Open AccessChanges in Sleeping and Basal Energy Expenditure and Substrate Oxidation Induced by Short Term Thyroxin Administration in Man
Author(s) -
Bracco David,
Morin Odette,
Liang Hong,
Jéquier Eric,
Burger Albert G.,
Schutz Yves
Publication year - 1996
Publication title -
obesity research
Language(s) - English
Resource type - Journals
eISSN - 1550-8528
pISSN - 1071-7323
DOI - 10.1002/j.1550-8528.1996.tb00539.x
Subject(s) - endocrinology , medicine , heart rate , excretion , energy expenditure , thyroid , basal metabolic rate , hormone , basal (medicine) , blood pressure , insulin
The present study was designed to explore the thermogenic effect of thyroid hormone administration and the resulting changes in nitrogen homeostasis. Normal male volunteers (n=7) received thyroxin during 6 weeks. The first 3‐week period served to suppress endogenous thyroid secretion (180μg T 4 /day). This dose was doubled for the next 3 weeks. Sleeping energy expenditure (respiratory chamber) and BMR (hood) were measured by indirect calorimetry, under standardized conditions. Sleeping heart rate was continuously recorded and urine was collected during this 12‐hour period to assess nitrogen excretion. The changes in energy expenditure, heart rate and nitrogen balance were then related to the excess thyroxin administered. After 3 weeks of treatment, serum TSH level fell to 0.15 mU/L, indicating an almost complete inhibition of the pituitary‐thyroid axis. During this phase of treatment there was an increase in sleeping EE and sleeping heart rate, which increased further by doubling the T 4 dose (ΔEE: +8.5 ± 2.3%, Δ heart rate +16.1 ± 2.2%). The T 4 dose, which is currently used as a substitutive dose, lead to a borderline hyperthyroid state, with an increase in EE and heart rate. Exogenous T 4 administration provoked a significant increase in urinary nitrogen excretion averaging 40%. It is concluded that T 4 provokes an important stimulation of EE, which is mostly mediated by an excess protein oxidation.