Document Detail


ATP-sensitive K+ channel knockout compromises the metabolic benefit of exercise training, resulting in cardiac deficits.
MedLine Citation:
PMID:  15561907     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Exercise training elicits a metabolic and cardiovascular response that underlies fitness. The molecular mechanisms that orchestrate this adaptive response and secure the wide-ranging gains of a regimented exercise program are poorly understood. Formed through association of the Kir6.2 pore and the sulfonylurea receptor, the stress-responsive ATP-sensitive K(+) channels (K(ATP) channels), with their metabolic-sensing capability and broad tissue expression, are potential candidates for integrating the systemic adaptive response to repetitive exercise. Here, the responses of mice lacking functional Kir6.2-containing K(ATP) channels (Kir6.2-KO) were compared with wild-type controls following a 28-day endurance swimming protocol. While chronic aquatic training resulted in lighter, leaner, and fitter wild-type animals, the Kir6.2-KO manifested less augmentation in exercise capacity and lacked metabolic improvement in body fat composition and glycemic handling with myocellular defects. Moreover, the repetitive stress of swimming unmasked a survival disadvantage in the Kir6.2-KO, associated with pathologic calcium-dependent structural damage in the heart and impaired cardiac performance. Thus, Kir6.2-containing K(ATP) channel activity is required for attainment of the physiologic benefits of exercise training without injury.
Authors:
Garvan C Kane; Atta Behfar; Satsuki Yamada; Carmen Perez-Terzic; Fearghas O'Cochlain; Santiago Reyes; Petras P Dzeja; Takashi Miki; Susumu Seino; Andre Terzic
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Diabetes     Volume:  53 Suppl 3     ISSN:  0012-1797     ISO Abbreviation:  Diabetes     Publication Date:  2004 Dec 
Date Detail:
Created Date:  2004-11-24     Completed Date:  2005-04-14     Revised Date:  2013-08-02    
Medline Journal Info:
Nlm Unique ID:  0372763     Medline TA:  Diabetes     Country:  United States    
Other Details:
Languages:  eng     Pagination:  S169-75     Citation Subset:  AIM; IM    
Affiliation:
Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic College of Medicine, Rochester, MN 55905, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Glucose / metabolism
Heart / physiopathology*
Heart Diseases / genetics*
Mice
Mice, Knockout
Physical Conditioning, Animal* / physiology*
Potassium Channels, Inwardly Rectifying / deficiency*,  genetics,  physiology*
Swimming
Grant Support
ID/Acronym/Agency:
GM08685/GM/NIGMS NIH HHS; GM65841/GM/NIGMS NIH HHS; HL64822/HL/NHLBI NIH HHS; R01 HL064822/HL/NHLBI NIH HHS; T32 GM065841/GM/NIGMS NIH HHS
Chemical
Reg. No./Substance:
0/Kir6.2 channel; 0/Potassium Channels, Inwardly Rectifying; 50-99-7/Glucose

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