T. Wolthers et al., CALORIGENIC EFFECTS OF GROWTH-HORMONE - THE ROLE OF THYROID-HORMONES, The Journal of clinical endocrinology and metabolism, 81(4), 1996, pp. 1416-1419
GH administration increases energy expenditure, independent of changes
in lean body mass, in healthy, obese, and GH-deficient subjects. This
may be causally linked to the well known GH-induced increase in perip
heral T-4 to T-3 generation, but experimental data are sparse. In this
study we have addressed whether 1) the calorigenic effects of GH admi
nistration could be reproduced by oral supplementation of T-3 in a dos
e selected to mimic the GH-induced increase in peripheral T-3 levels;
and 2) combined GH and T-3 administration have a synergistic effect on
resting energy expenditure (REE). Eight normal male subjects (aged 21
-27 yr; body mass index, 21.11-27.17 kg/m(2)) were randomly studied du
ring four 10-day treatment periods with 1) daily sc placebo injections
and placebo tablets, 2) daily sc GH injections (0.1 IU/kg . day) and
placebo tablets, 3) daily T, administration (40 mu g on even dates, 20
mu g on uneven dates) plus placebo injections, and 4) daily GH inject
ions plus T-3 administration. GH administration increased both free T-
3 (FT3) levels [mean +/- SE, 6.2 +/- 0.3 (control) vs. 7.3 +/- 0.5 (GH
) pmol/L; P < 0.05] and REE [mean +/- SE, 1959 +/- 67 (control) vs. 21
64 +/- 55 (GH) Cal/24 h; P < 0.01]. T-3 administration yielded compara
ble levels of FT3 (7.7 +/- 0.5 pmol/L; T-3 vs. GH, P = 0.37), but did
not increase REE (2015 +/- 48 Cal/24 h; T-3 vs. control, P = 0.23). Co
mbined GH and T-3 administration increased REE to a level higher than
that seen with T-3 alone (2279 +/- 68 Cal/24 h; T-3 vs. GH plus T-3, P
< 0.01). Significant increments in serum levels of insulin-like growt
h factor I and insulin were recorded with GH administration, but not w
ith T-3 alone. Resting heart rate increased to a similar degree after
GH administration and T-3 supplementation, respectively. Tympanic temp
erature remained unaltered in all four studies. The results suggest th
at the calorigenic effect of GH is not mediated solely through increas
ed conversion of T-4 to (3).