Recently, a family of uncoupling protein (UCP) genes has been discovered. The role
of these genes is unknown, but it has been suggested that they are involved in regulating
resting metabolic rate. In this study, we hypothesised that thyroid hormone status
may influence the expression of UCP2 mRNA. The adipose tissue levels of UCP2 mRNA
were measured in eight female subjects before and after treatment for thyrotoxicosis.
All subjects in the hyperthyroid condition had markedly enhanced plasma levels of
thyroxine (62.0 ± 6.9 vs. 17.9 ± 1.7, p = 0.012) and tri-iodothyronine (37.9 ± 6.9
vs. 5.9 ± 0.9, p = 0.012), accelerated heart rate (94 ± 7 vs. 69 ± 5, p = 0.012),
decreased BMI (24.5 ± 1.9 vs. 25.1 ± 1.9, p = 0.025) and decreased percentage body
fat (32.8 ± 4.4 vs. 37.1 ± 4.5, p = 0.018), as compared to the euthyroid state. Using
RT-competitive-PCR, the UCP2 mRNA levels were found to be 2.5-fold upregulated in
hyperthyroidism (10.4 ± 1.7 vs. 4.2 ± 1.3 amol/µgRNA, p = 0.012). In contrast, no
difference in expression levels of the reference gene 18SrRNA was seen in the hyperthyroid
versus the euthyroid state (317 ± 49 vs. 279 ± 25 amol/µgRNA, p = 0.48) but the difference
in UCP2 mRNA levels between the hyper- and euthyroid state remained when UCP2 was
related to 18SrRNA (p = 0.012). In conclusion, thyrotoxicosis markedly increases the
expression of UCP2 mRNA in adipose tissue, which suggests a role for thyroid hormones
in the regulation of this uncoupling protein in man.
Key words
Fat Cell - mRNA - Polymerase Chain Reaction - Thermogenesis - Thyrotoxicosis
