CONTEXT: A profound reduction of spontaneous as well as stimulated GH secretion has been consistently observed in obesity. Dopamine promotes GH release through activation of dopamine D2 receptors (D2Rs). Dopamine D2R availability in the brain is reduced in obese humans in proportion to body adiposity. We hypothesized that impaired dopamine D2R signaling is mechanistically involved in the deficient GH secretion associated with obesity.
OBJECTIVE: To test this hypothesis, we studied the effect of short-term bromocriptine (B) (a D2R agonist) treatment on spontaneous 24-h GH secretion in obese women, while body weight and caloric intake remained constant. DESIGN: This was a prospective, fixed order, cross-over study. SETTING: The study was performed in the Clinical Research Center at Leiden University Medical Center. PARTICIPANTS: There were 18 healthy obese women (body mass index 33.2 +/- 0.6 kg/m2) studied twice in the early follicular phase of their menstrual cycle. INTERVENTION(S): Eight days of treatment with B and placebo (Pl) was performed. MAIN OUTCOME MEASURE(S): Blood was collected during 24 h at 10-min intervals for determination of GH concentrations. GH secretion parameters were calculated using deconvolution analysis.
-------The figure really shows what's going on here, so I omitted the rest of the abstract. You can see that giving bromcriptine restored the pulsatile secretion of growth hormone in these obese patients. Basal GH secretion was not enhanced and also IGF-1 levels were not significantly changed.
Interestingly, other studies have been done looking at the effects of bromocriptine on other parameters. Theses studies showed that 24-hour glucose, insulin, and leptin levels were significantly reduced, whereas FFAs were enhanced after bromocriptine treatment.
J Clin Endocrinol Metab. 2006 Aug;91(8):3236-40.
Am J Physiol Endocrinol Metab. 2006 Nov;291(5):E1038-43.