Glucagon administration induces lowering of serum T3 and rise in reverse T3 in euthyroid healthy subjects.
Euthyroid sick syndrome is characterized by low serum T3 and raised reverse T3 (rT3). Most of the states with this syndrome are also documented to manifest hyperglucagonemia. Furthermore, several recent studies have suggested that glucagon may play a role in T4 monodeiodination in some of these states such as starvation and uncontrolled diabetes mellitus. Therefore, hyperglucagonemia was induced by intravenous glucagon administration in euthyroid healthy volunteers and thyroid hormone levels were determined at frequent intervals up to six hours. Plasma glucose and insulin rose promptly on glucagon administration, thus establishing the physiologic effect of glucagon. Serum T4, free T4, T3 resin uptake, and TSH concentrations remained unaltered throughout the study period. Serum T3 declined to a significantly low level (P less than 0.05) between 60-90 minutes. Serum rT3 rose significantly (P less than 0.05) by four hours and the rise was progressive till the end of the study period. Therefore, these results suggest that hyperglucagonemia may be one of the factors responsible for lowering of T3 and a rise in rT3 in euthyroid sick syndrome.
D005260:Female; D005934:Glucagon / Q000494:pharmacology*; D006801:Humans; D007328:Insulin / Q000097:blood; D008297:Male; D013997:Time Factors; D014284:Triiodothyronine / Q000097:blood*; D014285:Triiodothyronine, Reverse / Q000097:blood*
D007328:Insulin; D014284:Triiodothyronine; D014285:Triiodothyronine, Reverse; D005934:Glucagon