Effect of impaired glucose uptake on postexercise glycogen repletion in skeletal muscles of insulin-treated streptozotocin-diabetic fasted rats
Ferreira, Luis D.M.C.-B., Xu, Dan, Palmer, T. Norman, and Fournier, Paul A. (2005) Effect of impaired glucose uptake on postexercise glycogen repletion in skeletal muscles of insulin-treated streptozotocin-diabetic fasted rats. Metabolism: clinical and experimental, 54 (11). pp. 1420-1427.
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During recovery from intense exercise performed while fasting, the replenishment of muscle glycogen stores from glucose requires the activation of glucose transport. This study examines if insulin-treated streptozotocin (STZ) diabetes in rats impairs the rate of muscle glucose utilization and glycogen repletion when no food is ingested during recovery from high-intensity exercise. Rats fasted for 24 hours were injected with high doses of STZ (150 mg/kg) to cause severe diabetes, and their glycemia was normalized for 10 days with twice-daily insulin injections. High-intensity exercise in these rats resulted in a marked increase in plasma glucose, which remained higher than preexercise levels thereafter, whereas in control animals, the rise in glycemia was only of a short duration. During recovery, the rates of 2-deoxy-[3H]glucose utilization in muscles rich in fast twitch red fibers (red and mixed gastrocnemius muscles) were much lower in STZ-diabetic than in control rats, but were not affected by diabetes in muscles comprised mainly of fast twitch white fibers (white gastrocnemius muscle). Despite these effects on glucose utilization, STZ diabetes had no inhibitory effect on the rate and extent of glycogen deposition and fractional velocities of glycogen synthase across all muscles. In conclusion, although insulin-treated STZ diabetes in fasted rats inhibits glucose transport rates in fast twitch red muscle fibers post–intense exercise, this has no effect on muscle glycogen repletion either because glucose transport does not control the rate of glycogen synthesis or because of a compensatory increase in the activity of lactate glyconeogenesis in these muscles.
|Item Type:||Article (Refereed Research - C1)|
|Keywords:||diabetes; glycogen; insulin|
|FoR Codes:||06 BIOLOGICAL SCIENCES > 0601 Biochemistry and Cell Biology > 060104 Cell Metabolism @ 100%|
|SEO Codes:||97 EXPANDING KNOWLEDGE @ 100%|
|Deposited On:||04 Dec 2010 20:03|
|Last Modified:||04 Jun 2013 01:35|
Last 12 Months: 0
|Citation Counts with External Providers:||Web of Science: 4|
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