IGF-I stimulates muscle glucose uptake during sepsis.
The purpose of the present study was to determine whether insulin-like growth factor (IGF)-I would increase whole body and muscle glucose uptake in septic rats that are known to be insulin resistant. Animals were infused with either saline, low-dose IGF-I, high-dose IGF-I, or a maximally stimulating dose of insulin for 2 h, and the glucose metabolic response was assessed using a euglycemic clamp in combination with [3-3H]glucose. Under basal conditions, sepsis increased the rates of whole body glucose uptake, glycolysis, and hepatic glucose production. Under euglycemic hyperinsulinemic conditions, septic rats demonstrated a marked insulin resistance as evidenced by the impaired rate of insulin-stimulated glucose uptake and muscle glycogen synthesis. In contrast, the infusion of either dose of IGF-I increased total glucose uptake, glycolysis, and glycogen synthesis in both control and septic rats to the same extent. Furthermore, there was no difference in the IGF-I stimulation of glucose uptake (as determined by [14C]-2-deoxyglucose) in the gastrocnemius, soleus, and heart between control and septic rats. These results indicate that the glucose metabolic response to IGF-I is intact in insulin-resistant septic rats.
Lang
C H
CH
Department of Surgery, State University of New York, Stony Brook, New York 11794-8191, USA.
D000818:Animals; D005947:Glucose / Q000378:metabolism*; D007262:Infusions, Intravenous; D007328:Insulin / Q000494:pharmacology; D007334:Insulin-Like Growth Factor I / Q000494:pharmacology*; D008297:Male; D009132:Muscles / Q000187:drug effects* / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D018805:Sepsis / Q000378:metabolism*
D007328:Insulin; D007334:Insulin-Like Growth Factor I; D005947:Glucose