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Tytuł pozycji:

Glycogen overload by postexercise insulin administration abolished the exercise-induced increase in GLUT4 protein.

Tytuł :
Glycogen overload by postexercise insulin administration abolished the exercise-induced increase in GLUT4 protein.
Autorzy :
Chou CH; Center for General Education, National Chi-Nan University, Nantou, Taiwan, ROC.
Tsai YL
Hou CW
Lee HH
Chang WH
Lin TW
Hsu TH
Huang YJ
Kuo CH
Pokaż więcej
Źródło :
Journal of biomedical science [J Biomed Sci] 2005 Dec; Vol. 12 (6), pp. 991-8. Date of Electronic Publication: 2005 Dec 01.
Typ publikacji :
Journal Article; Research Support, Non-U.S. Gov't
Język :
English
Imprint Name(s) :
Publication: 2009- : London : BioMed Central
Original Publication: Basel ; New York : S. Karger Medical and Scientific Publishers, c1994-
MeSH Terms :
Physical Conditioning, Animal*
Glucose Transporter Type 4/*metabolism
Glycogen/*metabolism
Insulin/*administration & dosage
Animals ; Blood Glucose ; Glucose/metabolism ; Glucose Tolerance Test ; Glucose Transport Proteins, Facilitative ; Insulin/metabolism ; Insulin Resistance ; Male ; Models, Biological ; Models, Statistical ; Monosaccharide Transport Proteins/metabolism ; Muscle, Skeletal/metabolism ; Muscles/metabolism ; Rats ; Rats, Sprague-Dawley ; Temperature ; Time Factors
Substance Nomenclature :
0 (Blood Glucose)
0 (Glucose Transport Proteins, Facilitative)
0 (Glucose Transporter Type 4)
0 (Insulin)
0 (Monosaccharide Transport Proteins)
0 (Slc2a4 protein, rat)
9005-79-2 (Glycogen)
IY9XDZ35W2 (Glucose)
Entry Date(s) :
Date Created: 20051202 Date Completed: 20060525 Latest Revision: 20131121
Update Code :
20211105
DOI :
10.1007/s11373-005-9019-9
PMID :
16319996
Czasopismo naukowe
To elucidate the role of muscle glycogen storage on regulation of GLUT4 protein expression and whole-body glucose tolerance, muscle glycogen level was manipulated by exercise and insulin administration. Sixty Sprague-Dawley rats were evenly separated into three groups: control (CON), immediately after exercise (EX0), and 16 h after exercise (EX16). Rats from each group were further divided into two groups: saline- and insulin-injected. The 2-day exercise protocol consisted of 2 bouts of 3-h swimming with 45-min rest for each day, which effectively depleted glycogen in both red gastrocnemius (RG) and plantaris muscles. EX0 rats were sacrificed immediately after the last bout of exercise on second day. CON and EX16 rats were intubated with 1 g/kg glucose solution following exercise and recovery for 16 h before muscle tissue collection. Insulin (0.5 microU/kg) or saline was injected daily at the time when glucose was intubated. Insulin injection elevated muscle glycogen levels substantially in both muscles above saline-injected group at CON and EX16. With previous day insulin injection, EX0 preserved greater amount of postexercise glycogen above their saline-injected control. In the saline-injected rats, EX16 significantly increased GLUT4 protein level above CON, concurrent with muscle glycogen supercompensation. Insulin injection for EX16 rats significantly enhanced muscle glycogen level above their saline-injected control, but the increases in muscle GLUT4 protein and whole-body glucose tolerance were attenuated. In conclusion, the new finding of the study was that glycogen overload by postexercise insulin administration significantly abolished the exercise-induced increases in GLUT4 protein and glucose tolerance.

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