Document Detail


Exercise improves impaired ventricular function and alterations of cardiac myofibrillar proteins in diabetic dyslipidemic pigs.
MedLine Citation:
PMID:  15465890     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Chronic diabetes is often associated with cardiomyopathy, which may result, in part, from defects in cardiac muscle proteins. We investigated whether a 20-wk porcine model of diabetic dyslipidemia (DD) would impair in vivo myocardial function and yield alterations in cardiac myofibrillar proteins and whether endurance exercise training would improve these changes. Myocardial function was depressed in anesthetized DD pigs (n = 12) compared with sedentary controls (C; n = 13) as evidenced by an approximately 30% decrease in left ventricular fractional shortening and an approximately 35% decrease in +dP/dt measured by noninvasive echocardiography and direct cardiac catheterization, respectively. This depression in myocardial function was improved with chronic exercise as treadmill-trained DD pigs (DDX) (n = 13) had significantly greater fractional shortening and +dP/dt than DD animals. Interestingly, the isoform expression pattern of the myofibrillar regulatory protein, cardiac troponin T (cTnT), was significantly shifted from cTnT1 toward cTnT2 and cTnT3 in DD pigs. Furthermore, this change in cTnT isoform expression pattern was prevented in DDX pigs. Finally, there was a decrease in baseline levels of cAMP-dependent protein kinase-induced phosphorylation of the myofibrillar proteins troponin I and myosin-binding protein-C in DD animals. Overall, these results indicate that 20 wk of DD lead to myocardial dysfunction coincident with significant alterations in myofibrillar proteins, both of which are prevented with endurance exercise training, implying that changes in myofibrillar proteins may contribute, at least in part, to cardiac dysfunction associated with diabetic cardiomyopathy.
Authors:
F Steven Korte; Eric A Mokelke; Michael Sturek; Kerry S McDonald
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.     Date:  2004-10-01
Journal Detail:
Title:  Journal of applied physiology (Bethesda, Md. : 1985)     Volume:  98     ISSN:  8750-7587     ISO Abbreviation:  J. Appl. Physiol.     Publication Date:  2005 Feb 
Date Detail:
Created Date:  2005-01-14     Completed Date:  2005-05-24     Revised Date:  2013-09-26    
Medline Journal Info:
Nlm Unique ID:  8502536     Medline TA:  J Appl Physiol (1985)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  461-7     Citation Subset:  IM    
Affiliation:
Department of Medical Pharmacology and Physiology, University of Missouri School of Medicine, Columbia, MO, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Diabetes Mellitus, Experimental / complications,  diagnosis,  physiopathology*,  therapy*
Exercise Therapy / methods*
Hyperlipidemias / complications,  diagnosis,  physiopathology,  therapy
Male
Muscle Proteins / metabolism*
Myocardium / metabolism*
Physical Endurance
Protein Isoforms / metabolism
Recovery of Function / physiology
Swine
Treatment Outcome
Ventricular Dysfunction, Left / diagnosis,  etiology,  metabolism,  physiopathology*,  therapy*
Grant Support
ID/Acronym/Agency:
HL-10474/HL/NHLBI NIH HHS; HL-62552/HL/NHLBI NIH HHS; RR-13223/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
0/Muscle Proteins; 0/Protein Isoforms

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


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