Early posthypoglycemic insulin resistance in man is mainly an effect of beta-adrenergic stimulation.
The insulin effect following hypoglycemia was studied with the euglycemic clamp technique in seven healthy subjects. Following an initial euglycemic clamp hypoglycemia was induced and after glucose recovery a second clamp was performed. Glucose production (Ra) and utilization (Rd) were studied with [3-3H]glucose. Each subject was studied four times; during infusion of placebo, propranolol, somatostatin, and a control study where hypoglycemia was prevented. Hypoglycemia induced an insulin resistance with a lower steady state glucose infusion rate following the hypoglycemia during placebo as compared to the control study (2.5 +/- 0.5 and 4.8 +/- 1.0 mg/kg min, respectively, P less than 0.05). The insulin resistance was due to an attenuated insulin effect on both inhibition of Ra (impaired by 37%) and stimulation of Rd (impaired by 61%). The insulin-antagonistic effect was completely prevented by propranolol but only partly by somatostatin. Thus, early posthypoglycemic insulin resistance (2.5-3.5 h after hypoglycemia) is a sustained effect mainly due to beta-adrenergic stimulation.
D000328:Adult; D005260:Female; D005947:Glucose / Q000378:metabolism*; D006339:Heart Rate; D006801:Humans; D007003:Hypoglycemia / Q000503:physiopathology*; D007328:Insulin / Q000502:physiology*; D007333:Insulin Resistance; D008297:Male; D011433:Propranolol / Q000494:pharmacology*; D013004:Somatostatin / Q000494:pharmacology; D013997:Time Factors
D007328:Insulin; D013004:Somatostatin; D011433:Propranolol; D005947:Glucose