Context. Leptin release is regulated by factors other than fat mass alone. Previous observations provide indirect evidence for an inhibitory effect of dopaminergic neurotransmission on leptin secretion. This study was done to establish the effect of bromocriptine treatment on circadian plasma leptin concentrations in obese humans.

Objective. To study the acute effects of bromocriptine (a D2R agonist) on circadian leptin levels in obese women, while body weight and caloric intake remained constant.

Design. Prospective, single blind, cross-over study (2004).

Setting. Clinical Research Center

Participants. Eighteen healthy obese women (BMI 33.2 ± 0.6 kg/m²) were studied twice in the early follicular phase of their menstrual cycle.

Intervention(s). Treatment with bromocriptine (B) or placebo (Pl) for eight days

Main Outcome Measure(s). Blood was collected during 24 h at 20-minute intervals for determination of leptin concentrations at the last day of medical treatment (B or Pl). Mean 24 h serum concentrations were determined for insulin, glucose, free fatty acids and triglycerides.

Results. Short-term treatment with bromocriptine reduced leptin concentration (Pl 33.6 ± 2.5 vs. B 30.5 ± 2.5 ng/L, P = 0.03). FFA concentrations were increased by bromocriptine treatment. The increase of FFA was inversely related with the decline of leptin levels. The decline of glucose, insulin or prolactin concentrations in response to bromocriptine was not correlated with the reduction of leptin.

Conclusion. Activation of dopamine D2 receptors by bromocriptine lowers circulating leptin levels in obese women, which suggests that dopaminergic neurotransmission is involved in the control of leptin release in humans.