Studies on the mechanism of insulin resistance after injury in the mouse.
Acute insulin resistance developed after scald injury in the mouse. After 2h plasma glucose and insulin concentrations were each raised about two-fold. Glucose metabolism was studied in vitro in soleus muscles isolated at this time. Glycolysis and glycogen synthesis, and their stimulation by insulin, were unchanged in muscles from scalded mice, and insulin-stimulated transport of 2-deoxyglucose slightly increased, showing that the insulin resistance seen in vivo is not maintained in isolated tissues. Binding of insulin to liver cell membranes prepared from scalded mice was unaltered, whilst that of glucagon was slightly but significantly reduced, showing that changes in polypeptide-hormone receptors can occur within this short time. It was concluded that the acute loss of sensitivity to insulin after injury does not result from a change in insulin receptor sites and presumably reflects an impairment of glucose metabolism in vivo mediated by circulating hormones.
D000818:Animals; D001692:Biological Transport; D002056:Burns / Q000150:complications*; D002462:Cell Membrane; D003847:Deoxyglucose / Q000378:metabolism; D005947:Glucose / Q000378:metabolism; D006003:Glycogen / Q000096:biosynthesis; D006019:Glycolysis; D007333:Insulin Resistance; D008099:Liver / Q000378:metabolism; D008297:Male; D051379:Mice; D009132:Muscles / Q000378:metabolism*; D011972:Receptor, Insulin
D006003:Glycogen; D003847:Deoxyglucose; D011972:Receptor, Insulin; D005947:Glucose