Document Detail


Effects of weight loss and physical activity on skeletal muscle mitochondrial function in obesity.
MedLine Citation:
PMID:  15585590     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The current study was undertaken to address responsiveness of skeletal muscle mitochondrial electron transport chain (ETC) activity to weight loss (WL) and exercise in overweight or obese, sedentary volunteers. Fourteen middle-aged participants (7 male/7 female) had assessments of mitochondrial ETC activity and mitochondrial (mt)DNA in vastus lateralis muscle, obtained by percutaneous biopsy, before and after a 16-wk intervention. Mean WL was 9.7 (1.5%) and the mean increase in Vo(2 max) was [means (SD)] 21.7 (3.7)%. Total ETC activity increased significantly, from 0.13 (0.02) to 0.19 (0.03) U/mU creatine kinase (CK; P < 0.001). ETC activity was also assessed in mitochondria isolated into subsarcolemmal (SSM) and intermyofibrillar (IMF-M) fractions. In response to intervention, there was a robust increase of ETC activity in SSM (0.028 (0.007) to 0.046 (0.011) U/mU CK, P < 0.001), and in IMF-M [0.101 (0.015) to 0.148 (0.018) U/mU CK, P < 0.005]. At baseline, the percentage of ETC activity contained in the SSM fraction was low and remained unchanged following intervention [19 (3) vs. 22 (2)%], despite the increase in ETC activity. Also, muscle mtDNA content did not change significantly [1665 (213) vs. 1874 (214) mtDNA/nuclear DNA], denoting functional improvement rather than proliferation of mitochondria as the principal mechanism of enhanced ETC activity. Increases in ETC activity were correlated with energy expenditure during exercise sessions, and ETC activity in SSM correlated with insulin sensitivity after adjustment for Vo(2 max). In summary, skeletal muscle ETC activity is increased by WL and exercise in previously sedentary obese men and women. We conclude that improved skeletal muscle ETC activity following moderate WL and improved aerobic capacity contributes to associated alleviation of insulin resistance.
Authors:
Elizabeth V Menshikova; Vladimir B Ritov; Frederico G S Toledo; Robert E Ferrell; Bret H Goodpaster; David E Kelley
Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.     Date:  2004-12-07
Journal Detail:
Title:  American journal of physiology. Endocrinology and metabolism     Volume:  288     ISSN:  0193-1849     ISO Abbreviation:  Am. J. Physiol. Endocrinol. Metab.     Publication Date:  2005 Apr 
Date Detail:
Created Date:  2005-03-18     Completed Date:  2005-04-12     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  100901226     Medline TA:  Am J Physiol Endocrinol Metab     Country:  United States    
Other Details:
Languages:  eng     Pagination:  E818-25     Citation Subset:  IM    
Affiliation:
Division of Endocrinology and Metabolism, Department of Medicine, University of Pittsburgh, School of Medicine, Pennsylvania, USA.
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MeSH Terms
Descriptor/Qualifier:
Adult
Cohort Studies
DNA, Mitochondrial / chemistry,  genetics
Electron Transport / physiology
Exercise / physiology*
Female
Humans
Insulin Resistance / physiology
Male
Microscopy, Electron, Transmission
Mitochondria, Muscle / physiology*
Muscle, Skeletal / physiology*,  ultrastructure
Obesity / physiopathology*
Polymerase Chain Reaction
Sarcolemma / physiology,  ultrastructure
Weight Loss / physiology*
Grant Support
ID/Acronym/Agency:
5 M01-RR-00056/RR/NCRR NIH HHS; DK-49200-08/DK/NIDDK NIH HHS; P30-DK-462/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/DNA, Mitochondrial

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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