title: Glycogen overload by postexercise insulin administration abolished the exercise-induced increase in GLUT4 protein.
abstract: 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.
authors.affiliation: Center for General Education, National Chi-Nan University, Nantou, Taiwan, ROC.
authors.forename: Chia-Hau
authors.initials: CH
authors.lastname: Chou
authors.forename: Yin-Lan
authors.initials: YL
authors.lastname: Tsai
authors.forename: Chien-Wen
authors.initials: CW
authors.lastname: Hou
authors.forename: Hsing-Hao
authors.initials: HH
authors.lastname: Lee
authors.forename: Wei-Hsiang
authors.initials: WH
authors.lastname: Chang
authors.forename: Tzi-Wen
authors.initials: TW
authors.lastname: Lin
authors.forename: Tung-Hsiung
authors.initials: TH
authors.lastname: Hsu
authors.forename: Yi-Jen
authors.initials: YJ
authors.lastname: Huang
authors.forename: Chia-Hua
authors.initials: CH
authors.lastname: Kuo
mesh_terms: D000818:Animals; D001786:Blood Glucose; D005947:Glucose / Q000378:metabolism; D005951:Glucose Tolerance Test; D051246:Glucose Transport Proteins, Facilitative; D051275:Glucose Transporter Type 4 / Q000378:metabolism*; D006003:Glycogen / Q000378:metabolism*; D007328:Insulin / Q000008:administration & dosage* / Q000378:metabolism; D007333:Insulin Resistance; D008297:Male; D008954:Models, Biological; D015233:Models, Statistical; D009004:Monosaccharide Transport Proteins / Q000378:metabolism; D018482:Muscle, Skeletal / Q000378:metabolism; D009132:Muscles / Q000378:metabolism; D010805:Physical Conditioning, Animal; D051381:Rats; D017207:Rats, Sprague-Dawley; D013696:Temperature; D013997:Time Factors
chemical_list: D001786:Blood Glucose; D051246:Glucose Transport Proteins, Facilitative; D051275:Glucose Transporter Type 4; D007328:Insulin; D009004:Monosaccharide Transport Proteins; C495694:Slc2a4 protein, rat; D006003:Glycogen; D005947:Glucose