Glucagon Administration Induces Lowering of Serum T₃ and Rise in Reverse T₃ in Euthyroid Healthy Subjects

Summary

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 < 0.05) between 60-90 minutes. Serum rT₃ rose significantly (P < 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.

Key-Words:

Glucagon, Thyroxine - L-Triiodothyronine - Reverse T ₃