Abstract
The aim of the present study was to examine mitochondrial function in cells from persons
with subclinical hypothyroidism and euthyroid controls. The participating persons
were examined clinically and had basal oxygen consumption (VO2 ) determined. The concentrations of thyroid hormones and thyrotropine stimulating
hormone were determined, and mitochondrial function in isolated mononuclear blood
cells was examined by enzymatic methods [citrate synthase activity (CS)] and by flow
cytometry (mitochondrial membrane potential by TMRM fluorescence and mitochondrial
mass by MTG fluorescence). The ratio of T4 /T3 was lowered in subclinical hypothyroidism patients compared to controls (2.5±0.5
vs. 2.9±0.4, p=0.005). VO2 was increased in persons with subclinical hypothyroidism compared to controls (adolescents:
134±27 ml O2 /min*m2 vs. 119±27 ml O2 /min*m2 , p=0.006, adults: 139±14 ml O2 /min*m2 vs. 121±17 ml O2 /min*m2 , p=0.001). The mitochondrial function, represented by citrate synthase activity,
MTG, and TMRM fluorescence were all increased (CS in subclinical hypothyroidism vs.
controls: 0.074±0.044 nmol/mg*min vs. 0.056±0.021 nmol/mg*min, p=0.005; MTG fluorescence
in subclinical hypothyroidism vs. controls: 7 482±1 733 a.u. vs. 6 391±2 171 a.u.,
p=0.027; TMRM fluorescence in subclinical hypothyroidism vs. controls: 1 3449±3 807
a.u. vs. 1 1733±4 473 a.u, p=0.04). Our results indicate an increased mitochondrial
stimulation, eventually caused by increased deiodination of T4 to intracellular bioactive iodothyronines in adults and adolescents with subclinical
hypothyroidism.
Key words
hyperthyroidism - subclinical hyperthyroidism - thyroid function - thyroid hormones
References
Correspondence
jkve@regionsjaelland.dk
