheim M.
Clinique neurologique, Hôpitaux universitaires, F-67091 Strasbourg Cedex, France.

Epidemiological, clinical, paraclinical and molecular study of a cohort of 102 patients affected with autosomal recessive progressive cerebellar ataxi

Neurogenetics. 2009 May 14. [Epub ahead of print]

Epidemiological, clinical, paraclinical and molecular study of a cohort of 102 patients affected with autosomal recessive progressive cerebellar ataxia from Alsace, Eastern France: implications for clinical management.
Anheim M, Fleury M, Monga B, Laugel V, Chaigne D, Rodier G, Ginglinger E, Boulay C, Courtois S, Drouot N, Fritsch M, Delaunoy JP, Stoppa-Lyonnet D, Tranchant C, Koenig M.
Département de Neurologie, Hôpital Civil, Centre Hospitalier Universitaire de Strasbourg, 1, place de l'Hôpital, 67000, Strasbourg, France, anheim@titus.u-strasbg.fr.

The biology of PGC-1α and its therapeutic potential

The biology of PGC-1α and its therapeutic potential


Christoph Handschina, b,
aBiozentrum, University of Basel, Klingelbergstrasse 50-70, CH-4056 Basel, Switzerland
bInstitute of Physiology and Zurich Center for Integrative Human Physiology (ZIHP), University of Zurich, Winterthurerstrasse 190, CH-8057 Zurich, Switzerland
Available online 14 May 2009.

Ataxia de Friedreich- Friedreich's ataxia (en la atención primaria)

Aten Primaria. 2009 May 7.
Ataxia de Friedreich- Friedreich's ataxia.

[Article in Spanish]

Ortiz Uriarte R, García Ribes M, Gutiérrez VM, Sorlí JV, Valderrama Zurián FJ, Mingarro Castillo MM, Ejarque Domènech I.Grupo de trabajo semFYC Genética clínica y enfermedades raras; Centro de Salud, La Cavada, Cantabria, España.PMID: 19427070 [PubMed - as supplied by publisher]

A Study Investigating the Long-Term Safety and Efficacy of Deferiprone in Patients With Friedreich's Ataxia

A Study Investigating the Long-Term Safety and Efficacy of Deferiprone in Patients With Friedreich's Ataxia

http://www.clinicaltrials.gov/ct2/show/NCT00897221?term=friedreich

This study is not yet open for participant recruitment.
Verified by ApoPharma, May 2009
First Received: May 8, 2009 No Changes Posted
Sponsored by: ApoPharma

Information provided by: ApoPharma
ClinicalTrials.gov Identifier: NCT00897221

Practical guide to neurogenetics

http://www.thelancet.com/journals/laneur/article/PIIS147444220970122X/fulltext?rss=yes Practical guide to neurogenetics


Practical Guide to Neurogenetics
Thomas Warner, Simon HammansElsevier Saunders, 2008Pp 344. $65·95. ISBN-978-0750654104

Exercise, PGC-1α, and metabolic adaptation in skeletal muscle

Appl. Physiol. Nutr. Metab. 34(3): 424–427 (2009) doi:10.1139/H09-030 Published by NRC Research Press / Publié par les Presses scientifiques du CNRC

Full text: http://article.pubs.nrc-cnrc.gc.ca/RPAS/rpv?hm=HInit&journal=apnm&volume=34&calyLang=eng&afpf=h09-030.pdf

Exercise, PGC-1α, and metabolic adaptation in skeletal muscle

Zhen Yan

Endurance exercise is protective for mice with mitochondrial myopathy

J Appl Physiol 106: 1712-1719, 2009. First published March 12, 2009; doi:10.1152/japplphysiol.91571.2008 8750-7587/09 $8.00

HIGHLIGHTED TOPIC Regulation of Protein Metabolism in Exercise and Recovery

Endurance exercise is protective for mice with mitochondrial myopathy

Tina Wenz,1 Francisca Diaz,1 Dayami Hernandez,1 and Carlos T. Moraes1,2
Departments of 1Neurology and of 2Cell Biology and Anatomy, University of Miami School of Medicine, Miami, Florida
Submitted 8 December 2008 ; accepted in final form 9 March 2009

Address for reprint requests and other correspondence: C. T. Moraes, Dept. of Neurology, Miller School of Medicine, Univ. of Miami, 1095 NW 14th Terrace, Miami, FL 33136 (e-mail: cmoraes@med.miami.edu

p53/CEP-1 Increases or Decreases Lifespan, Depending on Level of Mitochondrial Bioenergetic Stress.

Aging Cell. 2009 Apr 22. [Epub ahead of print]

p53/CEP-1 Increases or Decreases Lifespan, Depending on Level of Mitochondrial Bioenergetic Stress.

Ventura N, Rea SL, Schiavi A, Torgovnick A, Testi R, Johnson TE.
Institute for Behavioral Genetics, University of Colorado at Boulder, Box 447, Boulder, CO 80309, USA.

Oxidative stress induces degradation of mitochondrial DNA

http://nar.oxfordjournals.org/cgi/content/short/37/8/2539?rss=1

http://nar.oxfordjournals.org/cgi/reprint/37/8/2539 (Full text)

Nucleic Acids Research Advance Access originally published online on March 5, 2009 Nucleic Acids Research 2009 37(8):2539-2548; doi:10.1093/nar/gkp100

Oxidative stress induces degradation of mitochondrial DNA

Inna Shokolenko, Natalia Venediktova, Alexandra Bochkareva, Glenn L. Wilson and Mikhail F. Alexeyev*
Department of Cell Biology and Neuroscience, University of South Alabama, Mobile, AL 36688, USA
*To whom correspondence should be addressed. Tel: +1 251 460 6789; Fax: +1 251 460 6771; Email: malexeye@jaguar1.usouthal.edu

Received September 4, 2008. Revised January 25, 2009. Accepted February 8, 2009.

Fly Study Suggests That Gene May 'Bypass' Disease-Linked Mitochondrial Defects

Fly Study Suggests That Gene May 'Bypass' Disease-Linked Mitochondrial Defects

Article Date: 06 May 2009 - 6:00 PDT
http://www.medicalnewstoday.com/articles/149070.php

Matching Supply and Demand

Science 24 April 2009:Vol. 324. no. 5926, p. 440DOI: 10.1126/science.324_440b
Editors' Choice: Highlights of the recent literature

http://www.sciencemag.org/cgi/content/full/324/5926/440-b?rss=1

Biochemistry:

Matching Supply and Demand

Valda Vinson

Nat. Struct. Mol. Biol. 16, 390 (2009).

J. Chem. Phys. 130, 155101 (2009); DOI:10.1063/1.3109902 Published 16 April 2009

N. K. Voulgarakis, K. Ø. Rasmussen, and P. M. Welch
Theoretical Division and Center for Nonlinear Studies, Los Alamos National Laboratory, Los Alamos, New Mexico 87545, USA

Dendrimers as synthetic gene vectors: Cell membrane attachment

http://www.medicalnewstoday.com/articles/148319.php

First Large-Scale Computer Simulation Of Gene Therapy

Effectiveness and safety of treatments for degenerative ataxias: A systematic review

http://www3.interscience.wiley.com/journal/122371107/abstract?CRETRY=1&SRETRY=0

Effectiveness and safety of treatments for degenerative ataxias: A systematic review

M.Mar Trujillo-Martín, PhD 1 *, Pedro Serrano-Aguilar, MD, PhD 2 3, Fernando Monton-Álvarez, MD, PhD 4, Romen Carrillo-Fumero, PhD 1

1Canary Islands Research and Health Foundation (Fundación Canaria de Investigación y Salud-FUNCIS), Santa Cruz de Tenerife, Canary Islands, Spain 2Planning and Evaluation Unit, Canary Islands Health Authority, Santa Cruz de Tenerife, Canary Islands, Spain 3CIBER Epidemiología y Salud Pública (CIBERESP), Spain 4Department of Neurology, University Hospital of Na Sa de la Candelaria, Santa Cruz de Tenerife, Canary Islands, Spain

email: M.Mar Trujillo-Martín (matrumar@gobiernodecanarias.org)

^*Correspondence to M.Mar Trujillo-Martín, Servicio de Evaluación y Planificación, Servicio Canario de la Salud, Pérez de Rozas, 5-4^a planta, 38004 Santa Cruz de Tenerife, España

Potential conflict of interest: None reported.

Funded by:
Spanish Ministry of Health
Consumption in cooperation
Fundación Canaria de Investigación y Salud (FUNCIS)

Keywords

rare diseases • degenerative ataxia • systematic review • treatment effectiveness • treatment safety

Received: 13 October 2008; Accepted: 3 March 2009

Digital Object Identifier (DOI)

Evidence That Phosphorylation of Iron Regulatory Protein 1 at Serine 138 Destabilizes the [4Fe-4S] Cluster in Cytosolic Aconitase by Enhancing 4Fe-3Fe

Originally published In Press as doi:10.1074/jbc.M807717200 on March 6, 2009 J. Biol. Chem., Vol. 284, Issue 19, 12701-12709, May 8, 2009

Evidence That Phosphorylation of Iron Regulatory Protein 1 at Serine 138 Destabilizes the [4Fe-4S] Cluster in Cytosolic Aconitase by Enhancing 4Fe-3Fe Cycling^*

Kathryn M. Deck, Aparna Vasanthakumar, Sheila A. Anderson, Jeremy B. Goforth¹, M. Claire Kennedy, William E. Antholine^¶, and Richard S. Eisenstein²

From the Department of Nutritional Sciences, University of Wisconsin-Madison, Madison, Wisconsin 53706, the Biochemistry Department, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, and the ^¶National Biomedical ESR Center, Department of Biophysics, Medical College of Wisconsin, Milwaukee, Wisconsin 53226-3548

Received for publication, October 6, 2008 , and in revised form, March 5, 2009.

This paper is dedicated to the memory of Helmut Beinert.

^* This work was supported in part by National Institutes of Health Grants DK 66600 (to R. S. E.) and National Biomedical ESR Center Grant EB001980. This work was also supported by United States Department of Agriculture Cooperative States Research Education and Extension Service Grant 2006-35200-16604 and University of Wisconsin-Madison Hatch Project 4885 (to R. S. E.).

The on-line version of this article (available at http://www.jbc.org/) contains supplemental Figs. S1 and S2.

¹ Supported by National Institutes of Health Training Grant T32 DK007665.

² To whom correspondence should be addressed: University of Wisconsin, Dept. of Nutritional Sciences, 1415 Linden Dr., Madison, WI 53706. Tel.: 608-262-5830; Fax: 608-262-5860; E-mail: eisenste@nutrisci.wisc.edu
.

PGC-1α-induced improvements in skeletal muscle metabolism and insulin sensitivity

Appl. Physiol. Nutr. Metab. 34(3): 307–314 (2009) doi:10.1139/H09-008 Published by NRC Research Press / Publié par les Presses scientifiques du CNRC

PGC-1α-induced improvements in skeletal muscle metabolism and insulin sensitivity

Arend Bonen