Summary
Clonidine, an imidazoline derivative, is an antihypertensive agent which reduces sympathetic
tone by acting in the central nervous system to stimulate alpha-2 adrenoceptors. There
is evidence that dopamine and norepinephrine modulate the secretion of GH. Stimulation
of GH release is a well-known effect of clonidine in man. Obesity is characterized
by an impairment of GH release in response to various stimuli. The aim of this work
is to study GH release in response to alpha-2 adrenoceptors stimulation by clonidine
in obesity. 12 volunteer obese subjects were studied. 10 normal weight subjects, sex
and age matched, were controls. The GH responsiveness was tested with a single oral
dose of clonidine (0.15 mg). Blood was sampled for GH radioimmunoassay at 0', 30',
60', 90', 120', 150', 180'. Serum GH basal levels were not significant different in
obese subjects compared to controls. In obese subjects, no significant changes occurred
in blood GH concentration after clonidine. In normal weight controls, instead, a significant
increase of GH values was reached at 90' (P < 0.05) and at 120' (P < 0.05) after clonidine.
The impairment of GH release after clonidine in obese subjects might be in a reduced
serotonin release or in a failure of the hypothalamic-pituitary system to stimulate
plasma GH caused by a diminished GH releasing factor stimulatory effect or by an excessive
endorphin or somatostatin secretion in obesity.
Key words
Growth hormone - Clonidine - Obesity