Glucose uptake and glycogen synthesis in muscles from immobilized limbs.
The purposes of this study were to determine whether the defects in glucose metabolism in muscles of immobilized limbs of mice were related to alterations in insulin binding, insulin responsiveness, glucose supply, and insulin activation of glycogen synthase. These were tested by in vitro methodology. A significant lessening in the insulin-induced maximal response of 2-deoxyglucose uptake into the mouse soleus muscle occurred between the 3rd and 8th h of limb immobilization, suggesting a decreased insulin responsiveness. Lack of change in the specific binding of insulin to muscles of 24-h immobilized limbs indicates that a change in insulin receptor number did not play a role in the failure of insulin to stimulate glucose metabolism. It's inability to stimulate glycogen synthesis in muscle from immobilized limbs is due, in part, to a lack of glucose supply to glycogen synthesis and also to the ineffectiveness of insulin to increase the percentage of glycogen synthase in its active form in muscles from 24-h immobilized limbs.
D000818:Animals; D003847:Deoxyglucose / Q000378:metabolism; D005947:Glucose / Q000378:metabolism*; D006003:Glycogen / Q000096:biosynthesis*; D006593:Hexokinase / Q000378:metabolism; D006614:Hindlimb; D007103:Immobilization; D007328:Insulin / Q000378:metabolism / Q000502:physiology; D008297:Male; D051379:Mice; D009132:Muscles / Q000201:enzymology / Q000378:metabolism*
D007328:Insulin; D006003:Glycogen; D003847:Deoxyglucose; D006593:Hexokinase; D005947:Glucose