T3 and GH have been implicated in the regulation of mitochondrial biogenesis. 
Since thyroid hormone promotes the synthesis of growth hormone, its control of 
human mitochondrial biogenesis could arise through a permissive action on GH 
biosynthesis. This was studied in hypophysectomized rats treated with T3 and/or 
human GH by the continuous infusion of hormone for 6 days from mini-infusion 
pumps implanted sc. Increases in mitochondrial respiration, enzyme activities, 
and protein synthesis were found in isolated liver mitochondria from rats 
receiving T3. In contrast, GH alone had no effect, nor did it increase the 
response to T3. Since it has been argued that mitochondrial biogenesis results 
from a direct interaction (binding) of GH with mitochondria, GH-specific binding 
sites were measured with 125I-bGH, a specific somatogenic receptor ligand, in 
isolated mitochondrial membranes in vitro. In addition, the intracellular 
endocytic uptake of 125I-bGH injected in vivo was compared in purified 
subcellular membrane fractions and mitochondria. No evidence in favour of 
specific GH interaction on mitochondrial membranes was found by either test. It 
is concluded that T3 exerts a direct, rather than permissive, effect on 
mitochondrial biogenesis, and that high affinity binding sites for GH are not 
present in rat liver mitochondria.